Download A Ganaw - Aneurysmal sub arachnoid hemorrhage

02 November 2012
No. 35
Aneurysmal sub arachnoid
hemorrhage
A Ganaw
Commentator: NH Gokul
Moderator: L Padayachee
Department of Anaesthetics
CONTENTS
INTRODUCTION ................................................................................................... 3
CIRCLE OF WILLIS .............................................................................................. 3
RISK FACTORS ................................................................................................... 4
PATHOPHYSIOLOGY .......................................................................................... 5
DIAGNOSIS .......................................................................................................... 6
GRADING OF SAH ............................................................................................... 7
COMPLICATIONS ASSOCIATED WITH SAH ..................................................... 8
CNS complication .............................................................................................. 8
Pathophysiology ............................................................................................. 11
TREATMENT OF CEREBRAL VASOSPASM AND CEREBRAL ISCHEMIA .... 12
SYSTEMIC COMPLICATION ............................................................................. 14
Pathophysiology ............................................................................................. 14
SURGICAL AND ENDOVASCULAR METHODS FOR TREATMENT OF
RUPTURED CEREBRAL ANEURYSMS ............................................................ 17
TIME OF SURGICAL INTERVENTION ............................................................... 18
ANESTHETIC MANAGEMENT .......................................................................... 18
Premedication.................................................................................................. 19
Monitoring ........................................................................................................ 19
Maintenance..................................................................................................... 20
Temporary clipping ......................................................................................... 20
Intraoperative aneurysmal rupture ................................................................. 20
Emergence ....................................................................................................... 21
ANESTHESIA FOR INTERVENTIONAL RADIOLOGY ...................................... 22
CONCLUSION .................................................................................................... 26
REFERENCES.................................................................................................... 27
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INTRODUCTION
Most of spontaneous SAH is due to rupture of saccular aneurysm, the prevalence
of intracranial saccular aneurysm by radiographic and autopsy series is 5 %,
about 20 to 30% of patients have several aneurysms. 1
Aneurysmal SAH occurs at rate of 3 to 25 per 100000 population, mostly occurs
between 40-60 years however young children and elderly can be affected , the
incidence of SAH is higher in women than men which may be due to hormonal
status, African Americans are at higher risk of SAH than Caucasian Amicans. 1, 2
CIRCLE OF WILLIS
The circle of Willis is an anastomotic structure, it is formed when the internal
carotid artery go into the cranial cavity bilaterally and divides into the anterior
cerebral artery and middle cerebral artery ,the anterior cerebral artery are then
united by an anterior communicating artery . Posteriorly the basilar artery formed
by the left and right vertebral arteries, it branches to give a left and right posterior
cerebral artery. Posterior cerebral arteries join the internal carotid system
anteriorly through posterior communicating arteries. 3, 4
Page 3 of 28
Subarachnoid haemorrhage and anaesthesia for neurovascular surgery Charlotte Moss Sally
Wilson, Anesthesia and Intensive Care Medicine 2011
RISK FACTORS
Most of spontaneous SAHs are result from rupture of intracranial aneurysm
therefore risk factors for aneurysm formation overlap with risk factors for SAH. 1
 Cigarette smoking; it is associated with 11 fold increase risk of SAH; it is
most important preventable risk factor. 1,2
 Hypertension; it is associated with 3 fold increase risk of SAH; it is major risk
factor for SAH.
 Alcohol abuse
 Genetic risk; the risk of SAH increases by 7 fold in first degree relatives of
patient, in addition number of rare inherited conditions(Autosomal dominant
polycystic kidney, Ehler Danlos syndrome) are associated with cerebral
aneurysm and SAH,1,5
 Use of sympathomimetic drugs such as (cocaine)1
 Female sex, it is due to estrogen deficiency (estrogen replacement therapy
reduces the risk), so it is higher in postmenopausal women than
premenopausal.1
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 Antithrombotic therapy, it increases severity of the haemorrhage, there is no
data to proof whether antithrombotic therapy increase the risk of
aneurysmal rupture or not.5,1
 Statins lowers the risk of ischemic cerebrovascular events, however some
concern that statin use and low cholesterol levels may increase risk of
intracerebral haemorrhage.
 Aneurysm size of 7 mm increases risk of rupture and increases risk of SAH
1,5
 Aneurysm morphology such as bottleneck shape and the ratio of size of
aneurysm to parent vessels are associated with rupture of aneurysm.
The risk of SAH increases in symptomatic patient with large unruptured
cerebral aneurysm, located either on posterior communicating artery or on the
vertebrobasilar system especially in symptomatic patient. 5
PATHOPHYSIOLOGY
Smoking , chronic hypertension and alcohol abuse lead to weakened arterial
tunica media , Chronic exposure to intravascular shear stress lead to pouching of
the weakened wall, especially in the vicinity of bifurcations where turbulent flow is
prominent . The aneurysmal rupture is directly proportional to the size of the
aneurysm, which is rising from 0, 05% in aneurysms less than 10 mm, to 6% for
those greater than 25 mm. More than 80 % of cerebral aneurysm arises from the
anterior carotid circulation (anterior and posterior communicating and middle
cerebral arteries), with only 10 - 20% arising from the posterior vertebrobasilar
circulation. Subsequent to aneurysmal rupture, blood spreads quickly within CSF,
rapidly increasing ICP , this sudden increase in the ICP
leads to severe
headache, cerebral oedema and hydrocephalus.
Bleeding usually lasts for a few seconds however rebreeding is common and
occurs within the first 24 hours. 1, 2 the presence of blood and breakdown products
of hemoglobin in the subarachnoid space is responsible for meningeal irritation,
meningism.and vasospasm1.2. Inflammation seems to play a vital role in the
pathogenesis and growth of intracranial aneurysms; prominent mediators include
the nuclear factor (NF-кB), tumor necrosis factor, macrophages, and reactive
oxygen species. Though there are no controlled studies in humans, 3-hydroxy-3methylglutaryl coenzyme A reductase inhibitors (statin”) and calcium channel
blockers could impede aneurysm formation by the inhibition of NF-кB and other
pathways.5, 6
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CLINICAL MANIFESTATION
Headache is the hallmark of aSAH in awake patient who describes it as worst
headache in his life , this headache is sudden onset and immediately reaching
maximal intensity (thunderclap headache ). Sentinel headache is also reported by
10% to 43% of patients, which is minor headache, it is symptoms of minor
Hemorrhage
(sentinel bleed or warning leak) .5, 7 the most of these minor
hemorrhages occur within 2 to 8 weeks before major hemorrhage.5 The headache
may be associated with nausea and/or vomiting, stiff neck, photophobia, brief loss
of consciousness, or focal neurological deficits (including cranial nerve palsies).
Seizures occur in about 26% of patients within the first 24 hours of SAH , most
of the time before medical care is accessed , it is commonly in SAH associated
with intracerebral hemorrhage, hypertension, and middle cerebral and anterior
communicating artery aneurysms.5,8
DIAGNOSIS
● Non contrast head CT scan
It is the cornerstone of SAH diagnosis, it confirms presence of blood clot in
subarachnoid space in most of the cases if the scan is performed in first 24
hours, also it may provide an idea of the cause of the bleeding and site of the
aneurysm. In addition to that it is useful in diagnosis of intraventricular and
subdural hematoma1, 2, and 5. CT scan sensitivity is highest in the first 3days
(close to 100 %) and progressively decreases over time to about 58% in 5th
day .1, 5
.
● Lumbar puncture
It is mandatory if there is strong feeling of SAH in spite of normal CT scan
especially after the 5th day when the sensitivity of CT scan greatly decreases,
the typical findings are an elevated opening pressure and presence of
xanthochromia which can lasts for 2 weeks after SAH.1, 5
Xanthochromia represents hemoglobin degradation products in CSF, and
indicates that the blood has been in CSF for at least 2 hours.
● Brain MRI
MRI has advantages over CT brain in detection of subacute subarachnoid
haemorrage (after 4 days), when head CT scan is negative and there is clinical
suspicion of SAH, and possibly avoiding need of lumbar puncture, the
disadvantage most of SAH patient confused, and they require sedation for at
least 45 minutes for MRI.1,5,8
● Digital subtraction angiography
Once diagnosis of SAH has been completed, the source of bleeding must be
identified with angiographic studies, Digital subtraction angiography (DSA) is
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the gold standard for detection of intracranial aneurysm and study of
anatomical features of cerebral blood vessels. 1
● CT and MR Angiography
Both CT and MR angiography are useful for screening and pre-surgical
planning, they can detect aneurysms ≥ 3mm with high degree of sensitivity,
however they are less sensitive than conventional angiography .1 CTA can be
achieved immediately after the diagnosis of SAH by head CT scan when the
patient still in scanner, CTA is more practical than MRA in acute setting. CTA
is used as alternative to conventional angiography in SAH patient, especially
in acute setting and rapidly declining patient who needs emergent craniotomy
for hematoma evacuation1.
CTA can substitute catheter cerebral
angiography in older patient with degenerative vascular disease provided that
the quality is excellent and investigation is performed cautiously.5 Negative
CTA should be followed by 2- and 3- dimensional cerebral angiography in
case of diffuse SAH. MRA is rarely indicated in SAH, because of limited
routine availability, difficulty in scanning acutely sick patient, patient
compliance and motion artefact, long study time and cost .5
GRADING OF SAH
Hard work has been made for development of scales to clinically grade patient
with SAH, to assess the severity of initial injury, to guide treatment decision, to
provide prognostic information regarding outcome, and to standardize patient
evaluation for scientific study purposes.9
● World Federation of Neurosurgeons SAH Scale (WFNS)
It is simple and widely accepted classification; it describes the clinical condition
of the patient.
WFNS scale
GCS
I
II
III
IV
V
15
14-13
14-13
12-7
6-3
Motor
deficit,
aphasia+/hemiparesis
or
hemiplegia
Absent
Absent
Present
Present/Absent
Present/Absent
Table 1 World Federation of Neurosurgeons SAH Scale.
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● The Hunt and Hess scale
It was projected in 1968 as an adjustment to an older system initially described
by Botterell and colleagues in 1956, the scale was prepared to stratify the
surgical risk, and to help the surgeon on making appropriate decision in
appropriate time.9
Grade Clinical description
I
Asymptomatic n minimal headache and slight nuchal regidity
II
Moderate to severe headache, nuchal rigidity, no neurological
deficit other than cranial nerve palsy.
III
Drowsiness, confusion or mild focal deficit.
IV
Stupor, moderate to severe hemiparesis, and possibly decelerate
rigidity and vegetative disturbances.
V
Deep coma, decelerate rigidity, moribund appearance
Table 2 Hunt and Hess scale.
● Fisher Scale
In 1980, the Fisher Scale was projected to predict cerebral vasospasm after SAH;
the scale quantifies the amount of blood seen on CT scan.9
Group
I
II
III
IV
Blood on CT scan
No subarachnoid detected
Diffuse or thin vertical layer < 1 mm thick
Localized subarachnoid clot and /or vertical layer > 1
mm thick
Intraventricular or intra-parenchymal clot with diffuse
or on SAH
Table 3 fisher grade scale.
COMPLICATIONS ASSOCIATED WITH SAH
CNS complication
i. Re-bleeding
The maximal risk of re-bleeding is in the first 2-12 hours, most of re-bleeding
(73%) occurs within the first 72 hours of initial hemorrhage.5 Re-bleeding is
associated with very high mortality and morbidity.5
Early re- bleeding is associated with worse prognosis than late re- bleeding.
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Many factors are considered as predictor for re-bleeding;

Hunt-Hess grade on admission

Maximal aneurysmal diameter

High initial blood pressure (systolic BP >160mmgh )

Sentinel headache preceding SAH

Longer interval from ictus to admission

Ventriculostomy before aneurysmal treatment
Re-bleeding diagnosis is based on deterioration of neurological status and
appearance of new hemorrhage in CT scan1.
Medical measures to prevent re-bleeding after SAH
 Blood pressure control (systolic BP <160 mmgH) between the time SAH
symptoms onset and aneurysm obliteration with treatable agents to maintain
cerebral perfusion, balance the risk of stroke, and prevent hypertension
related re-bleeding.
Nicardipine is used for smooth control of BP ,as well as Clevidipine, shortacting calcium channel blocker, is good option for acute control of BP,
however up to now there is no evidence support using it in SAH .1,5,8
.
 For patient with an unavoidable delay in obliteration of aneurysm ,and great
risk of re-bleeding ,short term (72 hours )therapy with tranexamic acid or
aminocaproic acid is advisable (provided there is no medical
Contraindication) to decrease risk of early bleeding .5
II. Hydrocephalus
One of the common complication of SAH, it is either acute or chronic;
 Acute hydrocephalus occur 15-87% of patients with SAH, it occurs as result
of obstruction of CSF flow by blood products or adhesion , it is managed by
external ventricular drainage ( EVD ) especially when obstructive
hydrocephalus is suspected or when the lumbar drainage is contraindicated
(sever high intracranial pressure ),it is also managed with lumbar drainage
which improves brain relaxation , decrease risk of vasospasm , acute
hydrocephalus is associated with increase mortality and morbidity secondary
to cerebral infarction and re-bleeding.1,5
 Chronic shunt-dependent hydrocephalus which occurs in 8.9%-48% of patient
with SAH, its due to decrease of CSF absorption at the arachnoid granulation,
it is usually treated with shunt placement.1,5






Factors may increase risk of hydrocephalus; 1
Elderly
Intraventricular hemorrhage
Hypertension
Hyponatremia at presentation
Low Glasgow score at presentation
Antifibrinolytic agents
Page 9 of 28
III. Seizures
More than 26% of patients with SAH experience seizure- like episodes,
majority of such patients reported onset of these seizures occurring before
medical care are accessed. There are variable risk factors for the development
of early seizures such as aneurysm in middle cerebral artery, thickness of SAH
clot, hypertension, intracerebral hematoma, re-bleeding, cerebral infarction,
poor neurological grade. Routine use of anticonvulsant is associated with
worse cognitive outcome, delayed ischemia, fever and vasospasm, however it
may be considered in patient with high risk of delayed seizure.5, 8
IV. Vasospasm
Its luminal narrowing of large cerebral blood arteries after SAH, leading to
cerebral ischemia, Vasospasm commonly occurs 3-5 days after initial
hemorrhage, with peak vasoconstriction occurring between days 5-14, it’s
resolving spontaneously after 21 days of SAH.5, 8, 10
It can manifests in many features such as reduced conscious level, focal
neurological deficit, simply nuchal rigidity, the exclusion of other causes such
as re-bleeding, hydrocephalus, sepsis and metabolic derangement is required
to confirm the diagnosis. Sometimes there is no correlation between severity
of vasospasm and the symptoms of ischemia, there are patients with severe
large artery spasm who never become symptomatic and others with quite
modest spasm who develop infarction.
Possibly various factors play important role in development of ischemia and
infarction, such as distal microcirculatory failure, poor collateral anatomy, and
genetic or physiological variations in cellular ischemic tolerance, It’s confirmed
angiographically in 70 %of patients with SAH, however it manifests as
symptomatic spasm in 36% of all patients with SAH .5, 8 Angiography is gold
standard diagnostic investigation for vasospasm (reduced arterial diameter). 12
Transcranial Doppler sonography (TCD) also can be used in diagnosis of
vasospasm which will reveal increased cerebral blood flow velocities.
Perfusion CT is a promising technology; however the risks of dye load and
radiation exposure are main disadvantage.5, 12
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Figure 1 TCD monitoring for cerebral vasospasm after subarachnoid hemorrhage. A, Normal TCD
waveform. B, Waveform from the same patient following development of cerebral vasospasm. Note
the greatly increased flow velocity of the blood travelling through the narrowed vessel 11.
Pathophysiology
It is complicated cascades in affected blood vessels and neurons and can be
divided into 2 categories; 10
1. Elevated intracellular calcium
After SAH, calcium influxes into smooth muscle and neuron is rapidly
increased through NMDA receptors and voltage-gated calcium channels, in
addition glutamate is increased and activates NMDA receptors, leading to
further calcium influx. In smooth muscle, high intracellular calcium
concentration enhances binding of calcium to calmodulin.
Calmodulin activates myosin light chain kinase (MLCK) to phosphorylate
myosin, which induces myosin-actin interaction and smooth muscle contraction
and blood vessels constriction.
Page 11 of 28
In neuronal cells, increase intracellular calcium leads to hyper activation of
enzymes such as protease, endonuclease, phospholipase, which destabilizes
cell body and membrane, leading to cellular injury and death.10
2. Vasoactive compound and vessel wall injury
In day 3-5 after SAH, oxy hemoglobin (RBC breakdown product) inhibits
nitric oxide (physiologic vasodilator), and stimulates leukocytes to produce
endothelin-1
(physiologic
vasoconstrictor),
resulting
in
potent
vasoconstriction. Furthermore breakdown of oxy hemoglobin leads to
release of re active oxygen species and iron which leading to oxidative
damage to blood vessels wall. In addition, production of vasoactive
compounds after SAH such as serotonin, norepinephrine, and angiotensin II
lead to potent vasoconstriction10
.
TREATMENT OF CEREBRAL VASOSPASM AND CEREBRAL ISCHEMIA
I. Nimodipine
It improves long-term neurological outcome if it is started on admission and
administered for 21 days, the recommended oral dosage is 60 mg 4hourly
(maximum daily dose 360 mg ),the role of nimodipine based general brain
protective mechanism as there is no proof to suggest that it treats
angiographically diagnosed vasospasm.2.11 The continuous intravenous infusion
of nimodipine is not recommended as it is not superior to oral nimodipine and
associated with high incidence of hypotension especially in hypovolemic patient.
(An adequate systolic BP of 130 -150mmHg takes priority over nimodipine
administration, and it should be stopped if a stable BP can’t be maintained.
Nimodipine should be given through a central line to avoid thrombophlebitis.
The recommended dose of IV nimodipine 1 mg /hour in the first 6 hours, then
1.5 mg/hour in next 6 hours, then increased to 2mg/hour (maximum dose).2.11
II. Triple-H therapy (hemodynamic augmentation therapy)
It is combination of induced hypertension, hypervolemia, haemodilution (HHH);
it is indicated in treatment of vasospasm in SAH, and prevention cerebral
ischaemia by optimization of cerebral blood volume and perfusion pressure in a
situation where cerebral blood flow is thought to be pressure dependent.
- HYPERTENSION
It increases cerebral perfusion pressure in face of increased cerebral
vascular resistance due to vasospasm ,Systolic blood pressure between 120
–150 mm Hg in unclipped, and 160 – 200 mm Hg in clipped aneurysms.2,11
- Haemdilution
Haematocrit of 30%-35%, it improves cerebral perfusion by reducing blood
viscosity and improving rheology.
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- Hypervolemia
CVP between 7-10 mmHg, and PAWP 13-15 mmHg, however there have
been sparse new significant records on the absence of benefit for
prophylactic hypervolemia compared with maintenance of euvolemia.2, 11, 5
Once DCI is confirmed, the initial management is the induction of
hemodynamic augmentation to improve cerebral blood flow and cerebral
perfusion. No randomized trials showing benefit from this intervention and a
Cochrane review failed to demonstrate support, but the rapid improvement of
many patients with this therapy and their worsening when it is stopped
prematurely are convincing proof of efficacy.2,5,8 in spite of this most
neurosurgeons don’t recommend augmentation therapy in unclipped
aneurysm. The augmentation therapy may cause myocardial ischemia,
respiratory failure, pulmonary embolism, hyponatraemia, therefore Triple-H
therapy is not recommended in presence of cardiac dysfunction.2
Aortic balloon device is the new technique for hemodynamic augmentation, it
is still under investigation.5
III. Ballon angioplasty
Cerebral angioplasty (for accessible lesion ) and /or intra-arterial vasodilator
infusion such as calcium channel blockers (for distal vessels) is indicated in
symptomatic patient with cerebral vasospasm ,especially who are not
responding to hypertensive therapy, and those with sudden focal neurological
deficits and focal lesions on angiography referable to their symptoms (before
angioplasty urgent catheter angiography to confirm segmental vasospasm ,
and CT brain to exclude infarction in the area supplied by the spastic
vessels).2,5 Cerebral angioplasty may lead to arterial dissection, rupture,
thrombosis, infarction, hemorrhage, and reperfusion injury leading to cerebral
oedema.11
IV. intra-arterial papaverine
Up to 300mg per hemisphere, it is used for treatment of distal vasospasm.
Disadvantages: may require repeating, relatively short-acting, neurotoxic,
associated with seizures, blindness, coma, irreversible brain injury.2.11
V. Magnesium sulphate
No evidence to support using of magnesium sulphate however there is some
suggestion of reduction in delayed ischemic deficits associated with
magnesium infusion .5
VI. Statins
Recent meta-analysis reported no role of statin in SAH however, a larger
phase 3 trial (SimvasTatin in Aneurysmal Subarachnoid Hemorrhage
[STASH]) is still in progress.5
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VII.Endothelin A-receptor antagonist
Clazosentan, (endothelin-1 receptor antagonist) had been presented to be
associated with a dose-dependent decrease in the frequency of vasospasm in
a phase IIb trial (Clazosentan to Overcome Neurological iSChemia and Infarct
OccUrring after Subarachnoid hemorrhage [CONSCIOUS-1]).
CONSCIOUS-2 found no improvement in clinical outcome in patient treated
with aneurysm clipping. CONSCIOUS-3 was in patient treated with coiling, it
was stopped before completion.5
VIII. Intra-arterial Nicardipine and/or Milrinone
IX. Intra-cisternal administration of vasodilators
SYSTEMIC COMPLICATION
The high morbidity and mortality associated with SAH is not only due to
neurological complication – medical complications also play major role in
increasing mortality and morbidity rates.13
I. Cardiac complication
It occurs in about 50 % of patients with SAH, it ranges from mild elevation in
cardiac enzymes and ECG changes to obvious clinical and echocardiographic
pathology, cardiac damage markers are associated with an increased mortality
and poor outcome and DCI.
Pathophysiology
● Mild myocardial injury
It is presented by mild elevation in serum cardiac troponin I(not reaching
diagnostic threshold of MI) , this elevation occurs in 20-68% of patients with
SAH , the degree of neurological injury as graded by the Hunt-Hess grade in
an independent predictor of myocardial injury in SAH patients. Serum troponin
is powerful predictor for cardiac and pulmonary complication such as
hypotension requiring vasopressor, LV dysfunction, pulmonary edema and
DCI, especially in patient presenting with a high grade on WFNS.
Serum troponin is more specific and sensitive indicator of myocardial injury
than creatine kinase-MB, therefore serum troponin level and trends must be
monitored through serial measurements particularly in SAH patients with past
history of cardiovascular disease.13
● Cardiomyopathy
Neurogenic stunned myocardium(NSM) is the most severe form of myocardial
injury in SAH , it occurs in 20%- 30% of patients with SAH , The elevated level
of sympathetic tone leads to calcium overload with reduced sensitization of
contractile filaments to this cation ,eventually causes myocardial depression ,It
is characterized by subendocardial contraction band necrosis,
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Echocardiography shows abnormal LV contractility and abnormal wall motion
which are reversible but sometimes may lead to cardiogenic shock.13
CK-MB levels, female gender and poor neurological grade are predictors of LV
dysfunction. Severe LV dysfunction decreases cardiac output and mean
arterial pressure leading to reduction in cerebral blood flow (CBF), furthermore
LV dysfunction may be associated with cerebral vasospasm and through it is
adverse effect on cerebral blood flow, therefore optimal heart function is critical
to prevent progression of neurological dysfunction and to promote recovery in
patients with SAH.2,5,13 The use of inotropes such as dobutamine or milrinone
may be required to optimize CO, in patient with LV dysfunction especially with
usage of Triple H therapy to treat vasospasm. In sever LV dysfunction
implementation of intra- aortic balloon pump may be required.2, 5, and 13
● ECG findings
It is common in SAH patients, particularly in first 3 days of presentation, during
the acute phase 50% - 100% of SAH patients will show different forms of ECG
changes such as13
ST segments changes in 15%-51 %.
T wave changes in 12%-92%.
QTc prolongation 11%-66%
Prominent U wave 4%-47%
Around 4–8% of SAH patients will have malignant arrhythmias such as
ventricular tachycardia (VT), torsade de pointe and asystole.13 Management of
arrhythmias in SAH patients depends upon the type of arrhythmia and
classification, clinical significance and the patient’s condition. As a first step, it is
vital to assure satisfactory oxygenation and correct electrolyte abnormalities
and metabolic disturbance. The use of b-blockers to treat cardiac
tachyarrhythmia in SAH should be balanced against hypotension and decrease
in CBF5, 13.
New study has found that arrhythmias are associated with poor outcome, in
spite no correlation was found between severity of cardiac arrhythmia and site
and extent of intracranial hemorrhage on CT scan, neurological condition, or the
location of ruptured malformation.14
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II. Electrolyte disturbance
The SAH associated with different forms of SAH such as hyponatraemia,
hypokalemia, hypocalcaemia and hypomagnesaemia.1, 5
Hyponatraemia
It is relatively common, it ranges at rate 10%-30%, it is an independent risk
factor for poor prognosis, and it can be developed from different mechanisms
after SAH.
- Cerebral salt wasting syndrome which caused by secretion of atrial and brain
natriuretic hormone , it is associated with negative sodium balance and
intravascular volume contraction ,it is common in patient with poor clinical
grade hydrocephalus , ruptured anterior communicating artery aneurysm,
Cerebral salt wasting syndrome can be treated with hypertonic saline solution
which increases cerebral blood flow, brain tissue oxygen and PH in patient
with SAH.
- SIADH is associated with increased free water and high CVP.2,5
III. Fever
One of the common medical complication of SAH, it is associated with the
severity of the injury, amount of hemorrhage, development of vasospasm.
Effective fever management may improve functional outcome.5
IV. Anaemia
It comprises brain oxygen delivery, correction of anaemia and high haemoglobin
value improve outcome after SAH, and however the thresholds for blood
transfusion have not been determined.5
V. Thrombocytopenia and deep venous thrombosis
Heparin induced thrombocytopenia is probably related to number of
angiographic procedures have been performed, Patients with heparin induced
thrombocytopenia type II seem to be at high risk of thrombotic complications,
vasospasm, and poor outcome. At this time uncertain whether there is practical
means of avoiding HIT (as it is essential in angiographic procedures), however
it is vital to know this complication to avoid further heparin exposure and to use
non heparin substitute under supervision of a haematologist.
DVT is relatively recurrent event after SAH, especially in immobilized patients.1,5
Page 16 of 28
Medical complication
Arrhythmia
Liver dysfunction
Neurogenic
pulmonary
oedema
pneumonia
ARDS, atelectasis
Renal dysfunction
Pulmonary embolism
incidence
35%
24%
23%
22%
20%
5%
<1%
Table 5 summery of medical comlication11
SURGICAL AND ENDOVASCULAR METHODS FOR TREATMENT OF RUPTURED
CEREBRAL ANEURYSMS
Ruptured aneurysms can be cured by microsurgical clipping or endovascular
coiling. Microsurgical clipping requires craniotomy and targets to prevent re
bleeding of the aneurysm via insertion a clip through its neck, thus, isolating the
aneurysm from circulation. This technique conveys a 98% certainty of elimination
of the risk of rupture.15
Guglielmi ( 1991) described blocking of an aneurysm by an endovascular
approach with electrolytically detachable platinum coils device which induces
secondary thrombosis of the aneurysm.5 The introduction of the new technique
gave rise to the need for identifying the patient population appropriate for
receiving endovascular treatment, in addition the frequency of use of this
technique varies widely therefore , there is a need of proof to establish the
efficacy and safety of endovascular coiling, particularly in a developing country15.
Koivisto and co-worker (2000) published first prospective randomized outcome
study of surgical versus endovascular coiling , they concluded that endovascular
treatment of intracranial aneurysms results in clinical outcomes equal to that of
surgical clipping.16
The International Subarachnoid Aneurysm Trial (ISAT) is the first multicenter
prospective randomized trial comparing the 2 options, they included 2143 patients
with ruptured intracranial aneurysms were randomly assigned to clipping ( 1070)
or coiling (1073) .5,15 Primary outcomes included death or dependent living, and
secondary outcomes included risk of seizures and risk of re bleeding.
Initially 1-year outcomes concluded a fall in death and disability from31% in the
clipping arm to 24% in the endovascular arm, this difference was mainly driven by
a reduction in the rate of disability among survivors (16% in the endovascular arm
and 22% in the clipping arm). The risk of epilepsy and significant cognitive decline
was also reduced in the endovascular group, but the occurrence of late re
bleeding (2.9% after endovascular repair versus 0.9% after open surgery),
Page 17 of 28
and only 58% of coiled aneurysms were completely obliterated compared with
81% of clipped aneurysms.5 Although these results have affected the approach to
patients with intracranial aneurysm in neurosurgical centers across the world, the
study has been criticized due to lack of generalizability, for example Posterior
circulation aneurysms, which account for 8% of patients admitted with
subarachnoid haemorrhage and up to 48% of ruptured aneurysms managed by
endovascular coiling at some centres, made up only 2·7% of the ISAT study
population.16
Tahir et al concluded no significant difference in the clinical outcome of coiling and
clipping of ruptured intracranial aneurysms; however, clipping is more cost
effective than coiling.
Clipping is recommended for middle cerebral artery aneurysms (difficult to treat
with endovascular technique) and Patients presenting with an intraparenchymal
hematoma >50 mL (high occurrence of critical outcome) 5
Endovascular coiling is preferred
technique for patients presenting with
vasospasm, elderly, poor clinical grade, and posterior cerebral aneurysms.5
TIME OF SURGICAL INTERVENTION Earl, typically
Early surgery ideally done within the first 24 hours of the hemorrhage, and
aggressive prophylactic measures to avoid DCI due to vasospasm ,have become
routine in most neurosurgical centers ,especially for patients with good
neurological condition (Hunt and Hiss grade I,II and III) ,and is also used very
often but not consistently in poor grade patients (IV ,V). The advantage of early
surgery is reduction the risk of re-bleeding, and allows for safe use of induced
hypertension to treat vasospasm .in addition early surgery has not been shown to
increase the risk of intraoperative complication compared with late surgery
however has disadvantage of being associated with poor operation condition.2,17
Late surgery provides excellent surgical condition but as was shown in
cooperative study high percentage of patient die before the planned surgery.2
The International Cooperative Study on the Timing of Aneurysm Surgery Trial
(ICSTAS), concluded that period from 4-10 day post SAH has been associated
with poor outcome. MF Lawson et al showed that endovascular treatment of
rupture aneurysm can be performed safely on day 4-10 post SAH.11
ANESTHETIC MANAGEMENT
Anesthetic concerns for clipping and coiling are comparable with noticeable
differences in the venue, possible blood loss and need for brain relaxation.
Preoperative assessment should include neurological status, co-morbidities and
complications. The clinical grade of the SAH correlates well with the ICP. Patients
with grade I or II SAH may be expected to have normal ICP, normal cerebral
autoregulation and a normal response to hyperventilation,
Page 18 of 28
While patients with grade III or IV SAH will have raised ICP, compromised
autoregulation and decreased CO2-reactivity.2, 4, 5, 18
The primary goals of anesthetic management are;
- Control the aneurysm’s transmural pressure gradient to avoid sudden
aneurysmal rupture. The aneurysm’s transmural pressure gradient (TMP) is
equal to the pressure within the aneurysm (arterial blood pressure) minus the
pressure outside/around the aneurysm (ICP) i.e. TMP=MAP-ICP.18
This highlights the dilemma of balancing acceptable cerebral perfusion versus
the risk of aneurysmal rupture therefore until the aneurysm is clipped blood
pressure should not be allowed to increase above the preoperative baseline.
Gradual decrease in ICP before opening the dura (ICP = 0) due to sudden
reductions in ICP lead to sudden increase in the aneurysm’s TMP.18
- Maintaining adequate cerebral perfusion and oxygen delivery to avoid
secondary injury2, 18.
- Avoiding sudden changes in intracranial pressure to avoid aneurysmal
rupture.
- Maximize surgical exposure and reduces retraction on the brain.
- Providing cerebral protection during ischemic period.
- Optimization of ventilation to achieve
1- Low mean airway pressure, to avoid increase in ICP
2-Normocapnia, at around 4.5kPa ( hypocapnia lead to cerebral
vasoconstriction and resultant ischaemia, and hypercapnia causes cerebral
vasodilatation and resultant increased ICP).2
- The prevention or treatment of cerebral oedema, via careful fluid
administration.
- Adequate preparation to manage expected intra-operative problems, such as
aneurysm rupture.
- Adequate analgesia to obtund painful stimuli, such as intubation and head
pin placement.
- Provision for rapid emergence, to enable early postoperative neurological
assessment.
Premedication
Poor-grade patients may already be in ICU, intubated and sedated. In others,
sedative premedication affects neurological evaluation and should be avoided,
however anxious patients with a good grade may benefit from a short acting
benzodiazepine2, 4
Monitoring
In addition to standard monitoring (pulse oxymetry, ECG, NIBP, gas analysis),
placement of arterial line under local anesthesia before induction of anesthesia is
mandatory to address any hemodynamic changes during induction. 5-lead ECG to
detect any arrhythmia. Central venous access is dependent on patient’s general
status, it is essential in poor grade patients or patients with significant
cardiovascular dysfunction to titrate vasopressor and to assess volume status pre
clipping, however the risk of placing central access outweighs any benefit for good
Page 19 of 28
grad patient.2,4,11,18 TEE is indicated for patient with myocardial dysfunction.
Neuromuscular relaxation should be monitored continuously to avoid the disaster
of a patient moving or coughing during the procedure which can lead to rupture of
aneurysm and increase in ICP. Neuromonitoring such as Evoked
potential(somatosensory evoked potential to detect reversible ischemia during
temporary vessel occlusion and brainstem auditory evoked potential to monitor
posterior circulation), ICP monitoring and intraventricular catheters especially in
patient with hydrocephalus4, 18.
- Bispectral index (BIS) monitoring
- Urine output monitoring.
- Temperature monitoring.2
Maintenance
The primary goals of maintenance are to provide compliant brain, maintenance
cerebral perfusion pressrure.2 Regarding patients outcome, no proof to suggest
that propofol TIVA is superior to isoflurane /sevoflurane inhalational-based
anaesthesia.2
Inhalation anaesthesia is accompanied with fentanyl or remifentanil, although high
dose of sufentanil is associated with increase of cerebral blood flow.
If higher doses of fentanyl or sufentanil need to be avoided, it is mandatory to
supplement painful events, such as the head pie with alfentanil, to blunt
hypertensive response that associated with pin placement.2
Other techniques, such as local anaesthetic infiltration or deepening the level of
anaesthesia, are not satisfactory to prevent hypertensive response that
associated with head pin placement.
Temporary clipping
Temporary clipping of feeder vessels is commonly used to improve surgical field
and to avoid intraoperative rupture during surgical dissection of aneurysms.it
substituted the use of global hypotension to reduce pressure gradient across the
aneurysm wall,
The main recommendations during clipping are:
- Blood pressure maintained at high normal levels, to ensure adequate collateral
circulation.
- Brain protection in some form (e.g. propofol, barbituarates), administered prior
to clipping.
- FiO2 increased to 100%.
- Clamping time should not be longer than 20 minutes.2,5,11
Intraoperative aneurysmal rupture
It is one of major complications, the risk of intra-op rupture is about 19%, and it
occurs at any time during the operation, it is associated with poor prognosis
especially if the rupture occurs during induction, therefore the surgery should
be postponed and patient reassessment is mandatory if the rupture is
suspected during induction.
Page 20 of 28
The intra-op rupture is due to sudden increase in the aneurysm’s TMPG or due
to surgical manipulation or dissection. Bleeding can be severe enough to cause
hemorrhagic shock. The anesthetic management is varies from center to
center, however the primary hemodynamic goal is maintenance of
normovolaemia, 5, 11 Temporary vessel occlusion is the ideal technique to
control of bleeding. When this is not possible, mean arterial pressure (MAP)
should be briefly dropped to 40 – 50 mm Hg, in order to simplify surgical
occlusion of the rupture. Cardiac arrest is induced by a rapid IV bolus of 12 mg
of adenosine into a large vein (arrest for 10 seconds)and the operative field is
suctioned and temporary clips (so-called “pilot” clips) are placed, however,
controlled studies are needed to validate this technique.2,4,5,11,18
Emergence
Fast-tracking techniques and early postoperative neurological evaluation are
preferred after uncomplicated surgery in good grade patients; however this
technique should be balanced against satisfactory analgesia to avoid
postoperative hypertension and agitation2.
Mild hypertension may augment cerebral perfusion particularly in patients with
vasospasm. Blood pressure > 20% of baseline can be treated with labetalol,
esmolol or hydralazine as extreme increases in blood pressure may lead to
postoperative hemorrhage4. If the patient fails to recover to the predictable GCS in
postoperative period, urgent brain CT is required to exclude intraoperative
bleeding18. Poor grade patients (III or IV) or who have had intra-operative
complications should be admitted in the ICU for postoperative ventilation,
continuous ICP monitoring and frequent neurological assessment4.
Intravenous paracetamol and codeine are most commonly used for analgesia,
long acting opioid such as morphine should be used carefully to avoid respiratory
depression, CO2 retention and postoperative nausea and vomiting, in addition
morphine may affect postoperative neurological assessment.2NSAID may
increase risk of bleeding and should be avoided. Prophylactic anti-emetics such
as ondansetron should be administered.
Antiepileptic prophylaxis should be considered for cases involving temporal or
frontal haematoma.2 All patients are at risk of venous thromboembolism, therefore
stockings should be worn with intermittent calf compression devices through the
perioperative period, low-molecular-weight heparin should be started on the 2nd
postoperative day providing there are no contraindications18.
Page 21 of 28
ANESTHESIA FOR INTERVENTIONAL RADIOLOGY
Anesthesia for INR can be exceptionally challenging to the anaethetist, due to it is
performed outside the operating theatre, in addition other potential problems such
as working in reduced light, poor access to the patient, and concerns of ionizing
radiation.
Anaesthetic concerns include prevention patient mobility, maintain physiological
stability, manipulating systemic and regional blood flow, dealing with
anticoagulation, and handling unanticipated complications during the
intervention.2, 19
I. Pre intervention assessment
Normal pre- anesthetic assessment with careful neurological examination is
mandatory in pre-intervention assessment.
Baseline arterial pressure, cardiovascular reserve, renal insufficiency,
coagulation should be evaluated, Patients with neck arthritis, back, or other
joints have limited ability to lay in supine position, and risk of airway
compromise with sedation.19 Allergic history especially to shellfish, iodine,
protamine is important and should be documented prior the intervention.
II. Anesthetic technique
Different anesthetic technique can be used in INR; there is limited data to
support any specific technique, in spite of this the needs of the neuroradiologist
and the procedure should be considered in selecting the anesthetic technique.19
General anesthesia
It is preferred by most of neuroradiologists as it provides an immobile,
comfortable patient with good image quality, and excellent control of the
respiratory and haemodynamic profile. The main disadvantages of general
anesthesia are the difficulty to achieve intraoperative neurological assessment,
as well as endotracheal intubation and extubation may induce hypertension,
coughing, and straining which can lead to raised ICP.19
Propofol, desflurane, and sevoflurane are the most anesthetic agents used in
general anesthesia, which can rapidly induce the anesthesia with minimum
haemodynamic changes, rapid control in depth of anesthesia, and a smooth
and rapid emergence from the anesthesia.
Nitrous oxide should be avoided, as it may cause enlargement of micro air
bubbles during injection of contrast or irrigation fluid.19 the laryngeal mask
airway (LMA) can be used for the management of the airway. It allows airway
control with less haemodynamic stress and smooth emergence from
anesthesia. Muscle relaxation and controlled ventilation can be used with LMA
provided there is no contraindication.
Page 22 of 28
Sedation
The main advantages of sedation are ability perform frequent neurological
assessment with the avoidance of haemodynamic stress associated with
intubation and extubation .however the risk of aspiration ,hypoxemia ,
hypercapnia and sudden movement should be considered in sedated patient.
Propofol and dexmedetomidine are most commonly used for sedation.19
III. Monitoring
In addition to standard monitoring, invasive arterial line for blood pressure
monitoring, and blood sampling is usually required in INR.
Catheterization of the bladder is mandatory due to significant volume of
heparinized flush solution and radiographic contrast is often used, and
administration of mannitol and Lasix may be necessary intraoperatively.
Temperature monitoring is vital to avoid hypothermia which can occur in the
neuroradiology suite.19
IV. Anticoagulation
It is mandatory to avoid thromboembolic complications during and after the
procedure, therefore all INR patients should be anticoagulated with
unfractionated heparin either bolus or continuous infusion after an initial bolus,
or at a weight-based bolus of 70 IU/kg to obtain a 2 to 3-fold increase in
Activated Clotting Time (250 s), if the rupture of aneurysm occurs rapid reversal
with protamine is required. After the procedure, heparin infusion may be
required to prevent thrombogenic effects of endothelial trauma and the
inherently thrombogenic nature of the materials instilled.19
If a patient has a wide neck aneurysm where a permanent stent in the neck of
the aneurysm would be needed to prevent coils migration into parent vessels,
dual antiplatelet therapy 5 days before the intervention is required (aspirin 300
mg daily, clopidogrel 75 mg daily), the aspirin is usually continued at a lower
dose 83mg -150 mg for 6 months, while clopidogrel is continued for 3 months
post intervention. If patient has a SAH with wide neck aneurysm and he is not
candidate for clipping surgery , endovascular intervention can be performed ,
patient is given loading dose of clopidogrel 300mg -600mg up n
commencement of procdure via NGT and then 75 mg daily for 3 months ,and
aspirin 83 mg – 150mg for 6 months.22
V. Complications of INR Procedures
It can be rapid and catastrophic, the good communication between the
neuroradiologist, anaesthetist, and the radiographer for the rapid management
of complications that may occur. Air way and ventilation are the primary
responsibility of the anesthetist. The complication can be divided into CNScomplication and non CNS complication. CNS complication either haemorrhagic
or occlusive, non CNS complications include contrast medium reaction, contrast
nephropathy, haematomas at puncture site.
Page 23 of 28
Haemorrhagic complications
It is associated with sudden increase in mean arterial pressure; the immediate
management include;
 Immediate reversal of heparin.
 Lowering systemic arterial pressure.
 PaCO2 should be maintained between 4.5 and 5.0 kPa
 Mannitol may be given to reduce cerebral oedema.
 Aneurysm perforation is treated via packing the defect with coils.
 Emergency craniotomy and clipping of aneurysm if coiling fails.
 New SAH may be complicated with acute hydrocephalus and requires
urgent ventricular drainage.
Occlusive complications
It can be due to thrombosis or due to malpositioned coils; the arterial pressure
should be raised to increase collateral blood flow.
Angiographically noticeable thrombus is cured via mechanical lysis using a
guide wire or local
- Infusion of saline.
- Thrombolytic agents are used to cure intraoperative thrombosis.
Contrast reactions
The fatal reaction occurs in 1 in 10000 exposures, the reactions may be due to
hypertonicity, direct cardiac depression, or idiosyncratic anaphylactoid
reactions. Prophylaxis treatment with steroids and antihistamine is
recommended for patient with previous reaction to contrast.
Contrast nephropathy
It is defined as a change in serum creatinine (SCr) over baseline (more than
25% above baseline) by 48 hr., or an absolute increase of > 0.5 mg/dl.20
One of the most common causes of renal failure, the risk factors include
diabetes mellitus, high dose of contrast, volume depletion, co-administration of
nephrotoxic medications and preexisting renal disease.
Modifiable risk factors
Contrast volume
Concomitant nephrotoxic
agents
Recent
contrast
administration
Non-modifiable risk factors
diabetes
Chronic kidney disease
Shock /hypotension
Advanced age >75 years
Advanced congestive heart
failure
Table 6 risk factors of CIN 20
Page 24 of 28
Pre-procedural management for high risk patients
- volume repletion
a. Administer 1 L of isotonic (normal) saline, started 3 hours before INR, and
continuing 6-8 hours after the operation.
b. Sodium bicarbonate (154mEq/l), starting with 3ml/kg/hour before INR, then
1ml/kg/hour for 6 hours post the intervention. However only one study
supported using sodium bicarbonate over normal saline and further studies
required to support use sodium bicarbonate.20
- patient medication
a. holding potentially nephrotoxic drugs(NSAID),aminoglycoside antibiotics,
b. N-acetylcysteine (600mg orally 12 hourly), 4 doses before contrast
injection.20
- pharmacotherapy
Such as vasodilators (dopamine/ fenoldopam), theophylline, calcium channel
blocker, and antioxidants (ascorbic acid) have all been tried without any
conclusive result.19
Intra-operative management for high risk patient
a. Minimize volume.
b. Low- or iso-osmolar contrast agents.20
Post- operative management
a. follow-up for 48 hours post intervention.
b. holds medications such as NSAID until renal function returns to normal.20
VI. Postoperative care
All patients should be admitted in high dependency unit after the operation,
unless there is indication for intensive care admission. Patients should stay
supine until the femoral sheath is removed. In patients with occlusive
conditions or vasospasm, high mean arterial pressure is required to maintain
cerebral perfusion pressure. Treatment with Nimodipine for 3 weeks is
required in aneurysmal SAH. 19 PONV can be due to contrast and anaesthetic
agents and should be treated aggressively.
Continuous neurological assessment is also mandatory to identify any new
neurological deficit. Reevaluation for aneurysm regrowth is strongly
recommended at 6 months post intervention, and then another reassessment
at 18 months from initial intervention is suggested. Catheter arteriography is
the gold standard for reevaluation; however the role of CT angiography and
MRI is investigation21. Stable aneurysm if there is no changed in size,
configuration, and volumetric occlusion, the improved aneurysm if there is
progressive occlusion, worsened aneurysm if the aneurysm has grown in size
or changed in arteriographic configuration.
Page 25 of 28
Reevaluation is also to exclude development of new aneurysms21.
CONCLUSION
Subarachnoid haemorrhage is a life threatening condition, it is associated with
high mortality and morbidity either from neurological ictus or from systemic effect,
most importantly cardiac effect, the management of SAH requires urgent
resuscitation to prevent complication such as re bleeding and to optimize cerebral
oxygenation and perfusion .Anaesthesiologists play vital role in management of
SAH patient .
Page 26 of 28
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Cerebral Aneurysms P.M. Meyer AJNR 31 _ Jan 2010 _
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