9. Autorregulación cerebral Pacientes con isquemia cerebral pierden la autorregulación Mantener PPC La reactividad vascular cerebral a cambios en la presión arterial de dióxido de carbono (PCO2 ) usualmente esta preservada
20. RESANGRADO Y VASOESPASMO DESPUÉS DE HSA 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
21. Neurosurg Rev (2006) 29: 179–193 VASOESPASMO CEREBRAL vasoespasmo angiográfico estrechamiento de la columna de medio de contraste en las arterias cerebrales. vasoespasmo clínico consecuencia isquémica del vasoespasmo cerebral diversos grados de déficit neurológico
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29. ALTERACIONES DEL SODIO ↓ ↓ ↑ OK, ↑ ↓ Na VOLUMEN TTO CAUSA SIADH OK, ↑ Restringir líquidos ADH Cerebro perdedor de sal ↓ ↓ SSN o hipertónica Fludrocortisona PNA y C Diabetes insípida - Poliuria Vasopresina dosis ? ADH Mantener EUVOLEMIA
Nontraumatic subarachnoid hemorrhage is a neurologic emergency characterized by the extravasation of blood into the spaces covering the central nervous system that are filled with cerebrospinal fluid. The leading cause of nontraumatic subarachnoid hemorrhage is rupture of an intracranial aneurysm, which accounts for about 80 percent of cases and has a high rate of death and complications.1 Nonaneurysmal subarachnoid hemorrhage, including isolated perimesencephalic subarachnoid hemorrhage, occurs in about 20 percent of cases and carries a good prognosis with uncommon neurologic complications.2 This review focuses on aneurysmal subarachnoid hemorrhage. As many as 46 percent of survivors of subarachnoid hemorrhage may have long-term cognitive impairment, with an effect on functional status and quality of life.3,4 The disorder is also associated with a substantial burden on health care resources, most of which are related to hospitalization.5. It accounts for 2 to 5 percent of all new strokes and affects 21,000 to 33,000 people each year in the United States.6-8 The incidence of the disorder has remained stable over the past 30 years,1 and although it varies from region to region, the aggregate worldwide incidence is about 10.5 cases per 100,000 person-years.9
The major identified modifiable risk factors include cigarette smoking, hypertension, cocaine use, and heavy alcohol use.20-22 Patients with a family history of first-degree relatives with subarachnoid hemorrhage are also at a higher risk.21,23 Heritable connective-tissue disorders associated with the presence of intracranial polycystic kidney disease, the Ehlers–Danlos syndrome (type IV), pseudoxanthoma elasticum, and fibromuscular dysplasia
A marked difference in fatality rates—for example ranging between China/Beijing and Russia/Moscow from 23% (95% CI 13–23) to 51% (95% CI 42–60)—may indicate the importance of medical management and treatment. Once an aneurysm has ruptured, treatment is focussed on the prevention of re-bleeding and prevention of secondary injury from ischaemia (vasospasm).
The major factors associated with poor outcome are the patient’s level of consciousness on admission, age, and the amount of blood shown by initial computed tomography (CT) of the head. Several grading systems are used to assess the initial clinical and radiologic features of subarachnoid hemorrhage. The two most widely used clinical scales are those of Hunt and Hess and the World Federation of Neurological Surgeons. The latter is currently preferred since it is based on the sum score of the Glasgow Coma Scale (a very reliable method for evaluating the level of consciousness) and the presence of focal neurologic signs. The higher the score, the worse the prognosis. The amount of blood seen on initial head CT scanning can be easily evaluated. A thick subarachnoid clot and bilateral ventricular hemorrhage are both predictive of poor outcome and can be reliably graded on head CT.
Dilataciones arteriales anormales por debilidad de la capa elástica arterial; frecuentemente en bifurcaciones por turbulencia de flujo sanguíneo
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. la autorregulación cerebral se ve afectada. curva de autorregulación cerebral a la derecha
Subarachnoid hemorrhage should always be suspected in patients with a typical presentation which includes a sudden onset of severe headache (frequently described as the “worst ever”), with nausea, vomiting, neck pain, photophobia, and loss of consciousness. Physical examination may reveal retinal hemorrhages, meningismus, a diminished level of consciousness, and localizing neurologic signs. The latter finding usually includes third-nerve palsy (posterior communicating aneurysm), sixth-nerve palsy (increased intracranial pressure), bilateral lower-extremity weakness or abulia (anterior communicating aneurysm), and the combination of hemiparesis and aphasia or visuospatial neglect (middle cerebral-artery aneurysm). Retinal hemorrhages should be differentiated from the preretinal hemorrhages of Terson’s syndrome, which indicates a more abrupt increase in intracranial pressure and increased mortality.
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%, 4 : 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 In general, the higher the clinical grade, the more likely are cerebral vasospasm, elevated ICP, impaired cerebral autoregulation, impaired vascular CO2 reactivity, cardiac arrhythmias and dysfunction, 20 hypovolaemia, and hypo- natraemia. 24 Patients with Hess and Hunt grade I and II (Table 1) are likely to have normal ICP and preserved cerebrovascular reactivity; thus, they can be expected to respond to hyperventilation with cerebral vasoconstriction. In contrast, patients with Hess and Hunt grade III and IV are likely to have increased ICP and impaired cerebrovas- cular reactivity; hyperventilation is thus unlikely to result in reliable cerebral vasoconstriction. A low Glasgow Coma Scale score (<8) is usually associated with increased ICP
The latter is currently preferred since it is based on the sum score of the Glasgow Coma Scale (a very reliable method for evaluating the level of consciousness) and the presence of focal neurologic signs. The higher the score, the worse the prognosis. The amount of blood seen on initial head CT scanning can be easily evaluated
Head CT scanning should be the first study performed in any patient with suspected subarachnoid hemorrhage. The characteristic appearance of extravasated blood is hyperdense. Since small amounts of blood can be missed, all scans should be performed with thin cuts through the base of the brain. Because of rapid clearance of blood, delayed head CT scanning may be normal despite a suggestive history, and sensitivity drops to 50 percent at seven days. Head CT scanning can also demonstrate intraparenchymal hematomas, hydrocephalus, and cerebral edema and can help predict the site of aneurysm rupture, particularly in patients with aneurysms in the anterior cerebral or anterior communicating arteries. Head CT scanning is also the most reliable test for predicting cerebral vasospasm and poor outcome.
15% aneurismas multiples ngiografía cerebral selectiva se debe realizar en los pacientes con HSA para documentar la presencia y anatómicas características de los aneurismas (clase I, nivel de evidencia B). 4. ARM y la CTA puede ser considerado cuando convencionales La angiografía no se puede realizar de manera oportuna
Urgente evaluación y tratamiento de los pacientes con HSA que se sospecha tanto, se recomienda (clase I, nivel de evidencia B). on
The daily percentage probability for the development of symptomatic vasospasm or re-bleeding after subarachnoid hemorrhage. Day 0 denotes onset of subarachnoid hemorrhage.
Angiographic vasospasm is defined as a narrowing of the contrast medium column in major cerebral arteries. Clinical vasospasm is defined as the ischaemic consequences of cerebral vasospasm resulting in various degrees of neurological deficits.
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
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
Intacranial hypertension is present to some degree in most patients following a SAH. Intracranial pressure gradually returns to normal by the end of the first week. If an intracerebral hemorrhage, intraventricular hemorrhage, vasospasm, or hydrocephalus develops, intracranial hypertension may be severe and require treatment. Patients may require emergency ventriculostomy, steroids, diuretics, or intubation and hyperventilation. ICP should be lowered gradually, especially in patients with unclipped aneurysms . Abrupt lowering of ICP by lumbar puncture, ventricular drainage, or rapid infusion of mannitol can induce rebleeding .
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
In general, elderly patients or patients in poor medical condition are often better suited for endovascular coiling. Aneurysms of the vertebrobasilar circulation or aneurysms deep in the skull base, such as paraophthalmic aneurysms, may be more easily accessed by an endovascular approach.
Currently, the two main therapeutic options for securing a ruptured aneurysm are microvascular neurosurgical clipping and endovascular coiling. Historically, microsurgical clipping has been the preferred method of treatment. Although the timing of surgery has been debated, most neurovascular surgeons recommend early operation. Evi 46,47 The authors found that for this particular subgroup of patients, a favorable outcome, which was defined as survival free of disability at one year, occurred significantly more often in patients treated with endovascular coiling than with surgical placement of clips. The risk of epilepsy was substantially lower in patients who underwent endovascular coiling, but the risk of rebleeding was higher. Also, in patients who underwent follow-up cerebral angiography, the rate of complete occlusion of the aneurysm was greater with surgical clipping. In general, elderly patients or patients in poor medical condition are often better suited for endovascular coiling. Aneurysms of the vertebrobasilar circulation or aneurysms deep in the skull base, such as paraophthalmic aneurysms, may be more easily accessed by an endovascular approach.
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. 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.
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. 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 The cardiac abnormalities are probably the result of excessive myocardial release of catecholamines from sympathetic nerve terminals triggered by the SAH, result- ing in calcium overload and necrosis of myocytes In most cases, myocardial dysfunction seems to corre- late more with the degree of neurological deficit than with the severity of ECG abnormalities.
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. Electrolyte disturbances SAH is frequently accompanied by hyponatraemia, hypokalaemia, hypocalcaemia, and hypomagnesaemia. Hyponatraemia develops in approximately 30% of cases as a result of either the cerebral salt wasting syndrome or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The cerebral salt wasting syndrome is caused by the secretion of brain and atrial natriuretic hormone, which leads to a negative sodium balance, hyponatraemia, and intravascular volume depletion. 120 The therapeutic options for the cerebral salt wasting syndrome are limited. Appropriate treatment consists of i.v. infusion of normal saline, rarely of hypertonic saline. Administration of fludrocortisone and hydrocortisone pre- vented or attenuated intravascular volume depletion and decreased the incidence of negative sodium balance. 36 68 121 SIADH is accompanied by retention of excess free water. Although fluid restriction would be the theoretical treatment of choice, salt-containing i.v. solutions are usually used during SAH to ensure a normal to high intravascular volume 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 EVITAR ETOMIDATO ASOCIADO MIOCLONIA Y ACTID¿VIDAD CONVULSIVA
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
Los anestésicos volátiles ( > 1.5 MAC) deterioran la autorregulación en un grado dependiente de la dosis. Después de 2-5 horas de administración continua, el FSC comienza a retornar al VN. Favorecen fenómeno de robo circulatorio. Isoflurano: favorece la absorción de LCR. 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].
Mantenimiento de la anestesia Cualquier IV (excepto ketamina) Etomidato convulsión Protección del edema cerebral Halogenado subMAC, hiperventilación Control PIC Anticiparse a estímulos dolorosos
Adversosíneo aumento inicial PIC Hiponatremia, hiperkalemia, acidosis Evitar caída brusca de PIC Consequently, the therapeutic effect of a combination of mannitol and frusemide on ICP and brain bulk was consistently larger and more prolonged than that of either drug alone.
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.
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