18. 4 – 3 – 2 – 1 – 0 – Vasoespasmo sintomático Resangrado I I I I I I I I I I I I 0 1 2 3 4 5 6 7 8 9 10 11 12 Días después de HSA % probabilidad Complicaciones
41. Los anestésicos volátiles ( > 1 MAC) deterioran la autorregulación en un grado dependiente de la dosis . Anesthesiology Clin N Am 2002; 20: 377–388 Surgical Neurology 66 (2006) 382–388 Anestésicos
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Notas del editor
Incidentally discovered IAs have an annual rate of rupture around 0.5% to 2%, 80% HSAE se debe a ruptura de aneurismas Puede haber subdiagnostico, no reciben atencion, o mal diagnostico from 2.0 cases per 100 000 population in China to 22.5 per 100 000 in Finland.13 Community-based studies reported an incidence that ranged from 8.1 per 100 000 in Australia and New Zealand to 23 per 100 000 in Japan.14–16 One Japanese study suggested that if early deaths attributed to SAH were included, the rate would be as high as 32 per 100 000.17
El pico es a los 55 años. are associated with IA development. Ehlers-Danlos syndrome type IV, adult polycystic kidney disease, fibrous dysplasia, neurofibromatosis type 1, Marfan syndrome [15], andAVMare associated with IA [16]. With the development of noninvasive diagnostic methods, screening for IA has become easier [17]. Screening is indicated for patients with adult polycystic kidney disease [18] and those who have two immediate relatives with IA [19]. Certain factors increase risk of SAH in patients with IA. About 75% of patients with SAH are women [20]. Men with IA tend to have a higher risk of SAH before the fifth decade of life, after which women have a higher risk of rupture [21]. The mean age of patients with SAH from IA is 52 years, and incidence of hemorrhage increases with age until at least the eighth decade of life [21,22]. Rupture can also occur during pregnancy, most frequently during the thirtieth to fortieth week or in the postpartum period. Cigarette smoking [23], hypertension [24], and moderate to heavy alcohol consumption (especially binge drinking) [25] increase the risk of SAH. En la persona que ya tuvo un *aneurisma el riesgo de formación de uno nuevo va de 1 a 2 por año.
: coágulo grueso SA y hemorragia biventricular.
10 % antes de la atencion medica
Arterias: dos carotidas internas (anterior) y dos vertebrales (posterior), que se anastomosan. Las CI dan ramas a la oftalmicas y despues a la comunicante poserior y luego a la coroidal anterior y finalmente se bifurca en la cerebral anterior (unida la de cada lado por la comuninante anterior) y la cerebral media (que es pobre de anastomosis, por lo cual es suceptible a la isquemia). Las vertebrales dan las cerebelares posteriores, que luego se anastomosan para formar las basilares. Estas finalmente se bifurcan y originan las cerebrales posteriores. 90% circulación anterior 39% CoA. 30% carótida interna. 22% cerebral media. 8% circulación posterior Tamaño Pequeños: 78% < 12 mm Grandes: 20% 12- 24 mm Gigantes: 2% > 24 mm Múltiples: 5.4 a 33%
Baja compliance cerebral
esta es curva de elasticidad: cambios de presión, ante determinados cambios de volumen (se llega a un punto en que ante cambios mínimos de volumen ocurren grandes cambios de presión). la distensibilidad es lo contrario: cambios de volumen ante cambios de presión (el cerebro tiene mucha elasticidad, poca distensibilidad)
Aumento súbito de la PIC iguala PAM – paro circulatorio cerebral (pérdida de consciencia) Dilataciones vasculares adquiridas Cambios degenerativos de la muscular Debilidad capa elástica
La HSA usualmente se acompaña de disminución del flujo sanguíneo cerebral (FSC) y de la tasa metabólica cerebral (TMC). Se altera la autorregulación cerebral, desplazándose la curva a la derecha, y esto acompañado de vaso espasmo cerebral puede llevar isquemia cerebral. Es por esto es tan importante una adecuada presión de perfusión cerebral (PPC) en el manejo de la HSA. La reactividad vascular cerebral a cambios en la presión arterial de dióxido de carbono (PCO2 ) usualmente esta preservada en la HSA, excepto en los pacientes con pobre estado neurológico, por lo tanto, la hiperventilación puede ser una medida para disminuir la PIC y el volumen sanguíneo cerebral de forma temporal.
En general a más alto grado clínico, más probabilidad de vaso espasmo cerebral, elevada PIC, daño de la autorregulación cerebral, daño de la reactividad al CO2, arritmias y disfunción cardiaca, hipovolemia e hiponatremia Mortalidad 1 y 2: 5 %, 3 10%, 3 : 35% y 5 50%
1 y 2 tambien se espera que tienen intactos la reactividad al co2, por lo que la hiperventilacion puede ser una medida terapeutica en ellos. Ademsa un gllasgow de 8 se relaciona con HEC
Debe ser obtenido en forma temprana en todos los pciantes porque la cantidad de sangrado observado es el marcador mas confiable de resultado, y ademsa da una idea del plan a seguir Sensibilidad de 98 a 100 en las primeras 12 horas y baja a 93 cuando se hace las primeras 24 horas y de 57 a 98% a los primeros 7 dias. Todos los pacientes 98% diagnóstico a las 12 h Hematomas, hidrocefalia, edema cerebral Predicción de vasoespasmo Pronóstico
El mejor predictor pronostico, predice vasoespasmo
En una revisión sistemática de la literatura reciente mostró que la terapia con calcioantagonistas redujo el riesgo de resultado desfavorable (déficit neurológico tardío o infarto cerebral confirmado por imágenes) con un riesgo relativo (RR) de 0,82, intervalo de confianza (IC) del 95% (0,72 - 0,93), reducción del riego absoluto de 5,1%, y un número necesario a tratar (NNT) de 20. Cuando se utilizó nimodipina oral como único calcioantagonista el RR de eventos adversos fue de 0,7 (0,58-0,84). Para todos los calcioantagonistas el RR de muerte fue 0,9 (IC de 95%: 0,76 - 1,07). Para nimodipina el RR de déficit neurológico tardío 0,65 (IC de 95%: 0,51 - 0,82), con un NNT de 8 y el de infarto confirmado por imágenes de 0,7 (IC de 95%: 0,58 - 0,85), con un NNT de 757,58.
The daily percentage probability for the development of symptomatic vasospasm or re-bleeding after subarachnoid hemorrhage. Day 0 denotes onset of subarachnoid hemorrhage.
Más frecuente primeras 2 semanas Probabilidad 4% el primer día Luego 1.5% día, hasta día 15 (20%). 50% a los 6 meses. 3% por cada año. Tratamiento quirúrgico temprano vs. tardío Iguales resultados: 0 a 3 días y 11 a 14 días Mortalidad: 20% Buen resultado: 60% Cuando hay resangrado es el peor pronostico neurologico. Los facorres de riego asociados son ; la magnitud del sangrado inicial, la demora entre los sintomas y la consulta, la HTA al ingreso y las caracteristicas del aneurisma. Previous studies delineated several patterns of rebleeding.134,135 In the prospective Cooperative Aneurysm Study,136 rebleeding was maximal (4%) on the first day after SAH and then constant at a rate of 1% per day to 2% per day over the subsequent 4 weeks. Several prospective follow-up cohorts137,138 have demonstrated that the risk of rebleeding with conservative therapy is between 20% and 30% for the first month after hemorrhage and then stabilizes at a rate of 3% per year.139 Rebleeding occurs most comonly during the first 24 hours following initial SAH. Recurrent aneurysmal hemorrhage is a devastating complication associated with increased morbidity and mortality. Because of the incidence of rebleeding with conservative management of SAH, early aneurysm clipping (days 0–3) is currently recommended for patients who are alert on admission HTA mayor de 160 se relaciona con mayor risgo de sangrado… Hypertension is a common risk factor for hemorrhagic stroke and increases the risk of serious complications if not effectively controlled during the early post-event phases. It is logical to conclude that elevated or rapidly changing blood pressure may increase the likelihood of rebleeding following subarachnoid hemorrhage. However, no clear benefit of antihypertensive therapy to reduce the incidence of rebleed in has been established. As a result, no specific antihypertensive recommendations were made in the 1994 Guidelines. Algunos centros no manejan HTA si la Pam no supera los 130, miestras que otros tienen como metas mantener sistolicas de 140 a 160 maximo. Blood pressure should be monitored and controlled to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I, Level of Evidence B). 2. Bedrest alone is not enough to prevent rebleeding after SAH. It may be considered a component of a broader treatment strategy, along with more definitive measures (Class IIb, Level of Evidence B). 3. Although older studies demonstrated an overall negative effect of antifibrinolytics, recent evidence suggests that early treatment with a short course of antifibrinolytic agents combined with a program of early aneurysm treatment followed by discontinuation of the antifibrinolytic and prophylaxis against hypovolemia and vasospasm may be reasonable (Class IIb, Level of Evidence B), but further research is needed. Furthermore, antifibrinolytic therapy to prevent rebleeding may be considered in certain clinical situations, eg, in patients with a low risk of vasospasm and/or a beneficial effect of delaying surgery (Class IIb, Level of Evidence B).
Cerebral vasopasm is a major cause of morbidity and mortality in SAH patients Angiographic evidence of vasospasm can be detected in up to 70% of patients. However, clinical vasospasm with ischemic deficits is observed in approximately 30% of patients, most often between days 4–12, with a peak at 6–7 days following SAH [10]. The diagnosis of vasospasm is confirmed by angiography. The transcranial Doppler (TCD) is a safe, repeatable, noninvasive method to identify and quantify vasospasm, and can be used to evaluate the effectiveness of various therapies. The mechanism responsible for vasospasm is unknown; however, structural and pathologic changes have been demonstrated in the vessel wall. There is also evidence that vasospasm after SAH correlates with the amount of blood in the subarachnoid space, and removal of extravasated blood decreases the occurrence and severity of ischemic deficits. The component in blood implicated in causing cerebral arterial vasospasm is oxyhemoglobin. Another method for treating symptomatic vasospasm is cerebral angioplasty. Transluminal angioplasty can be used to dilate constricted major cerebral vessels in patients refractory to conventional treatmen These procedures are usually performed under general anesthesia to minimize movement and permit accurate placement of the intraarterial balloon used to dilate the cerebral vessels. The risks of angioplasty include aneurysm rupture, intimal dissection, vessel rupture, ischemia, and infarction
El nimodipino, es un calcio antagonista, mejora los resultados en HSA (53). Se usa de dosis de 60mg cada 4 horas VO o por sonda nasogástrica, debe ser iniciado en el momento del ingreso y continuado por 21 días. Si una adecuada presión arterial sistólica (130- 150mmHg) no puede ser mantenida, prima en manejo de la presión sobre la administración de nimodipino. Comment. Hypovolemia and hypotension after aSAH are strongly linked to adverse outcome and should be avoided in all patients. The existing data do not support the prophylactic use of triple-H therapy in patients with aSAH who do not have clinical evidence of vasospasm. In patients with symptomatic vasospasm,hemodynamic augmentation may reverse neurologic deterioration; however, an adequately powered randomized trial is needed to test the hypothesis that triple-H therapy has a favorable effect on neurologic outcomes or survival and is safe when compared with a strategy of normovolemia and normotension. Further study is needed to better understand the effects of increased cardiac output, as opposed to hypertensive therapy, on CBF and on the reversal of symptomatic vasospasm. At this time, TBA and intraarterial vasodilators administration are reasonable options in treating vasospasm refractory to medical management. However,the relative efficacy and harm of TBA vs.medical management needs further substantiation. This might take the form of a randomized trial comparing immediateangioplasty vs. triple-H therapy in patients who have developed symptomatic vasospasm. In patients with symptomatic vasospasm in whom triple-H therapy and endovascular options have either failed or are contraindicated, consideration should be given to IABC or to neuroprotective interventions such therapeutic hypothermia and pentobarbital coma (see below).
The therapeutic goal of triple-H therapy is to increase CBF, increase CPP, and improve the rheological blood characteristics. For this purpose, systolic arterial pressure is increased (by administration of i.v. fluid or cardiovasoactive drugs) to approximately 120–150 mm Hg in unclipped and 160–200 mm Hg in clipped aneurysms; central venous pressure is maintained at 8–12 mm Hg (or pulmonary artery wedge pressure at 15–18 mm Hg); and haematocrit is decreased to approximately 0.3–0.35. Most
Objetivos: Analgesia y sedacion de ser necesario, si reqiere use opiodes. Evite simepre hiperglicemia porque esta se relaciona con malos resultados neurologicos Mantenga siempre temperaturas por debajo de 37.5 Controle estado hidroelectrolitico. Profilaxis de convulsiones con fenitina 20 por kilo hasta que se clampe. Proteccio gastrica a todos con cualquier cosa. Mantener presion sistolica por debajo de 160 Blood pressure should be maintained within normal limits, and if necessary, intravenous antihypertensive agents such as labetalol and nicardipine can be used.23 Once the aneurysm is secured, hypertension is allowed, but there is no agreement on the range. Analgesia is often required, and reversible agents such as narcotics are indicated. Two important factors that are associated with poor outcome are hyperglycemia and hyperthermia, and both should be corrected.39,40 Prophylaxis of deep venous thrombosis should be instituted early with sequential compressive devices, and subcutaneous heparin should be added after the aneurysm is treated. Calcium antagonists reduce the risk of poor outcome from ischemic complications, and oral nimodipine is currently recommended.41 Prolonged administration of antifibrinolytic agents reduces rebleeding but is associated with an increased risk of cerebral ischemia and systemic thrombotic events.42 Early treatment of aneurysms has become the mainstay of rebleeding prevention, but antifibrinolytic therapy may be used in the short term before aneurysm treatment. Airway and cardiovascular system Monitor closely in intensive care unit or preferably in neurologic critical care unit Environment Maintain reduced noise level and limit visitors until aneurysm is treated Pain Administer morphine sulfate (2–4 mg IV every 2–4 hr) or codeine (30–60 mg IM every 4 hr) Gastrointestinal prophylaxis Administer ranitidine (150 mg PO twice daily or 50 mg IV every 8–12 hr) or lansoprazole (30 mg PO daily) Deep venous thrombosis prophylaxis Use thigh-high stockings and sequential compression pneumatic devices; administer heparin (5000 U SC three times daily) after treatment of aneurysm Blood pressure Keep systolic blood pressure at 90–140 mm Hg before aneurysm treatment, then allow hypertension to keep systolic blood pressure <200 mm Hg Serum glucose Maintain level at 80–120 mg/dl; use sliding scale or continuous infusion of insulin if necessary Core body temperature Keep at ≤37.2°C; administer acetaminophen (325–650 mg PO every 4–6 hr) and use cooling devices if necessary Calcium antagonist Administer nimodipine (60 mg PO every 4 hr for 21 days) Antifibrinolytic therapy (optional) Administer aminocaproic acid (first 24–48 hr, 5 g IV, followed by infusion at 1.5 g/hr) Anticonvulsants Administer phenytoin (3–5 mg/kg/day PO or IV) or valproic acid (15–45 mg/kg/day PO or IV) Fluids and hydration Maintain euvolemia (CVP, 5–8 mm Hg); if cerebral vasospasm is present, maintain hypervolemia (CVP, 8–12 mm Hg, or PCWP, 12–16 mm Hg) Nutrition Try oral intake (after evaluation of swallowing); for alternative routes, enteral feeding preferred Other treatment Surgical clipping Perform procedure within first 72 hr Endovascular coiling Perform procedure within first 72 hr Common complications Hydrocephalus Insert external ventricular or lumbar drain Rebleeding Provide supportive care and emergency treatment of aneurysm Cerebral vasospasm Maintain hypervolemia or induced hypertension with phenylephrine, norepinephrine, or dopamine; provide endovascular
Terapia endovascula Menos secuelas Menos convulsiones Mejor en ancianos Mejor en circulación posterior Más resangrado Morbilidad 3.7% - 5.3% Mortalidad 1.1 – 1.5% Ruptura 1 – 2.7% Mortalidad 0 – 40% Cirugia Hematoma intraparenquimatoso Cuello ancho Efecto de masa Morbilidad 4 - 11% Mortalidad 1 – 3% Ruptura 6 – 13% ISAT international subaracnoid aneurysm trial, aletatorizo 2134 pacientes para manejo po cx o po tev, encontro una disminucion de 22 % de mortalidad a una ñso y el beneficio se mantuv a 7 años. Los de tev mas resangrado.
Continuar calcio antagonistas, estroides y anticonvulsivantes si los viene recibiendo. Evaluar historia cardiovascular y EKG. Determinar la necesidad de ecocargiograma, enzimas cardiacas, monitorio perioperatorio. Premedicar: HYH 3 y 4 no reqiuerem. Los demas si tiene un nivel elevado de ansiedad, deben recibir dosis bajas de benzodiacepinas, en forma cuidadosa para no generar hipercapnia. Si hay alteracion del estado de consciencia se recomienda proquinetico.
Alteraciones STST, T, QT, arritmias ventriculares Correlación con sangrado Resolución 10 días - 6 sem Aturdimiento miocárdio cardiogénico: se relaciona con el grado de deterioro neurologico, mas que con los hallazgos en el ekg, se creee que es debido a liberacion masiva de catecolaminaas por la HSAE, con sobre carga de calcio y necrosis de los kiocitos. Puede ser tan grave que lleve a falla ventricular y EAP y muerte. la mayoría de estos cambios electrocardiográficos son de origen neurogénico más que cardiogénico y el dilema es, si la sospecha de lesión cardiovascular con lleva o no a retardar la cirugía. En estos casos especiales se deben realizar enzimas miocárdicas y evaluar la función ventricular con ecocardiografía, con el fin de hacer cambios en el monitoreo intraoperatorio, como la utilización del catéter de la arteria pulmonar o la realización del procedimiento por terapia endovascular. La decisión de posponer la cirugía se debe sopesar con el riesgo.de re sangrado y vaso espasmo. Electrolyte abnormalities frequently occur secondary to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion or diabetes insipidus. Hyponatremia is the most common electrolyte disturbance detected, and is often associated with a high urinary sodium and osmolality, which is expected with SIADH. Unlike a patient with SIADH, however, the patient with SAH usually has a contracted intravascular volume despite hyponatremia. This cerebral saltwasting syndrome may be caused by release of an atrial natriuretic factor from the damaged brain. The recommended therapy is to maintain normovolemia with isotonic saline solutions. Other factors contributing to intravascular volume contraction in these patients are supine diuresis secondary to increased thoracic blood volume, negative nitrogen balance, decreased erythropoiesis, increased catecholamine levels, and iatrogenic blood loss. Fluid balance and electrolyte abnormalities should be corrected prior to surgery. Electrocardiographic abnormalities are commonly associated with ruptured cerebral aneurysms [25]. The ECG changes include ST-segment depression or elevation, T-wave inversion or flattening, U-waves, prolonged Q-T intervals, and dysrhythmia. The ECG changes are not necessarily associated with increased operative morbidity and mortality or consistent increases in serum myoglobin or creatine kinase. They usually resolve within 10 days following SAH, and require no special treatment. When indicated, cardiac troponin-I levels should be drawn to determine the clinical significance of these abnormalities [26]. When cardiac dysrhythmia and occasional frank subendocardial ischemia result in cardiac failure, appropriate treatment must be instituted. ECG abnormalities (e.g. QTc prolongation, repolarization abnormalities) have been reported in 25–100% of cases,40 101 123 along with an increase in serum concentration of cardiac troponin in 17–28% and of creatine kinase MB isoenzyme in 37%,11 22 109 123 and left ventricular dysfunction in 8–30% of cases.20 47 124 The most severe form of cardiac injury associated with SAH is the syndrome of neurogenic-stunned myocardium, which is characterized by reversible left ventricular systolic dysfunction, cardiogenic shock, and pulmonary oedema.46
Electrolyte abnormalities frequently occur secondary to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion or diabetes insipidus. Hyponatremia is the most common electrolyte disturbance detected, and is often associated with a high urinary sodium and osmolality, which is expected with SIADH. Unlike a patient with SIADH, however, the patient with SAH usually has a contracted intravascular volume despite hyponatremia. This cerebral saltwasting syndrome may be caused by release of an atrial natriuretic factor from the damaged brain. The recommended therapy is to maintain normovolemia with isotonic saline solutions. Other factors contributing to intravascular volume contraction in these patients are supine diuresis secondary to increased thoracic blood volume, negative nitrogen balance, decreased erythropoiesis, increased catecholamine levels, and iatrogenic blood loss. Fluid balance and electrolyte abnormalities should be corrected prior to surgery. Electrocardiographic abnormalities are commonly associated with ruptured cerebral aneurysms [25]. The ECG changes include ST-segment depression or elevation, T-wave inversion or flattening, U-waves, prolonged Q-T intervals, and dysrhythmia. The ECG changes are not necessarily associated with increased operative morbidity and mortality or consistent increases in serum myoglobin or creatine kinase. They usually resolve within 10 days following SAH, and require no special treatment. When indicated, cardiac troponin-I levels should be drawn to determine the clinical significance of these abnormalities [26]. When cardiac dysrhythmia and occasional frank subendocardial ischemia result in cardiac failure, appropriate treatment must be instituted. ECG abnormalities (e.g. QTc prolongation, repolarization abnormalities) have been reported in 25–100% of cases,40 101 123 along with an increase in serum concentration of cardiac troponin in 17–28% and of creatine kinase MB isoenzyme in 37%,11 22 109 123 and left ventricular dysfunction in 8–30% of cases.20 47 124 The most severe form of cardiac injury associated with SAH is the syndrome of neurogenic-stunned myocardium, which is characterized by reversible left ventricular systolic dysfunction, cardiogenic shock, and pulmonary oedema.46
Electrolyte abnormalities frequently occur secondary to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion or diabetes insipidus. Hyponatremia is the most common electrolyte disturbance detected, and is often associated with a high urinary sodium and osmolality, which is expected with SIADH. Unlike a patient with SIADH, however, the patient with SAH usually has a contracted intravascular volume despite hyponatremia. This cerebral saltwasting syndrome may be caused by release of an atrial natriuretic factor from the damaged brain. The recommended therapy is to maintain normovolemia with isotonic saline solutions. Other factors contributing to intravascular volume contraction in these patients are supine diuresis secondary to increased thoracic blood volume, negative nitrogen balance, decreased erythropoiesis, increased catecholamine levels, and iatrogenic blood loss. Fluid balance and electrolyte abnormalities should be corrected prior to surgery. Electrocardiographic abnormalities are commonly associated with ruptured cerebral aneurysms [25]. The ECG changes include ST-segment depression or elevation, T-wave inversion or flattening, U-waves, prolonged Q-T intervals, and dysrhythmia. The ECG changes are not necessarily associated with increased operative morbidity and mortality or consistent increases in serum myoglobin or creatine kinase. They usually resolve within 10 days following SAH, and require no special treatment. When indicated, cardiac troponin-I levels should be drawn to determine the clinical significance of these abnormalities [26]. When cardiac dysrhythmia and occasional frank subendocardial ischemia result in cardiac failure, appropriate treatment must be instituted. ECG abnormalities (e.g. QTc prolongation, repolarization abnormalities) have been reported in 25–100% of cases,40 101 123 along with an increase in serum concentration of cardiac troponin in 17–28% and of creatine kinase MB isoenzyme in 37%,11 22 109 123 and left ventricular dysfunction in 8–30% of cases.20 47 124 The most severe form of cardiac injury associated with SAH is the syndrome of neurogenic-stunned myocardium, which is characterized by reversible left ventricular systolic dysfunction, cardiogenic shock, and pulmonary oedema.46
Alteraciones en electrolitos e hiperglicemia se relaionan con pobres desenlaces.
Basica que incluya EGK de 5 derivadas, con analizador de ST. Diuresis, temperatura y relajacion. PAI es obligatoria. CVC: no es mandatorio, aunque en elgunos centros es de rutina, se recomienda basicamente en los mas enfermitos (disfuncion miocardica, vasoespasmo, riesgo de presentarlo.) Trasnductor en la base del craneo para medir la PPC SVY: aporte y demanda de oxigeno en forma global, invertigación en paciente con HSA, no probada su utilidad en monitoreo intraoperatorio. Electorencefalograma: permite determinar la tolerancia al pinzamiento y protección cerebral al usar pentotal. Potenciales evocados: funcion neuronal durante el pinzamiento, si aumento tiempo de conduccion o perdida del registro: riesgo de lesion neurológica. Dopler transcraneano: monitoria del FSC durante la anestesia, evalua efecto de hierventilacion, hipotensión y presencia de vasoespasmo
The anesthetic goals for intracranial aneurysm surgery are to avoid aneurysm rupture, maintain cerebral perfusion pressure and transmural aneurysm pressure, and provide, a ‘‘slack’’ brain. Patients in WFNS scale I or II who appear anxious should receive premedication. Cerebral perfusion pressure (CPP) is maintained by using drugs in doses that avoid sudden or profound decreases in systemic blood pressure or increases in ICP. To minimize the risk of hypertension and aneurysmal rupture during induction of anesthesia, intravenous lidocaine and the beta-adrenergic antagonist (esmolol) or labetalol are recommended. Following induction, ventilation is mechanically controlled to maintain normocarbia, if ICP is normal. If intracranial hypertension is present, the PaC02 is lowered to 30–35 mmHg. A deep plane of anesthesia must be established prior to insertion of head pins, scalp incision, turning the bone flap, and opening the dura to avoid a hypertensive response . When intracranial hypertension is present, anesthesia should be deepened with additional doses of thiopental and fentanyl until the skull is opened. Several techniques can be instituted during aneurysm surgery to provide a ‘‘slack’’ brain and facilitate dissection. These are hyperventilation of the lungs, osmotic diuresis, barbiturate administration, and CSF drainage during the procedure. Controlar gradiente de presión transmural del aneurisma Adecuada PPC y oxigenación Evitar variaciones en PIC Evitar daño secundario Condiciones quirúrgicas Despertar rápido y suave Tener en cuenta tambien si hay Riesgo de VAD o riego de aspiración (0.05%)
The two variables that require considerable attention are CPP and TMPG of the aneurysm. CPP is calculated as the difference between mean arterial pressure (MAP) and ICP (CPP¼MAP2ICP). The TMPG of the aneurysm is calculated as the difference between the pressure within the aneurysm (equal to MAP) and the pressure outside the aneurysm (equal to ICP) (TMPG¼MAP2ICP). Thus,TMPG and CPP are governed by the same variables (MAP and ICP). The objectives are to maintain TMPG as low as possible to reduce the risk of aneurysm rupture, and CPP as high as needed to provide adequate cerebral oxygenation. Overall, it seems sensible to maintain blood pressure at preoperative levels until the aneurysm is secured. If treatment of the increased ICP becomes necessary before opening of the dura, such treatment should not be overly aggressive because an abrupt decrease in ICP causes an equally abrupt increase in the TMPG of the aneurysm. Opening of the dura in the presence of markedly elevated ICP may have the same detrimental effect.
Mantenimiento de la anestesia Cualquier IV (excepto ketamina) Etomidato convulsión Protección del edema cerebral Halogenado subMAC, hiperventilación Control PIC Anticiparse a estímulos dolorosos
Pre acondicionamiento Isquémico Hipotermia Barbitúricos Estatinas Antihipertensivos Oxigeno hiperbatico Ischaemic preconditioning may be observed in patients with recurrent transient ischaemic attacks.91 Determination of the exact molecular mechanisms involved in ischaemic preconditioning is under active investigation. Depending on the organ and preconditioning stimulus, ischaemic precond itioning may induce tolerance within minutes or days and is effective for hours or days. Rapid ischaemic preconditioning appears to involve activation and phosphorylation of ATPsensitive Kþ channels in cell membranes and inner mitochondrial membranes.92 Delayed preconditioning may result from induced gene expression or protective proteins. Delayed preconditioning in the brain often requires multiple applications of the trigger daily before ischaemia and may protect the brain for a week. Various important pathways have been identified and have been comprehensively reviewed. Studies to determine the relevance of ischaemic preconditioning in humans are difficult to perform, and only two retrospective studies are available suggesting the protection of recurrent transient ischaemic attacks in stroke patients. Opioids limit the need for higher-dose volatile anesthetics [67] and may be useful in avoiding cerebral vasodilation and increased CBF. With their minimum alveolar concentration-sparing effect opioids are useful adjuncts for blood pressure control during aneurysm surgery. During maintenance of anesthesia opioids can be administered as intermittent boluses or by continuous infusion. If rapid emergence is desired to perform an early neurologic examination, a short-acting agent like remifentanil should be considered [68]. The short half-life of this agent and the induction of acute opioid tolerance may be associated, however, with severe early postoperative incision pain [69].
Adversosíneo aumento inicial PIC Hiponatremia, hiperkalemia, acidosis Evitar caída brusca de PIC
No pasar el limite de tiempo, si se necesita se debe soltar, esperar 5 minutos minimo para que se de la reperfusion y volver a clipar. TPS 3–5 mg/kg, manitol Hipotermia no. Potencial daño del vaso Fenilefrina dosis de 25 az 100 ug o labetalos bolitos de 10 mg deliberate hypotension during aneurysm dissection, the risk-benefit ratio must be assessed for each patient [27]. The potential benefit of hypotension must be weighed against the risk of causing cerebral ischemia or ischemia to other organs. Patients with a history of cardiovascular disease, occlusive cerebrovascular disease, intracerebral hematoma, fever, anemia, and renal disease are not good candidates for induced hypotension. Such patients should only be subjected to moderate reductions in systemic blood pressure (20–30 mmHg), if at all. The most commonly used agents to induce hypotension are sodium nitroprusside, isoflurane, and esmolo temporary clipping [28,29]. The temporary occlusion of a feeding artery produces an acute reduction in focal blood flow and a slack aneurysm, thus eliminating the need for induced hypotension and its systemic effects. Depending on the location of the aneurysm, either somatosensory evoked potentials or brain stem auditory evoked potentials can be used to monitor the safety of temporary occlusion [ When the aneurysm is secured, intraoperative fluid deficits are replaced and additional volume is administered. At the time of aneurysm dissection, blood is available for transfusion in case the aneurysm ruptures. A bolus of thiopental (3–5mgkg1) may be given before temporary occlusion of a major intracranial vessel and before aneurysm clipping. If temporary occlusion lasts longer than 10 minutes, recirculation should be established, and additional thiopental administered before reapplying the temporary clip. Following aneurysm clipping, the central venous pressure and pulmonary capillary wedge pressure are raised to 10–12 mmHg or 12–18 mmHg, respectively, with crystalloid, colloid, or blood. A postoperative hematocrit between 30–35% is desirable.
Mantener ppc: quiere decir; no permita hipotension pensando reducir el seangrado, mantega normo o hipertension. Inmediatamente empiece lev a chorro y trasfunda si es necesario. Si no tambien use vasopresores.
Efecto máximo 30 – 60 minutos Pupilas isocóricas vs. anisocóricas Causas sistémicas: Causas sistñemicas: hipotermia, hipoglicemia, alteraciones electrolíticas, acidosis, etc.
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