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Anesthetic management ofCerebral Aneurysm By Dr. Veena Boswal Under the guidance of Dr. Poonam Kalra
Definitions A cerebral aneurysm is a cerebrovascular disorder in which weakness in the wall of a cerebral artery or vein causes a localized dilatation or ballooning of the blood vessel A common location of cerebral aneurysms is on the arteries at the base of the brain, known as the Circle of Willis
Anatomy The Circle of Willis is a circle of arteries that supply blood to the brain Components1. Anterior cerebral artery (left and right)2. Anterior communicating artery3. Internal carotid artery (left and right)4. Posterior cerebral artery (left and right)5. Posterior communicating artery (left and right) The basilar artery and middle cerebral arteries, though they supply the brain, are not considered part of the circle
Epidemiology Exact incidence is unclear but probably about 4%. An annual incidence of rupture is about 15-20 per 100,000 population Age : At any age but peaks at 40-60 years Sex : Male to Female 2 : 3 but more males below 40 and more females after 40years Sites : 30% ICA 40% ACA( Anterior Communicating) 20% MCA 10% Vertebro-basilar systems Rupture : 90% <12mm, 5% in 12-15mm, 5% >15mm
Aetiology It had been thought to be a congenital disease but is now thought to be primarily acquired (although there is a congenital component in some cases) Most are of the saccular or berry aneurysms and this type of aneurysm is unique to the cerebral circulation Rupture is thought to relate to the size of the lesion. This clearly is due to Laplaces Law T = 2PR and the fact that the wall also becomes thinner as the aneurysm enlarges The lesions almost always occur at the bifurcation of vessels . It is thought that the process starts with degeneration of the internal elastic membrane at the apex of a bifurcation. This is the site of the maximum hemodynamic stress The pressure within the aneurysm is at systemic levels and thus rupture is most likely to occur at moments of raised BP. The larger the aneurysm the greater the likelihood of rupture, however most rupture when they are <12mm
Presentation The vast majority present with Sub Arachnoid Haemorrhage Occasionally with pressure symptoms related to direct pressure on nerves, eg. 3, 4, or 6 nerve palsies Many are now presenting with incidental findings on MRI or CT scans Those patients who present with a SAH will in fact have had some type of symptoms in the few days prior to the major bleed Minor bleeds precede the major haemorrhage in 50% of patients. The patients may have Hypertension either as the cause or the result of the bleed. Brainstem ischaemia is thought to be the cause of the secondary form
Signs and Symptoms The Signs and Symptoms of SAH are due to1. Raised ICP2. Damage due to intra-cerebral bleeds3. Regional vasospasm4. Generalised vasospasm
Continued.. The Signs and Symptoms are :1) Result of Initial Rupture : There is an initial abrupt rise in ICP that produces a severe headache ± loss of consciousness. Blood in the CSF produces meningism (photophobia, neck stiffness, and headache)2) Focal signs : The most commonly occurs 7 days later from vasospasm, but if occurring initially may be due to the direct effects of the jet of blood, intracerebral bleeding, or from herniation3) Hydrocephalus : Common, usually due to impaired CSF passage through the basal cisterns. Occasionally large basilar aneurysms may produce IV ventricular obstruction and hydrocephalus
Classification Systems Botterell’s Clinical GradingGrade Criteria1) Conscious with or without Meningeal Signs2) Drowsy without significant Neurological3) Deficit Drowsy with Neurological Deficit and probable cerebral clot4) Major Neurological Deficit present.5) Moribund with Failing Vital Centers and Extensor Rigidity.
Modified Hunt and Hess’s Clinical GradesGrade Criteria0) Unruptured Aneurysm1) Asymptomatic or have mild headache or neck stiffness2) Headache and neck stiffness but no neurological abnormalities other than cranial nerve palsies Drowsy, confused or have mild focal deficits3) Stuporosed and have moderate or severe4) hemiparesis
World Federation of Neurological Surgeons GradingWNFS Grade GCS Score Motor Deficit1) 15 Absent2) 14 – 13 Absent3) 14 – 13 Present4) 12 – 7 Present or5) 6 - 3 Absent Present or Absent
Diagnosis of SAH This is usually on CT scan (SAH or haematoma mainly but you may be able to see the aneurysm on a plain CT MRI or CT angiography will have a much better detection rate Ultimately Cerebral Angiography will be done to determine whether there is an aneurysm and how it should best be treated
Management An angiogram is done as soon as possible to allow rational management decisions to be made (aneurysms are not always demonstrated in presumed subarachnoid bleeds and the absence of an aneurysm obviously has a major impact on the patient’s management) As the patients who have survived the initial bleed are at risk of re-bleeding it would seem sensible to repair the aneurysm as soon as possible. Almost all neurosurgeons will now operate as soon as is practical except in Grade IV and V patients Those with severe vasospasm unresponsive to pharmacologic treatment may also be clipped to allow the use of more marked induced hypertension Obviously the patient who has a major intracranial bleed with mass effects or obstructive hydrocephalus (blockage of the arachnoid villi or the basal cisterns) will require urgent surgery. In these cases the surgery may be restricted to relieving these problems rather than the definitive repair
In case Angiography (and thus definitive diagnosis of Aneurysm) is delayed due to any reasons, the intervening period is a dangerous one with 20% suffering a re-bleed, with a >60% mortality The goals of this period1. Prevent re-bleeds2. Prevent or treat vasospasm3. Detect hydrocephalus4. Avoid respiratory problems5. Optimise the general medical state of the patient
The patient is confined to bed and they are to avoid things that may increase their BP eg straining at stool (given laxatives) Their BP control is difficult and depends on their clinical status. As a rule hypertension should be controlled however if they have vasospasm a common treatment is to raise their BP If there is no obvious vasospasm then the BP is controlled on empirical grounds to about 160 systolic and 100 diastolic Epsilon aminocaproic acid may be used to prevent the clot around the aneurysm from being dissolved. In general it has not proved useful Generally the patient’s fluid status needs to be very carefully assessed and it may be necessary to measure the CVP, of course the U/O and fluid balance should be carefully measured The prolonged bed rest predisposes to respiratory problems and these should be aggressively treated
Vasospasm It is one of the worst problems in this condition causing ischaemia and subsequent cerebral oedema that further compromises the cerebral circulation Radiological evidence of large vessel vasoconstriction is present in about 60-80% of patients But is Clinically and hemodynamically significant in 33% of patients The peak incidence is around 7th day from initial event. The exact mechanism for it is unclear but appears to be due to the presence of blood breakdown products . FFA derivatives such as the prostaglandins and leukotrienes, oxyhaemoglobin and the oxygen radicals.
Clinical Manifestations – Are due to Cerebral Ischemia:1. Decrease in Level of Consciousness2. New Onset of Focal Signs3. Mutism Diagnosis :1. Confirmed by Angiography2. Non Invasive TCD USG may be used to demonstrate increased cerebral artery Flow Velocities
Treatment :1. Pharmacological : Calcium Channel Blockers – Nimodipine is used. Beneficial effects occur either at Distal Vessel Site or at a Cellular level2. Surgical : Early Surgery (within 48 hrs of SAH) with extensive irrigation of cisterns, removes the causative agent (blood byproducts) of vasospasm. Intraoperative cisternal injection of Papaverine may be done to reduce vasospasm3. Reduction of ICP : To improve Cerebral Perfusion and alleviate the ischemic state, reduction of ICP may be tried in patients with elevated ICP
4. Triple H Therapy : Hypervolaemia, Haemodilution, and Hypertension Hypervolaemia – Increase CVP to 10 mm Hg or PAWP to 12 to 20 mm Hg. Colloids or Crystalloids may be used. Hetastarch and Dextrans should be used sparingly due to potential of coagulopathy Hypertension – To increase CPP, Vasopressors (dopamine, dobutamine or phenylephrine) may be used to titrate the blood pressure level till reversal of symptoms or to a maximum of SBP of 160 -200 mm Hg in aneurysm clipped patients and upto 120 – 150 mm Hg in patients with non clipped aneurysms. The BP is maintained until vasospasm resolves (usually in 3 to 7 days) Hemodilution – Based on correlation of hematocrit and blood viscosity. The cerebral blood flow improves with reduction of blood viscosity. Hematocrit of 33% provides optimal balance between viscosity and oxygen carrying capacity of blood
Intracranial Pressure1. ICP rises rapidly after SAH. May also increase from mass effect of clot, cerebral edema or hydrocephalus due to blocked aqueduct or communicating hydrocephalus due to arachnoidal adhesions from extravasated blood that interferes with reabsorption of CSF2. Vasospasm can also exacerbate ICP increase because the reduction in CBF is accompanied by vasodilatation of distal vessels3. ICP correlates well with clinical grade. Normal in Grade 1 or 2 and raised in grade 4 or 5 (Botterell’s grades)4. Never normalize ICP too rapidly because it leads to a rapid increase in Transmural Pressure across the aneurysm wall, thus further increasing chances of bleeding
Impairment of Autoregulation : These patients may have an impaired ability to autoregulate CBF and the Degree of impairment correlates directly to Clinical Grade. Thus it is advisable not to allow the Perfusion pressure to decrease below the lower limit of autoregulation perioperatively specially in Gradewise poor patients. Thus it presents a relative contraindication to Induced Hypotension in these patients Reactivity to CO 2 : Cerebrovascular response to Hyperventilation is generally preserved after SAH . Thus hyperventilation remains effective in reducing CBF during perioperative management in these patients
Pre-operative Assessment These patients need very careful pre-op assessment1. CVS : Baseline BP (to give some idea of the safe level of hypotension) Fluid Status (the fluid balance of these patients is very important, they should not be overloaded otherwise they may develop CCF but if they are dry, cerebral circulation maybe compromised and vasospasm, if present, may be rendered haemodynamically significant. If hyponatremia is allowed to develop cerebral oedema may result2. RESP : Prolonged bed rest runs the risk of atelectasis and pneumonia if this is present, it should be cleared to the patient prior to surgery. Patients with COPD may also need a higher FiO 2 intra- op3. CNS : A simple pre-op assessment will help in the rapid post-op assessment of the patient. Pupil size, gross motor weakness, presence of aphasia and any specific cranial nerve signs are sufficient4. GEN : As for any pre-op examination
Pre-op Tests1. Blood Biochemistry : Electrolyte abnormalities are common and should be corrected pre-op. Renal functions should be assessed as this be a consideration in reducing the BP if induced hypotension is used. Blood Sugar should be normalised as hyperglycaemia has been shown to worsen neurological deficits in the presence of cerebral ischaemia2. CBC : Anaemia should be corrected pre-op3. Coags : INR/APTT4. ECG: This should be done on the day prior to surgery as these patients have a high incidence of ECG abnormalities and these are changeable over the time that surgery is delayed5. CXR : As a general assessment of RESP and CVS pathology6. Echo : Patients with questionable cardiac function should have a pre- operative echocardiography7. Other tests may be indicated in specific situations
Pre-Medication Adequate Explanation is the Best Premedication. Aim of pre-med is to alleviate anxiety to prevent shooting of blood pressure In general, pre-med is best omitted to allow accurate assessment of patient’s pre-op neurologic status In patients with Elevated ICP pre-medication with barbiturates or narcotic should be used judiciously to prevent respiratory depression and hence hypercapnia induced increases in CBF In very anxious, grade 1 SAH patients, titrated doses of sedatives might be used till anxiety is relieved
Radiological Management of Aneurysms Angiographic Coiling of an Aneurysm Usually done under GA Coiling works by placing extremely coiled material inside the Aneurysm. The material coating the coils is extremely thrombogenic and the aim is for the aneurysm to thrombose and a new intima to grow over the inlet of the aneurysm. A variable number of the coils are placed until the aneurysm is full of them The usual anaesthesia is similar that for operative neurosurgery with relaxation, intubation and ventilation The patients will develop a diuresis from all the contrast material and should be catheterised after induction
Risks of Angiographic Coiling:1. The aneurysm may rupture with the angiographic manipulation2. Secondly part of the coil could embolise out of the aneurysm into a more distal artery3. The thrombus formation may extend out of the aneurysm and cause thrombus formation in the feeding vesselsAneurysm rupture is uncommon and can vary from a small leak to a full-blown rupture. Rupture can usually be controlled angiographically but if this fails the patient may need to go to theatre.It is imperative however not to let the BP become elevated and BP should be controlled with Propofol in the first instance. DO NOT used vasodilators to control the BP.
Intra-operative Anaesthesia Principles The principles are :1. Avoid increases in transmural aneurysm pressure2. Provide good conditions for the aneurysm surgerya) "slack" brainb) Reduce aneurysmal pressure during clipping byi) Induced hypotensionii) Surgically by Temporary clips3. Avoid damage to the brain
Monitoring1. CVS : ECG, Arterial line (IBP), CVP (cubital fossa)2. RESP : SpO2, End tidal CO2, oesophageal stethoscope3. NEUROMUSCULAR : Train of 4 (by PNS) (it is essential that these patients do not move)4. CNS : Either BIS/EEG or EPs5. RENAL : U/O, all these patients are catheterised the U/O provides an indication that the diuretics are working
Induction Principle of Induction is that rises in BP and falls in ICP should be avoided at this stage as that increases the transmural aneurysm pressure (the pressure in the aneurysm is at arterial levels) and makes rupture more likely; this is a disaster if it occurs Thiopentone (5-6 mg/kg) or carefully titrated Propofol (1.5 – 2.5 mg/kg) may be used. These tend to reduce CBF and hence ICP Narcotics ( sufentanyl, fentanyl, remifentanyl) tend to increase ICP ( due to autoregulation mediated compensatory cerebral vasodilation in response to systemic hypotension) Thus Normotension should be ensured before their usage. Their Combination with Thiopentone is safe as the opposing effects on ICP usually cancel each other. Mild Hyperventilation may be instituted in patients with elevated ICP.
Continued.. Succinylcholine is often used for muscle relaxation for intubation (found to be clinically safe although theoretically it increases ICP) Atracurium (hypotension) and Pancuronium (tachycardia and hypertension) are associated with Hemodynamic disturbances and hence avoided Vecuronium might be used but long latency obviates its use Rocuronium, due to short latency may be the NDMR of choice in Neurosurgical Anaesthesia Complete muscle relaxation should be ensured using PNS before attempting laryngoscopy
Laryngoscopy and Intubation Prophylaxis against BP rise during laryngoscopy may be given in form of High dose Narcotics, Beta adrenergic antagonists, IV or Topical Lignocaine, Second dose of Thiopentone( 1-2 mg/kg), high MAC Isoflurane IV adjuncts best for poor SAH grades Deep Inhalational anaesthetics may be used in good SAH grades but Avoided in those with increased ICP Laryngoscopy and Intubation should be smooth. If unacceptable rises in BP are encountered, attempt is aborted and resorted back to mask ventilation along with deepening of anaesthesia until it is safe to try again
Maintainance Maintenance best with Nitrous, Remifentanil (due to short duration of action), and a Propofol infusion. Avoidance of inhalational agents and the use of an intravenous agent that causes cerebral vasoconstriction helps to optimise cerebral conditions. BP should be kept within previously defined limits according to the patient’s baseline BP. Target is usually 20 mm Hg below baseline Prior Beta blockade is preferable to reduce reflex tachycardia due to hypotensive agents, to reduce the total requirement of hypotensive agents and to reduce rebound hypertension once the hypotensive agent is discontinued Mannitol (1.5 gm/kg) combined with Frusemide (0.3mg/kg) is given to shrink the brain and provide good operating conditions. It takes about 1 hour for the maximal effect so the mannitol should be started soon after the BP has settled down from intubation
Critical Periods Securing of head with Mayfield pins Skin Incision Periosteal Flap elevation and Bone cutting. These stimuli might cause an increase in BP and hence a preemptive bolus of Narcotic or Propofol is advised before these
Induced Hypotension As the pressure inside the aneurysm is at arterial levels it is usual to induce hypotension during the time of dissection and clipping It has been found that the aneurysm and its vascular tree are more mobile at MAPs of around 50 mmHg In general cerebral autoregulation preserves flow at MAPs of 50 mmHg (providing that there is not raised ICP) but in patients with pre-existing uncontrolled hypertension this lower limit may be considerable raised It is important that the MAP is measured at the level of the brain and not some point below this (due to very low margin for error) The usual thing to do is to reduce the MAP to about 60 mmHg as they are approaching the aneurysm and only go to 50mmHg with clipping Usual choice of agents is between Nitroglycerine and Sodium Nitroprusside with a prior beta blockade
Hypothermia As the survival of tissues has been shown to be prolonged by profound hypothermia (20- 25°C) it was felt that this might be beneficial in this type of surgery Very rarely used these days Reasons:1. For the average case it did not seem to cause a decrease in the mortality ( because there usually is no problem with adequate blood supply as the degree and period of hypotension is not usually great)2. It increases the incidence of post-op vasospasm
Post Clipping Once the aneurysm is clipped the BP is raised to the pre-op level. This should be done slowly over about 10 mins All the fluid loss including calculated insensible losses should be replaced prior to the end of surgery unless there was marked Cerebral Oedema pre-op The maintenance of adequate filling pressures and BP will help prevent vasospasm becoming clinically significant
Reversal The patient is not extubated until they are awake and breathing well BP should be controlled with Propofol or Narcotics infusion Further agents to control BP (B blockers, diazoxide) during extubation might be used if infusions are found unsatisfactory If Remifentanyl has been used then Fentanyl (50-100µg) should be given after the patient is awake and appears neurologically normal
Post Operative Management The patients should be assessed in the recovery ward prior to their return to ICU as there may be need to re- operate if major new neurological signs have occured. The worries post-op are1. Vasospasm2. Re-bleeds3. Infarction either due to the clip occluding a vessel or to thrombosis4. In the higher risk groups there may be continual decreased level of consciousness and the usual complications occur, eg pulmonary oedema Post op the Fluid status needs to be very carefully looked at with enough fluids given to maintain an adequate U/O but not to much as to cause cerebral or pulmonary oedema Close eye kept on their Electrolyte status as hyponatraemia (causes cerebral oedema)
If new neurological deficits are encountered some time after an apparently successful surgery, CT scan is done to rule out Hematoma If normal, Angiography needs to be done to diagnose Vasospasm.Then the BP is raised until the neurological deficit goes or an arbitrary limit is reached
Conclusion Because of the systemic effects and surgical requirements, patient with cerebral aneurysms present a unique challenge to anaesthesiologist. As an anaesthesiologist we should have a thorough understanding of pathophysiology of SAH, a communication with the neurosurgeon regarding approach, a formulation of an anaesthetic plan and its implementation. There will always be patients who despite our best efforts, fail to benefit from the surgical procedure, however with proper planning optimal results can be hoped for.