Anaesthesia for interventional neuroradiology
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Transcript of Anaesthesia for interventional neuroradiology
Intro
A trend towards minimally invasive neurosurgery, an important
development in which has been the introduction of the Guglielmi
detachable coil (GDC) for endovascular aneurysm coiling.
Anaesthesia is required for neuroradiological diagnostic procedures such
as angiograms,computerized tomography (CT), and magnetic resonance
imaging (MRI) or for therapeutic intervention
Anaesthetic concerns INR procedures, including
1. maintaining immobility during procedures to facilitate imaging
2. rapid recovery from anesthesia at the end of procedures to
facilitate neurologic examination and monitoring or to provide for
intermittent evaluation of neurologic function during procedures
3. managing anticoagulation
4. treating and managing sudden, unexpected procedure-specific
complications during procedures (eg, hemorrhage or vascular
occlusion) which may involve manipulating systemic or regional
blood Pressures
5. guiding the medical management of critical care patients
Pre operative assessment
Patients who have had an SAH can have
marked derangement of various organ
systems
Pulmonary complications are the most
common non-neurological cause of death
Neurology
A brief history and short neurological examination
should be carried
1. Glasgow Coma Scale,
2. Grade of SAH
3. Any cranial nerve, visual field, and
4. Motor and sensory deficits
The nature, location, and size of the lesion and
previous treatment must also be ascertained.
Cardiovascular system Massive catecholamine release is the most likely cause of cardiac
dysfunction seen after SAH.
This may include dysrhythmias, abnormal ECG morphology (T
inversion, ST depression, Q waves, U waves, and prolonged QT),
elevated cardiac enzymes, and frequent left ventricular dysfunction
and pulmonary oedema.
Therapy with oral anticoagulants should be stopped and, if
necessary, converted to heparin, which can be stopped or reversed,
if required.
Respiratory system
In addition to the strong causal relationship
between SAH
cigarette smoking
reduced levels of consciousness
prolonged bed rest
predispose to atelectasis and pneumonia
Metabolic considerations Tight control of blood glucose is essential since hyper- and
hypoglycemia are associated with poor outcomes,particularly in the
presence of cerebral ischaemia.
Patients are often dehydrated with electrolyte disturbances such as
1. hypomagnesaemia,
2. hypernatraemia,
3. hyponatraemia associated with the syndrome of inappropriate
ADH secretion,
4. hypokalaemia, and
5. hypocalcaemia
Conduct of anaesthesia
Premedication Premedication should be individualized. A titrated dose of a
benzodiazepine (e.g. midazolam) provides anxiolysis, sedation of short
duration, and amnesia, although it can impair assessment of
neurological status and worsen confusion
Narcotics are best avoided because of potential respiratory depression
and hypercarbia.
H2 -receptor antagonists, alone or with metoclopramide, may be used
to reduce the risks of gastric aspiration.
Nimodipine is frequently used to reduce cerebral ischaemia
consequent to cerebral vasospasm.
Induction
The overriding priority is to maintain cardiovascular
stability, avoiding surges in arterial pressure that might
cause aneurysm rupture while maintaining adequate
perfusion of a possibly ischaemic cerebral circulation.
To this end, propofol is usually used to induce
anaesthesia combined with remifentanil, alfentanil, or
fentanyl; thiopentone and etomidate are alternatives.
Pressor responses can also be obtunded with i.v.
lidocaine or rapid, short-acting b-blockers (e.g. esmolol).
Before tracheal intubation, it is important to ensure that
neuromuscular block is profound; before administration of
neuromuscular blocking agent, the correct placement of
electrodes for peripheral nerve stimulation should be verified.
Rocuronium, atracurium, or vecuronium are suitable for
neuromuscular block. It is useful to use a cut endotracheal tube
so that the image intensifier does not push in or kink the tube
The laryngeal mask airway has also been used in this setting;
there is insufficient evidence to recommend its routine use
Maintainence
Sevoflurane is the volatile anaesthetic agent of choice
because of its low potential for increasing CBF – ICP and
its rapid offset.
Up to 1 MAC, there is preservation of the reactivity of
cerebral blood vessels to carbon dioxide and coupling of
CBF and CMRO2
Sevoflurane also provides faster recovery and
postoperative neurological assessment than isoflurane.
Nitrous oxide (N2O) elevates CBF and ICP and increases
the consequences of air embolism; it should not be used
The use of a TIVA technique incorporating propofol and a short-
acting opioid reduces CBF, ICP, and CMRO2.
Of the short-acting opioids, remifentanil is frequently used; it
provides stable haemodynamics and allows more rapid recovery
from anaesthesia than alfentanil or fentanyl
Rebound hypertension may develop on sudden discontinuation of
the infusion, necessitating a slow decrease in rate before
emergence.
Propofol and remifentanil, sevoflurane and remifentanil, and a
combination of propofol and remifentanil supplemented with
sevoflurane.
Ventilation Ventilation aims for mild hypocapnia to normocapnia (Paco2 4 – 4.5
kPa) to help control ICP
It is important to distinguish two general settings where
hyperventilation is used in anesthetic practice.
First, it is used to treat intracranial hypertension.
Hyperventilation is an important mainstay of the acute management of
an intracranial catastrophe to reduce cerebral blood volume acutely.
The second, far more common, application is to provide brain
relaxation after the skull is open with the intent of providing better
surgical access and, presumably, a lesser degree of brain retraction for
a given surgical approach
Delibrate hypertension
During acute arterial occlusion or vasospasm, the only practical
way to increase collateral blood flow may be an augmentation of
the collateral perfusion pressure by raising the systemic blood
pressure.
The extent to which the blood pressure has to be raised depends
on the condition of patients and the nature of the disease.
Typically, during deliberate hypertension, the systemic blood
pressure is raised by 30% to 40% above the baseline in the
absence of some direct outcome measure, such as resolution of
ischemic symptoms or imaging evidence of improved perfusion.
Phenylephrine usually is the first-line agent for deliberate
hypertension and is titrated to achieve the desired level of blood
pressure.
The EKG and ST segment monitor should be inspected carefully
for signs of myocardial ischemia.
The risk for causing hemorrhage into an ischemic area must be
weighed against the benefits of improving perfusion, but
augmentation of blood pressure in the face of acute cerebral
ischemia probably is protective in most settings.
There also is a risk for rupturing an aneurysm or arteriovenous
malformation (AVM) with induction of hypertension
Delibrate hypotension
The two primary indications for induced hypotension
are
1. to test cerebrovascular reserve in patients
undergoing carotid occlusion.
2. to slow flow in a feeding artery of brain AVMs before
glue injection (sometimes termed ‘‘flow arrest’’).
The most important factor in choosing a hypotensive
agent is the ability to achieve safely and expeditiously
the de-sired reduction in blood pressure while
maintaining patients physiologically stable
Anti coagulation Heparin is administered as an initial i.v. bolus
(5000 IU) or 70 units /kg followed by intermittent boluses or an infusion to keep ACT 2 – 3 times baseline; ACT is monitored hourly.
For reversal of heparin anticoagulation, protamine is used in a dose of 1 mg per 100 units of heparin or dosed according to the heparin dose – response curve.
Complications of protamine administration include I. hypotension, II. anaphylaxis,III. pulmonary hypertension
Direct thrombin inhibitors inhibit free and clot-bound
thrombin, and their effect can be monitored by
either activated partial thromboplastin time or ACT.
Lepirudin and bivalirudin, a synthetic derivative,
have half-lives of 40 to 120 minutes and
approximately 25 minutes, respectively.
Because these drugs undergo renal elimination,
dose adjustments may be needed in patients who
have renal dysfunction.
Temperature Control of body temperature is important; hyperthermia is associated with poor
outcome, and mild hypother-mia has not shown to improve
neurological outcome
Recovery A rapid and smooth recovery is desirable to
facilitate early neurological assessment and safe transfer to recovery areas.
Blood pressure is allowed to return to normal or up to a systolic pressure of 160 mm Hg.
An unsecured or incompletely secured aneurysm may call for induced hypotension.
Patients who have had neurological complications may need to be transferred to neurointensive care for continued sedation and ventilation
Complications Vascular complications are either
haemorrhagic or occlusive Vascular rupture or perforation may be: 1. spontaneous;2. due to hypertension during laryngoscopy,
emergence, inadequate depth of anaesthesia, or associated with the use of vasoactive drugs.
3. brought about by the microcatheter, guide wire, coil, or injection of contrast
Tumors & AV malformations
• Maintain lower blood pressure
a. Reduces flow through fistulous lesion
b. Greater precision for delivery of
cyanoacrylate glues
c. To prevent glue passage into the draining
veins or systemic venous system
Intracranial Aneurysms• 2 basic approaches 1. occlusion of proximal parent arteries 2. obliteration of the aneurysmal sac. (coil
embolization )
Risks – spontaneous rupture, leaky sac, vascular rupture secondary to manipulation
Alternate – stent assisted coiling methods • Risks - parent vessel occlusion,
thromboembolism, or vascular rupture.
AV malformations • Goal : To obliterate as many of the fistulae and
their respective feeding arteries as possible
• Method : embolization with cyanoacrylate glues
• Complications : 1. Acute hemorrhage2. Pulmonary embolism
Carotid Angioplasty & Stenting Anesthetist services are mostly
requested for compromised patients Relative contraindications to CAS
include –
• Antiplatelet agent intolerance, • Other pending surgery that precludes antiplatelet
agents, • Aortic arch disease (age)• Altered carotid morphology, including carotid
tortuosity, concentric calcification (which entails a risk of vessel rupture),
• Heavy thrombus burden, and unstable plaque