Since perfusion depends in part on the intravascular volume and MAP the boosting of CBF as accomplished by Triple H therapy or hypertensive hypervolemic hemodilution. The augmentation of blood pressure and the expansion of intravascular volume, the preservation of relative hemodilution (hematocriet of 32%) to promote blood flow through the cerebral microvasculature and the avoidance of hyponatremia.The key to the succesful use of Triple H therapy is its early application before mild ischemia evolves to infarction.
Because the risk of rebleeding can be as high as 19%, however,both hypertensive and hypervolemia are induced with caution in the period preceeding surgical securing of the aneurysm by clip ligation,wrapping,gluing or balloon occlusion.
With early operation the likelihood of bleeding from Triple H therapy is diminished.Other adverse intracerebral squelae of Triple H therapy include hemorrhage into area of infarctions, exacerbation of cerebral oedema and a rise in ICP. The systemic complication include myocardial infarction(2%),pulmonary oedema (7 t0 17%),coagulopathy (3%) and dilutional hyponatremia (3%).
For the anesthesiologist it's crucial to maintain the blood pressure and intra vascular volume in the normal range during surgery and to augment both as the aneurysm is being secured. Serial measurement of the Ht intraoperative and during recovery period will facilitate achievement of the appropriate degree of hemodilution through the administration of crystalloid and blood as necessary.
Hetastarch and dextran are contraindicated because of their potential for interference with coagulation.
Five percent albumin may be used in addition to crystalloid.
Previous reports of the management of hypervolemic hemodilution after SAH equated the optimal volume ex
pansion to a CVP of 10 mmHg and PCWP of 12 to 20 mmHg.
Vasopressor drugs,including dopamine,dobutamine,and phenylephrine may also be required to raise blood pressure to reverse the signs and symptoms of the ischemic deficit.
If the patient aneurysm has not been clipped the blood pressue is increased to 120 to 150 mmHg.Once aneurysm has been secured,the blood pressure in the range of 160 to 200 mmHg may be maintained,this is often employed to improve collateral blood flow during temporary clipping and in patients with areas of critical perfusion.This can usually be done with small boluses of phenylephrine (25 to 50 mcg) and appropriate modificates of the inhaled or continous iv anesthetic level but may require use of a phenylephrine infusion (start 20 to 40 mcg/min) and titrate up to main
tain the dersired blood pressure.
Some clinicians use a bolus of a brain protective agent such as thiopental,propofol,lidocaine and mannitol before the clipping are applied.
Mannitol 2g/kg before temporary occlusion has been advocated because it enhances the microcirculation and increases regional CBF in areas of ischemic.
Suzuki has added vit.E(500 mg) and dexamethasone (50 mg) to mannitol 100g as a Sendai cocktail.
Care must be taken not to seriously overshoot the blood pressure level especially before the temporary clips are in place.In short the neuro anesthesiologist to day must be ready to provide controlled hypertension as well as controlled hypotension. In addition to the example of temporary clipping various levels of controlled hypertension may be required for the patient with known vasospasm or concurent cerebrovascular occlusive disease.
Notably continuous infusion of calcium channel blockers such nicardipine may prove to be the optimal blood pressure controllers in vasospastic patients or in early surgery in general.
The resultant change in CBF may be indicated with the use of TCD monitor and improvement in vasospasm is signalled by a decrease in flow velocity.
However in patients with abnormal autoregulation CBF is pressure dependent and increase in MAP will increase CBF and may result in blood brain barrier damage and vasogenic oedema.
Patients with myocardial disease or unsecured aneurysm are at risk for myocardial ischemia and aneurysm rupture respectively.
Whether controlled hypotension or hypertension has been used resumption of normotension is the goal after the aneurysm itself has been successfully clipped.
This is important so that bleeders can be detected before the dura is closed. This can be usually achieved by lightening the isoflurane level in the case of hypotension or discontinuing phenylephrine and deeping the anesthetic after hypertension.
Mild hypothermia has been shown to be cerebroprotective by virtue of decreasing the release of excitatory neuro
tansmitter(e.g.glutamate) and increasing the release of inhibitory neurotransmitter(e,g.gamma amino butyric
acid).Hypothermia also reduces cerebral oxygen demand by 7 to 8% per one degree C and this effects continues after the EEG becomes isoelectric.
Mild hypothermia with a simple cooling-warming blanket and aim for oesophageal temperature of 32 t0 33 degrees C, because brain temperature are probably about 0,5 degree C higher.
Temperature below 32 degrees C are avoided because problems may theoretically begin with coagulation disorders and arrhythmia.
Doses of narcotic and relaxants should be appropriately reduced.It's important to begin the rewarming process sufficiently early so that post operative shivering does not occur.
Intraoperative aneurysm rupture:(1,2,3)
Rupture of the aneurysm during induction of anesthesia or intraoperative can be catastrophic.
More often the aneurysm ruptures during the approach to or handling of the aneurysm by the surgeon,infact this occurs to some degree in 25 to 40% cases.
Samson et all reported that 7% ruptures occured before dissection and 45% during clip aplication.
More serious ruptures are less common and require our input to lower blood pressure to reduce bleeding,and improve surgical exposure,and to replace blood loss if necessary.The surgeon may request pressure on both carotids to reduce the blood loss in the operation field and may have to clip a major pro-ximal artery to get control. Although uncontrolled hypotension may result from severe blood loss it's critical to attempt to maintain intravascular volume status and a short period of induced hypotension so that the situation does not deteriorate into cardiac arrest.
MAP < 50 mmHg may be requested in this lifethreatening situation and maybe provided by thiopental,propofol,esmo
lol,nitroprusside or isoflurane to facilitate clip ligation of the neck of the aneurysm or temporary proximal and distal occlusion of the parent vessel.When the parent vessel is occluded blood pressure is increased to normal during the period of temporary occlusion to enhance collateral perfusion.
If the bleeding is sufficient to cause acute hypovolemia ,induced hypotension may not be an option. In this case the blood that is lost is replaced immediately with whole blood, blood products or colloid to maintain vascular volume.
Recovery:(1,2)
In patients with initial good grade SAH,a rapid return of conciousness is aimed for allow early neurologic assessment
Provided no intowards events occured intraoperatively
grade I-II patients are extubated. In patients with WFNS grade III recovery depends on their preoperative concious level and ventilatory state, Grade IV-V patients are usually transfered to neurocritical unit for a 24-48h period of elective post operative ventilation.
After the aneurysm has been clipped the blood pressure allowed to rise to normal or high normal levels so that the security of the clip and excessive bleeding can be evaluated before the dura is closed.
If mild hypothermia has been used the thermal blanket is turned up to 39 to 40 degrees C to begin rewarming.
The level of isoflurane is reduced as tolerated.
Blood pressure control usually be obtained with labetalol given in incremental doses of 5,10,20 and 40 mg boluses (total 75 mg) which can be supplemented by additional 20 mg boluses if bradycardia is not excessive and blood pressure control is indequate. A small dose of sufentanil will usually produce a reasonable blood pressure control but the occasional patient still need nitroprusside.
When surgery is complete the anasthetic are discontinued and 100% oxygen is given. Residual neuromuscular blockade is reversed,the airway suctioned,and the patient extubated on regaining conciousness. Boluses of short acting opioids ,propofol or lignocaine can be used to facilitate extubation and control blood pressure.
Uncontrolled hypertension in the immediate post operative phase can precipitate intracerebral hemorrhage.
In patients with unsecured aneurysm the blood pressure is kept withi 20% of normal. If the patient remain hyperten
sive (systolic pressure > 200 mmHg) in recovery despite adequate pain relief,esmolol,labetalol or nifedipine is used.
If the patients fails to regain their preoperative neurologi
cal state the following need to be excluded :
-anesthetic causes (partial neuromuscular blockade).
-residual narcotic and sedative drugs.
-hypoxia and hypercarbia
-metabolic factors (hyponatremia)
-post tictal state.
It's important the airway is not compromised post operatively and hypercapnia and hypoxaemia are avoided.
Reintubation will be needed in those patient unable to protect their airway or maintain adequate gas exchange.
Once the above possible causes has been excluded, a CT scan is performed to exclude hydrocephalus,cerebral oedema,intracranial hemorrhage,hematoma or rebleed (multiple aneurysm).
If the scan is negative ,a cerebral angiography is needed to exclude vascular occlusion(e.g.misplaced clip).
Vasospasm can be detected using transcranial Doppler.
All patients are transfered to neurocritical unit or high dependency unit for their post operative management.
Cerebral vasospasm and delayed ischemic neurological deficits remain the major post operative complication once the aneurysm has been clipped.
SUMMARY :
The maintenance of adequate cerebral perfusion,the avoidance of hypotension and the prevention and treatment of elevated ICP,are important for a good recovery in patients with intracranial hemorrhage,cerebral trauma or encephalopathies.Therefore clinicians caring for these patients must have a thorough understanding of cerebral physiology and the factors that affect cerebral hemodyna
mics. Realizing that a balance exist between risk of aneurysmal rupture and maintanance of adequate CPP,one should attempt mild reduction of systemic blood pressure (1,e.30%) with close observation for signs of neurologic deterioration; this reduction in blood pressure often is accomplished by calcium antagonist used as treatment of prophylaxis of vasospasm.
The only therapy proven useful for symptomatic vasospasm is intravascular expansion,hemodilution and induced hypertension(triple H therapy).
Suggested reading :
1. Leisha S.Goodsiff & Matta F.Basil:Anesthesia for intravascular surgery;Matta F.Basil & Menon K.David;Textbook of Neuro Anesthesia and Critical Care,
Greenwhich Medical Media Ltd,London ,2000,pp.195-204
2.Stone JD,Bagdonoff :Anesthesia for Intracranial vascular surgery ;Stone JD,Sperry JR,The Neuro anesthesia Handbook,Mosby,St.Louis,Baltimore,Boston,1996,pp.332-51.
3.Newfield Philippa,Hamid.A.K.Rukaiya, Lam M Arthur;Anesthetic Management of Subarachnoid Hemorrhage;Albine S.Maurice;Textbook of Neuroanesthesia with Neurosurgical and Neuroscience perspective;Mc.Graw Hill USA,1997,pp.860-81.
4.Kaptok J.Mark,Flamin S Eugene;Cerebral Aneurysm:Surgical Consideration. Cottreels James,Smith S David;Anesthesia and Neurosurgery,4th edit.Mosby Company,St Louis,London;2001.pp.353-67
5.Morgan Edward,Mikhail S Mage:Anesthesia& craniotomy for intracranial Aneurysm& AV Malformation;Clinical Anesthesiology,third edit.McGraw Hill ,Newyork,Chicago,San Franscisco,2002,pp 578-9.
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