The induction of anesthesia is a critical juncture for the patient who has an unsecured intracranial aneurysm because rupture at this time can be fatal.
The smooth induction of anesthesia therefore requires mitigation against the sympathetically mediated hypertensive response to maneuvere such as laryngoscopy and intubation and the attendant increase in transmural pressure.Obliteration of coughing and straining once endotracheal tube is in place and maintanance of adequate cerebral perfusion pressure in a patient who may already have vasospasm and impairment of autoregulation is mandatory
The relationship between the transmural pressure across
the wall of the aneurysm and the wall tension the aneu
rysm is linear.Either an increase in the MAP(as during sympathetic stimulation in the face of light anesthesia
or decrease in the ICP (as by hyperventilation, adminis
tration of mannitol,CSF drainage,or opening of cranial vault at time when the SBP is elevated) will raise the transmural pressure and enhance the possibility of aneurysmal rupture.
The goal therefore,is to minimize the transmural pressure while maintaining the CPP during the induction of anesthesia.
The extent of which blood pressure is intentionally reduced
during induction of anesthesia depends on the clinical grade of the patient. The ICP of good grade patients (grade 0,I,II) is usually normal so that a decrease in blood pressure to 30 to 35% below wards value(or SBP of 100 mmHg) is not detrimental in the absence of evidence cerebral ischemia.Poor grade patients(grade IV,V) in contrast, already have intracranial hypertension and reduction in CPP, the combination of which may cause ischemia.A decrease in SBP of these patients may exacerbate the potential for cerebral ischemia while the SBP in a poor grade patient should be reduced less than in good grade patients, and for a shorter time, measures should be taken to blunt the sympathetic response to laryngoscopy and intubation.
Good grade patient do not require hyperventilation during anesthetic induction since they generally do not have a decrease intracranial compliance.
In the absence of increased ICP,the reduction in CBF cause by hyperventilation will reduce the ICP and increase transmural pressure (when the MAP remains constant or rises) risking rupture of the aneurysm.
Poor grade patient conversely may have an increase in ICP and will benefit from moderate hyperventilation to enhance cerebral perfusion. The iv induction of anesthesia is designed to confer loss of conciousness while maintaining cardiovascular and intracerebral homeostasis in the face of catechol amine stimulating maneuvers.Anesthesia can be induced after the placement of the arterial cannula if patient cooperative and at least one secure iv line.
Hypovolemia should be corrected before induction .Some clinicians usually use thiopenthal in 4 to 5 mg/kg doses, unless the patient has cardiac dysfunction.Other clinicians may prefer propofol because achieves rapid loss of con
ciousness,reduction in CBF,ICP and CMRO2 maintanance of cerebral autoregulation and cerebrovascular CO2 respon
siveness.
Slow incremental administration of smaller doses (1,0 to 1,5 mg/kg) will mitigate against systemic hypotension and the possibility of attendant compromise of cerebral perfusion.Propofol has the added advantages of prompt awakening and a decrease in the incidence of postoperative nausea and is appropriate for inclusion in the pharmaco
poeia of neuroanesthesia provided cerebral perfusion is maintained through the prevention or prompt treatment of any reduction in SBP.
Some clinicians use etomidate iv(0,1 to 0,3 mg/kg) but the other clinicians would not advocate the use of etomidate in this setting because marked hypertension sometimes result.The patient with notable cardiac dysfunction should receive a careful induction as for any anesthetic but anesthesiologist should watch for hypertension from inadequate anesthesia.
Clinicians may choose from some combination of a reduced dose of thiopenthal,narcotic and lidocaine or even a pure narcotic cardiac induction if ejection fraction is low. If possible large doses of narcotics that will delay resumption of spontaneous ventilation and wake up should be avoided.
The addition of narcotic (fentanyl 3 to 7 mcg/kg) or
(sufentanil 0,5to 1,0 mcg/kg),lidocaine 1,5 mg/kg and midazolam 0,1 to 0,2mg/kg iv,during the induction of anesthesia will futher blunt the patient's response to sympathetic stimulation as from laryngoscopy,intubation and the application of three points skull fixation devices.
After the patient loses the eyelash reflex, mask ventilation is assured and intubating dose of non depolirizing muscle relaxant is given and relaxation is monitored by the use of peripheral nerve stimulator.
The vecuronium is preferred because of the stable hemody-
namics produced and the reasonably fast onset in large doses. When the patient receiving phenytoin or carbama-
zepine double doses is used because these anticonvulsant increases the pharmacokinetic and pharmacodynamic for non depolizer.
Succinylcholine is probably is probably best avoided after SAH even if neurologic function is intact however,it may be used for rapid sequence induction if it is judged that the risk of aspiration justify it. It may be also used in the neurologically intact patient if the clinician does not wish to use a nondepolizer because of airway anatomy and does not feel comfortable in concious intubation in this setting.
If the airway appears to be difficult even a recent SAH does not contraindicated concious intubation because excellent blood pressure control is meaningless in the absence of oxygenation.
After the relaxant begins to work anesthesia is usually supplemented with a dose of narcotic.The narcotic administration is best delayed to avoid the chest rigidity sometimes produced that makes the efficacy of mask ventilation difficult to evaluate.Sufentanil is most com
monly because it appears to provide the best hemodynamic control in low doses.The doses ranges from 0,25 to 2,0 mcg/kg depending on the patient's blood pressure response to the induction agents, it is best to start with low doses and then supplement as needed.
The patient left with a large sufentanil burden may become hypotensive during the sometimes long period of neurosur-
gical preparation.
Wether sufentanil or fentanyl is chosen for this purpose,it's important to recall that low dose narcotics may take several minutes to take effect. If more immediate narcotic effects is desired alfentanil is a reasonable choice. However if laryngoscopy or intubation is prolonged, the alfentanil effect may wear off before the endotracheal tube cuff is finally inflated.
Remind that there is no place for high dose opioid anesthesia as this will result in catastrophic hypotension
reduced CPP and cerebral ischemia.
The patient with full stomach for aneurysma clipping can be delayed until 6to 8 hrs have gone by after eating but the patient may require emergency ventriculostomy or hema
toma drainage and have a full stomach it is reasonable to pretreat with metclopropamide,H2 blockers or non particulate antacid as is customary and to proceed with a modified rapid sequence induction in which careful cricoid pressure is continuously applied,the patient is very gently ventilate to keep peak pressure below 20 cm H2O and intubation is accomplished as quickly as possible without causing an unacceptable rise in blood pressure.The lungs are then ventilated with 100% oxygen and mild hypocap
nia(PaCO2 of 35 to 40 mmHg) when intracranial elastance is normal and PaCO2 25 to 30 mmHg when intracranial elastance is impaired.
The prior infiltration of the scalp and periosteum with local anethesia may also avoid the hypertensive response to the insertion of pins into the outertable of skull.
MAINTENANCE :(1,2)
The best anesthetic technique produces a slack brain so that retraction pressure is low while ensuring maximum cerebral protection by keeping cerebral metabolic requirement to a minimum. Those agents that maintain cerebral vaso reactivity to CO2 and autoregulation may reduce fluctuation in CBF,ICP and CPP when blood pressure changes with varying surgical stimuli.
A combination of a propofol infusion and opioid is increasingly used to maintain anesthesia during aneurysm surgery.Propofol rapid adjustment of anesthetic depth with more rapid recovery than either thiopentone or isoflurane.
Propofol has no intrinsic vasodilatory effect and therefore does not result in increases in CBF,CBV,or ICP. Furthermore propofol has been shown not to affect cerebral autoregula
tion or CO2 reactivity even at doses high enough to produce EEG isoelectricity Inhalational anesthetic agents have a dual effect on CBF: a reduction consequent on to the decrease in cerebral metabolism and increase secondary to
their direct cerebral vasodilatory effect.The net effect of an inhalational agents on CBF is therefore dependent on the level of cerebral metabolism at the time the agent is introduced.
When cerebral metabolism is low as in patients with SAH grades III or IV the net effect may be vasodilatory with increase in CBF and ICP accompanying the introduction of the agent.However in patients with good grade SAH I or II
in whom cerebral metabolism is high inhalational agents primarily reduce CBF secondary to reduction in cerebral metabolism.Therefore inhalational agents can be safe use in patients with good graded SAH. When there is uncertain
ty about the level of cerebral metabolism or when signs of significant cerebral oedema are present,total intravenous anesthesia is preferred option.
Inhalational agents with the exception of sevoflurane impair autoregulation in a dose dependent manner.
Therefore isoflurane in concentration less than 1,0% can be used in neurosurgery. Desflurane increases ICP and this may be related to its sympatho adrenal effects.Sevoflurane has been shown not to alter cerebral autoregulation in concen-
tration up to 1,5 MAC. However at 1,5 MAC sevoflurane brain oxygen consumption was shown to be reduced by 25% and therefore a degree of luxury perfusion may occur.
Nitrous oxide has a number of advantages, it has a rapid onset and ofsett, it easy to use and relatively in expensive.
However, its routine use in neuroanesthesia is discourage at some institution as there is evidence to suggest that N2O increases ICP and CBF by stimulating cerebral metabolism.
But when combination with isoflurane this effect can be attenuated by hyperventilation and propofol.
If the patient has a tight,swollen brain that is interfering with surgical exposure N2O is discontinued,the position of the patient's head is check for the possibility of kinked jugular vein and the PaCO2 rechecked.
Initial dose of mannitol is usually so large (200 g) that more mannitol is not likely to be helpful.
At this point a bolus of lidocaine (1,0 t0 1,5 mg/kg) then followed with a lidocaine infusion of 1 to 4 mg/minute can be begun.
This provides almost one third the maximum allowable concentration (MAC) of anesthetic contribution and a good effect on ICP.
If exposure continues to be problem the isoflurane is discon
tinued and a continuous infusion of thiopental 1,0 to 10.0 mg/minute after a small bolus (25 to 100 mg) is begun.
The anesthetic provided by lidocaine and thiopental with
residual narcotic is likely to be adequate because there are actually no painful and the patient temperature is 33 to 34 degrees C,reducing anesthetic requirement by 20% to 30%.If further narcotic is indicated. The first choice in this situa
tion would be low doses of fentanyl because it has been least implicated in this problem. It may be also reasonable to ensure that MAP is at a middle level because either low pressure(with autoregulation intact) or high pressure
(with autoregulation impaired) may increase CBV and ICP.
If possible it may be best to avoid further narcotic in view of recent studies claiming increases in ICP with alfentanil, fentanyl and sufentanil especially in patients with cerebral tumors and head trauma.
Fentanyl with its medium duration of action and its negligible cerebrovascular effects is the agent of choice in many neurosurgical intensive care units.
Remifentanil a new opioid with onset and short half life is being investigated for neurosurgery. Remifentanyl appears to compare favourably to fentanyl in patients undergoing elective supratentorial surgery,when combined with 0,5 MAC sevoflurane does not alter cerebral autoregulation in individuals undergoing non intracranial neurosurgical procedures.
Brain relaxation
The aim is to produce a slack brain so that retraction pressure can be kept in minimum to facilitate the surgical approach to the aneurysm and brain relaxation improved after the opening of the dura. There are several methods employed to reduce the brain bulk,CSF volume and
CBF. These include a 15-30 degree head up position,mild hypocarbia,mannitol and furesemide. Mannitol is usually administered (0,5 to 1g/kg)as 20% solution and probably acts on all three intracranial compartment via different
mechanism. It may reduce brain bulk by osmotic dehyd
ration, CBF by improving rheology of erythrocyte thus decreasing blood viscosity and CSF production.
Mannitol is also a free radical scavenger and its high osmolarity causes an immediate but transient increase in intravascular volume,CBF,CBV and ICP.
This followed by a reduction in ICP and CBV,which is maximum at 45 to 60 minutes. Therefore, care must be taken when using mannitol to patients with poor cardiac function as they may develop congestive heart failure, and pulmonary oedema. Furesemide can be used in conjuction with mannitol or it can be used alone in those patients with poor myocardial function who may be sent into cardiac failure with mannitol.
Hypertonic saline has been advocated as an alternative to mannitol although its action is transient and its overall effects remain untested in SAH.
The potential ischemic effects of marked hyperventilation must be balanced against the benefits of reducing CBV,
when used properly,hyperventilation is a quick and effective tool for reducing CBV, provided a measure of cerebral oxygenation is employed. Although it cannot detect regional ischemia, jugular bulb oxygenation(SJO2) reflect the balance between cerebral oxygen supply and demand it's probably unwise to induce hypocapnia if the SJO2 < 50%.
CBV can also be reduced pharmacologically by reducing cerebral metabolism and hence CBF.This is achieved by bolus iv administration of thiopentone (3 to 5mg/kg),
propofol (1 t0 2 mg/kg) or lignocaine (1,5 mg/kg).
The drainage of CSF facilitates surgical exposure,the surgeon may put in a ventricular catheter or drain the basal cysterna intraoperatively.
Alternatively a lumbar subarachnoid catheter is inserted after induction of anesthesia and before positioning for surgery.While the cranium is still closed,the avoidance of leakage of CSF is essential to prevent a decrease in ICP and the concomittant rise in transmural pressure.
If the ICP is elevated preoperatively,the subarachnoid puncture and escape of CSF may also lead to tonsilar herniation. Control hypotension has been used to decrease the likelihood of rupture by decreasing aneurysmal transmural pressure, mechanically improving the approach to handling and actual clipping of the aneurysm and reducing bleeding should it occur. Oral pretreatment with clonidine (0,05 mg/kg)or captopril (3mgkg) will facilitate the provision of desired levels of hypotension but may also result in excessive hypotension in some anesthetized patients.
Some clinicians involves tha manipulation of isoflurane levels on top of a narcotic base,a means blood pressure of 50 mmHg is generally achieved by this means. Other clinicians use a basic nitrous or narcotic anesthetic with nitroprusside for hypotension with equally good effects.
Futhermore Lam has shown that when isoflurane is used to produce hypotensive anesthesia to the lower limits of cerebrovascular autoregulation (e.g.50 mmHg,cardiac output and CBF are relatively well preserved making isoflurane at least theoretically advantagous).
On the otherhand nitroglycerine(NTG) might be a reasonable choice if mild hypotension is absolutely required in a patient with known significant coronary disease. As with tight brain situation a thiopental infusion can be used to provide hypotension with excellent operating condition,
if doses >30 mg/kg are used awakening is likely to be significantly delayed.
The MAP is not usually reduced below 50 mmHg in normotensive patients and chronically hypertensive patients may require a higher MAP(systolic best kept greater than the preoperative diastolic pressure).
However there are many problems associated with
controlled hypotension.
Many SAH patients will have impaired autoregulation or cerebral vasospasm and hypotension may therefore lead to local or global cerebral ischemia.
to be continued
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