Cerebral Vasopasm (PART 2)

TREATMENT :

Pharmacologic treatment:(1,4)


Numerous drugs have been investigated for prevention or treatment vasospasm but most are ineffective.


Calcium channel blockers (calcium antagonist) which nimodipine has been more extensively studied are the only drugs that have been shown to consistently reduce the mortality and morbidity from vasospasm in all patients with SAH irrespective of the grades. 


Nimodipine, a dehydropyridine calcium antagonist blocks the intracellular influx of extra cellular calcium, preventing arterial smooth muscle contraction. It was initially believed that this agent prevents constriction of vessels; however clinical trial have shown no change in the incidence or severity of angiographic vasospasm.


It is now postulated that improved outcome is related either to decrease in vasospasm in the microvasculature which is not visualized by angiography or to a modification of calcium influx into the damage cells which limited the extent of neural injury.


Interestingly none of these favourable studies with calcium antagonist prophylaxy was able to demonstrate any signifi
signicant change in the incidence or severity of vasospasm.


Nicardipine is another dehydropyridine calcium antagonist in high dose intravenous has been investigated for prevention of vasospasm.


Nicardipine studied in SAH therapy continuous iv infusion for 14 days after SAH has shown to decrease the incidence of vasospasm but compared with placebo,nicardipine has not shown to improve clinical of vasospasm outcome at 3 months.


Nimodipine,60 mg every 4 hours should be used enterally as soon after the ictus as possible ;preferably before 96 hrs.


It is continued for 14 to 21 days 


Hypotension is seen in about 5% of patients treated with enteral nimodipine and in 28% to 33% of patients treated iv nicardipine.


Therefore the BP should be monitored carefully;the hypo
tension is typically readily treatable with fluid adminstra 
tion.Pulmonary oedema,presumably as manifestation of high output congestive heart failure(CHF) has also been associated with dehydropyridine therapy.


An early clinical trial of tirilazad mesylate,a potent lipid peroxidation inhibitor in Europe,Australia and New Zealand demonstrated that at 6 mg per kg per day,a significant reduction in symptomatic vasospasm occured primarily
primarily in men.However a subsequent trial in North America involving 897 patients failed to demonstrate any improvement over placebo.


A subsequent trial with a higher dose(15mg/kg per day) in women demonstrated a slight improvement in mortality in patients with poor neurologic grade but no difference from the placebo group when all patients were considered.


Approaching from another direction,a clinical trial with a hydroxyl radical scavenger (nicaraven) reported a 35% reduction of the incidence of delayed ischemic deficit.


These result although promising,await confirmation with a larger clinical trial.


In retrospective study,patients taking aspirin before their SAH had reduced risk of delayed ischemic deficit and there
fore the use of aspirin post aneurysm clipping require further study.


 HYPERVOLEMIC,HYPERTENSIVE AND HEMODILUTION
 (TRIPLE H)(1,2)
 The rationale behind induced hypervolemia and hyper
 tension is that in SAH the ischemic area of the brain have 
 impaired autoregulation and thus CBF depends on the  
 intravascular volume and mean arterial pressure(MAP).

The aims of triple H therapy is to optimize cerebral 
 perfusion by increasing CBF and improving flow 
 characteristics by haemodilution.

Hypervolemia is achieved by the administration of some 
 combination of colloids,crystalloids and blood products.
 Colloid may at times be superior to crystalloid solution in 
 maintaining hypervolemia.

This therapy is most successful if instituted early when the 
 neurologic deficit are mild and before the onset of 
 infarction.However prophylactic treatment initiated before aneurysm clipping,is associated with a significant risk of rebleeding(19% in one series).


Other concerns include worsening of cerebra oedema,
increasing ICP,and causing hemorrhage into an infarcted area.Other systemic complications included pulmonary oedema(7% to 17%),myocardial infarction(2%),dilutional hyponatremia(3% t0 35%),and cogulopathy(3%).


To optimized theraphy and minimize the potential cardio
vascular and pulmonary complication,invasive monitors including direct arterial pressure,CVP or preferably a pulmonary artery catheter are essential.


Sufficient iv fluids are infused to increase the CVP to 10 mmHg or the pulmonary artery wedged pressure (PAWP) t0 12 to 20 mmHg.


In recent study where a starling curve was constructed in nine patients with a ruptured aneurysm ,Levy and Giannotta observed the increasing the PAWP from 8 to 14 mmHg correlated with significant increases in left ventricular stroked work  index,stroke volume index,and cardiac index.


However further volume expansion to increase PAWP to above 14 mmHg resulted in  a decline in the cardiac index.


The initial step is to increase cardiac output and BP with agressive volume expansion.In addition to maintanance fluids of 2-3 litres per day,colloids or packed red cell are used to obtain the following:
             -Hematocriet of 30-35%
             -PAWP of  8-14 mmHg
             -Cardiac Index(CI) of 4,5L/m2/min
             -Systemic vascular resistance(SVR) index of 1400-
              2000 dyne/sec/cm3.
             -SBP of 120 -150 mmHg in unclipped and 160-200 
              mmHg in clipped aneurysm.
 Although iv fluid alone is often effective is at times 
 insufficient to raise BP or reverse the ischemic symptoms;
 vasopressors are then initiated to induce hypertension .

The most widely used vasopressors are dopamine,dobu-
 tamine,nor adrenaline or phenylephrine.

If after volume expansion the above parameters cannot be achieved or there are no improvement in neurologic status
inotropes(usually dopamine 2,5-15 mcg/kg/min)are started.


The use of appropriate inotropes/vasopressors is guided by a pulmonary artery catheter.


In some cases nimodipine may have to be withdrawn as it can interfere with attempt to induce hypertension.


Triple H therapy may induce a vagal response,as well as profound diuresis ,requiring administration of large amounts of iv fluids.


Atropine (1 mg im every 3 to 4 hrs ) may be given to maintain the heart rate between 80 and 120 beats/min,and aquous vasopressin(pitressin)( 5 units im) may be adminis
tered to maintain the urine output at less than 200 ml/hr.


The BP is treated to a level necessary to reverse the signs and symptoms of vasospasm or to a maximum of 160 to 200 mmHg systolic,in patients whose aneurysm has been clipped 
If the aneurysm has not been clipped then SBP is increased to only 120 to 150 mmHg.


The elevated BP must be maintained until the vasospasm resolves which usually in 3 to 7 days.


Response to therapy can now be monitored non invasively using the TCD,improvement in vasospasm is associated with a decrease in flow velocity.


PET has been performed in patients not responding to triple H therapy,to diagnose any hypoperfused area which are not infarcted,which will benefit from an improvement in blood flow. CBF values <20 ml/100g/min,have been found in the affected hemispheres of patients with symptomatic vaso
spasm and values<12 ml/100g/min have been associated with irreversible changes.


The BP is manipulated using inotropes to see wether there is any increment in blood flow to these hypoperfused areas.


Hemodilution the last component of triple H therapy is based on the correlation of hematocriet and whole blood viscosity.As the Hematocriet and viscosity decrease,the cerebrovascular resistance corresponding decreases and CBF increases and the oxygen carrying capacity is decrease.


Experimental study that suggested that hematocriet of 33%
provides an optimal balance between viscosity and oxygen carrying capacity and this has been applied clinically.


Phlebotomy or blood transfusion are performed to maintain a hematocriet 33%.


 Non Pharmacologic treatment:
 Reduction of ICP:(1)
 In patient has elevated ICP ,cerebral perfusion may be 
 improved by lowering the ICP.
 Improvement in neurologic status with this treatment 
 alone has been reported.

 Interventional neuroradiology:

Percutaneous angioplasty (PTA):(2,4)


If the patient is in imminent danger from severe diffuse vasospasm refractory to triple H therapy ,these spastic arterial segment may be forcibly dilated by means of small low pressure balloon placed through intra arterial catheter.
In expert hands this associated with the permanent rever
sal of vasospasm and clinical improvement in one half to two thirs of patients but there is a risk that the vessels may rupture and dissect with this technique so the procedure should be restricted to experienced interventional neuro
radiologis.


 Intra arterial papaverine:(2)
 The proximal segment of the anterior cerebral arteries,and 
 distal middle cerebral arteries are not amenable to balloon 
 dilatory because of size or angle of take off.

 The instillation over several hours of high concentration
 of intra arterial papaverine has been associated with rever
 sal of vasospasm in some cases.

 Papaverine ,a phosphodiesterase inhibitor causes the accu
 mulation of cycle adenyl monophosphate within smooth 
 muscle leading to vasodilatation.

 There has been tendency for spasm to recur and the 
 infusion may have to be repeated but it is sometimes 
 associated with clinical improvement.

 However,papaverine can precipitate systemic hypotension 
 and intracranial hypertension so measures to support BP 
 and control ICP  must be immediately available.


 Prophylaxis:(2,3)

 Early surgery permits the mechanical removal of fresh 
 blood clot by suction and irrigation.

 As blood in the subarachnoid space precipitate cereb-
 ral vasospasm,it has been postulated that drugs which 
 dissolve this blood clot may reduce the incidence of 
 cerebral vasospasm and improve outcome.

 Once the offending aneurysm has been secured by a clip 
 it is possible to place tissue plasminogen activator within 
 the subarachnoid space,either at the time of surgery or 
 subsequently through catheters to faciltate the early 
 fibrinolysis the clot ,thus reducing the amount of decaying
 blood pressing against the arteries. 

This appear to be effective way of preventing vasospasm.
 However,a recent trial using tissue plasminogen activator 
 showed a reduction in angiographic vasospasm but no 
 improvement in symptomatic cerebral vasospasm or 
 neurologic deterioration.

 These fibrinolytic agents have a potential to cause 
 bleeding by dissolving normal clot,so only patients at high 
 risk of developing vasospasm should be choosen for this 
 type of prophylaxis.


 Summary 

 One of the most devastating complications of SAH is 
 cerebral vasospasm.

 which can cause delayed focal or diffuse ischaemic 
 neurologic deficits.

 The frequency of occurence as determined by angiography 
 is estimated to be 40% to 60%,however clinically significant 
 and symptomatic vasospasm occurs at lower frequency (20% to 30%).

 Blood in the subarachnoid space precipitate cerebral vaso
 spasm,the component in the blood implicated in pathoge
 nesis of vasospasm is currently thought to be oxyhemoglo
 bine.

 Progressive impairment in level of conciousness or increase 
 in focal neurologic deficit occuring more than four days 
 after bleeding episode should raise the suspicion of cereb  
 ral vasospasm.

 There is general belief that early surgery and the removal 
 of blood reduced the risk of developing cerebral vasospasm
 Numerous drugs have been investigated for prevention or 
 treatment of vasospasm but most are ineffective.

 Calcium channel blockers of which nimodipine has been 
 more extensively studied are the only drugs that have been 
 shown to consistently reduce the incidence of poor 
 outcome by 40% to 70%.

 Triple H therapy aims to increase cerebral perfusion by 
 increasing CBF and improving flow characteristic by 
 haemodilution.

 To optimize therapy and minimize the potential 
 cardiovascular and pulmonary complications,invasive 
 monitors including direct arterial blood pressure,CVP or
 preferably a pulmonary artery catheter are essential.
 If there is no improvement after volume expansion ,the use 
 of inotrope(dopamine,dobutamine and phenylephrine ) are 
 started.


 If the patient is imminent danger from severe diffuse 
 vasospasm or refractory to triple H therapy  then PTA can 
 be alternatif treatment.

 When cerebral arteries are not amenable to balloon 
 dilatory because of size or angle of take off,intra arterial 
 papverine can be choosen.

 REFERENCES :
1.Lam M Arthur :Cerebral aneurysm :Anesthetic 
   concidreation;Cottrell E James,Smith S David;Anesthesia 
   and Neurosurgery ;4th edit.Mosby A harcourt Health 
   Sciences Company ,2000:pp 373-6


2.Weir K Bryce:Intracranial Aneurysm and AV Malformation
   Surgical Consideration ;Albin S Maurice;Textbook of 
   Neuroanesthesia with Neurosurgical and Neuroscience 
   Perspective ;The Mc Graw Hill Companies Newyork,StLouis 
   San Franscisco,1997:pp 852-3.


3.Godsiff S Leisha,Matta FBasil:Intensive care management 
   of intracranial hemorrhage ;Matta F Basil,Menon K David
   Turner M John:Textbook of Neuroanesthesia and Critical 
   Care,Greenwich Medical Media Ltd,London
    2000,pp 335-9.


4.Chang W.J.Cherylee,Bleck P Thomas:Neuroscience Inten
   sive Care:StoneJ.D.Sperry J.Richard;The Neuroanesthesia 
   Handbook;Mosby Year Book Inc.USA,1996;pp457-60.

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Cerebral Vasopasm (PART I )

DEFINITION : (2,3,4)


Vasospasm is the prolonged intense constriction of the larger conduction arteries in the subarachnoid space,which initially surrounded by subarachnoid clot it is likely that spasmogens are released from the breakdown of red blood cell trapped by fibrin mesh in in the the abnormal environment of subarachnoid space.The etiology remain uncertain but appears to be related to the amount and distribution of blood in the subarachnoid space.


This may also be due to local mechanic pressure effects from the high pressure arterial bleeding of the aneurysm or from the clot itself.


Pathogenesis :(1,3)


The vasospastic artery has a structural and pathologic changes within the vessel wall, such as swelling and necrosis of the smooth muscle cells. Although the exact mechanism and cause of spasm have not been completely elucidated,a reasonable hypothesis is that one or more vasoactive substances contained in the blood in the basal cisterns induce changes in the cerebral arteries to cause severe constriction.


Several mediators have been postulated including serotonin
histamine,cathecolamine,prostaglandins,angiotensin,lipid
peroxidase,endothelin and oxyhemoglobin.


The component in the blood implicated in the pathogenesis of vasospasm is currently thouht to be oxyhemoglobin.


The cerebrovascular tone is regulated by a balanced between vasodilatating and vasoconstricting factors.


The suppressived interaction of oxyhemoglobin with endothelium derived relaxing factor nitric oxide (patent vasodilator) coupled with stimulated production of endo
thelin(potent vasoconstrictor) is the postulated cause
of vasocerebral spasm. In experimental vasospasm the increase in the perivascular concentration of oxyhemoglobin and deoxyhemoglobin parallels the time course of vasospasm. In support of this hypothesis,early intracra-
nial operation (within 48 hours) to remove extravasated subarachnoid blood has been shown to be effective in reducing the occurence of vasospasm and associated neurologic deterioration.


INCIDENCE:(1,3)


In study vasospasm accounted for 13,5% the overall morta
lity and major morbidity. 


Not all patients with subarachnoid hemorrhage(SAH) will develop vasospasm and its severity,time course and prognosis are largely inpredictable.


The incidence and severity of delayed cerebral vasospasm have been shown to correlate with the amount and location of blood in the basal cisterns. 


The frequency of occurence as determined by angiography is estimated to be 40% to 60%. 


However,clinically significant and symptomatic vasospasm occurs at a lower frequency (20% to 30%).


This difference may be explained by the varying degree of vasospasm. As established lower limit of cerebral blood flow(CBF) compatible with normal brain function is appro
ximately 15 to 20 ml/100 g/min.


Thus considerable reduction in CBF can occur from vaso
spasm without clinical symptoms.


When symptomatic vasospasm develops, approximately 50% of the patients will die or be left with serious residual neurologic deficits.


Typically angiographically detectable vasospasm is not seen until 72 hrs after SAH, the incidence peaks 7 days after SAH and it is seldom seen after 2 weeks.The onset of vasospasm is generally 3-5 days after SAH, and duration of 2-4 weeks.


CLINICAL MANIFESTATION: (1,2)


Clinical manifestation most commonly gradually but may also occur abruptly include a decrease in the level of conciousness new onset of focal sign and mutism. 
Hijdra et al found that the patients with delayed cerebral ischemia from vasospasm had a decreased in the level of conciousness that may be accompanied by but was never preceded by focal signs.


Progressive impairment in level of conciousness or increase in focal neurologic deficit occuring more than four days after SAH should raise the suspicion of cerebral vasospasm.


DIAGNOSIS: (2,3)


Cerebral angiography remains the gold standard for diagno
sing vasospasm which is seen as smooth vasoconstriction in cerebral vessel.


Vasospasm may be limited the area surrounding the rup
tured aneurysm or it may be widespread when it is asso
ciated with poor prognosis.


Although an angiogram remains the definitive diagnostic tool for vasospasm,and although transcranial Doppler ultrasonography (TCD) is unreliable as a measure of CBF in patients with SAH because vasospasm associated changes in vessel diameter, it has become valuable for diagnosing vaso
spasm non invasively prior the onset of clinical symptoms.


As the vessel diameter is reduced for a given blood flow,red blood cell velocity (FV) increases. 


Hence, cerebralvasospasm is considered present when FV > 12o cm/sec or the ratio between the FV in the middle cerebral aretery(MCA) and the FV in the internal carotid artery(ICA) exceeds 3, should decrease with effective treatment.


TCD is increasingly being used to diagnose vasospasm especially in sedated and ventilated patients, as it has advantage of being a noninvasive bedside test and TCD results did not have any adverse influence on management or outcome.


Cerebral angiography should be performed in any patient with clinically suspected vasospasm despite negative TCD findings.


Other methods which can be used to diagnose vasospasm include photonemision tomography and positron emission tomography(PET).


PET has been performed in patients not responding to triple Htheraphy,the aim is to diagnose any hypoperfused area which are not infracted.


Which will benefit from an improvement in blood flow.
CBF values <20 ml/100g/min have been found in the affected hemisphere of patients with symptomatic vasospasm and values <12ml/100g/min have been asso
ciated with irreversible changes.


to be confinued

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Subarachnoid Hemmorhage And Anesthetic Consideration (PART 5)

HYPERTENSIVE HYPERVOLEMIC HEMODILUTION (TRIPLE H):(1,3)

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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