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63.
NONTRAUMATIC INTRACRANIAL HEMORRHAGE
Deepak Sharma and Julia Metzner
CLINICALCASE
A 46- year- old woman with a history of diabetes mellitus
suered sudden onset of severe headache followed by a
loss of consciousness. She regained consciousness on hospital arrival following placement of an external ventricular
drain (EVD). She was drowsy but had no focal neurological decits. Her blood pressure is 136/ 90 mmHg, Na +
128 mEq/ L, K +3.2 mEq/ L, and blood glucose 256 mg/ dl.
Electrocardiogram (ECG) revealed ST segment depression
in leads II and AVL. Contrast computed tomography (CT)
shows subarachnoid hemorrhage (SAH) in the anterior
interhemispheric ssure and le sylvian ssure and a le
middle cerebral artery aneurysm.
PATHOPHYSIOLOGY OFTHE DISEASESTATE
Subarachnoid hemorrhage occurs when rupture of an arteriovenous malformation (AVM) or aneurysm leads to the
release of blood into the subarachnoid space. Less oen it
release of catecholamines, which leads to the extracranial
manifestations of SAH such as stress cardiomyopathy, cardiac arrhythmias, hyperglycemia, and neurogenic pulmonary edema.1 Brain natriuretic peptide (BNP) levels are
frequently elevated aer SAH, and a syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral
salt wasting can cause hyponatremia.
1
Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral
vasospasm, and seizures. Blockage of arachnoid granulations can lead to delayed, nonobstructive, communicating
hydrocephalus. Symptomatic cerebral vasospasm develops
in approximately 20%– 40% of patients with SAH, and
may cause permanent neurological decits. It is a reversible vasculopathy of the intracranial arteries associated with
impaired cerebral autoregulation, reduced cerebral perfusion, and ischemic insults known as delayed ischemic neurologic decits (DINDs). Cerebral vasospasm is a major
cause of morbidity and mortality in patients withSAH.
may be caused by trauma or a bleeding disorder. e blood
in the subarachnoid space spreads through the cerebrospinal uid (CSF) and causes meningeal irritation with nuchal
ASSESSMENT OFTHE PATIENT:PREOPERATIVE
EVALUATION
rigidity. Sudden accumulation of blood and obstruction of
the CSF drainage can cause an acute increase in intracranial pressure (ICP) and early obstructive, noncommunicating hydrocephalus, necessitating the emergent placement of
an EVD. Symptoms including headache, nausea, vomiting,
and loss of consciousness result from acutely increased ICP
and reduced cerebral perfusion. e increase in ICP following the rupture of an aneurysm causes some degree of tamponade that may decrease further bleeding. In addition to
SAH, aneurysms and AVMs can also rupture into the ventricular system or cause intracerebral hemorrhage.
e initial hemorrhage may be fatal in 20%– 30% of
patients. In survivors, cerebral autoregulation and cerebrovascular reactivity to carbon dioxide may be impaired.1 e
intracranial hemorrhage causes a sympathetic surge with
e preoperative assessment should incorporate clinical
grading of the SAH, typically using the modied Hunt
and Hess grading system (Table 63.1)2 or the World
Federation of Neurological Surgeons’ (WFNS) grading system (Table 63.2).3 ese grading systems not only
allow assessment of perioperative morbidity and communication between physicians but also indicate the severity
of cerebral pathophysiology as well as extracranial sequela
of SAH. Placement of an EVD early aer admission may
improve the neurologic condition of the patient by 1– 2
grades. e Fisher grading on CT scan is commonly used
to assess the risk of cerebral vasospasm by evaluating the
pattern of hemorrhage with SAH.4 While the surgery
cannot be delayed signicantly in patients with ruptured
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TABLE63.1 MODIFIED HUNT AND HESS GRADING SYSTEM
FORANEURYSMAL SUBARACHNOID HEMORRHAGE
Grade Neurological Status
2
It is important to know the date of rupture of the
cerebral aneurysm as cerebral vasospasm typically sets in
4– 5days later. Most patients with SAH usually have their
aneurysm secured before this time period to avoid both
0 Unruptured aneur ysm
1 Asymptomatic or mild headache and slight nuchal
rigidity
2 Severe headache, stiff neck, no neurologic decit
except cranial nerve palsy
3 Drowsy or confused, mild focal neurologic decit
4 Stuporous, moderate or severe hemiparesis
5 Coma, decerebrate posturing
1 higher grade is assigned if cerebral vasospasm or presence of serious systemic disease
(hypertension, diabetes, severe atherosclerosis or chronic obstructive pulmonary disease)
the risk of cerebral vasospasm during the procedure and to
minimize the time interval when rebleeding could occur.
Review of the cerebral angiogram helps assess collateral
cerebral circulation and identify other nonruptured aneurysms, in addition to examining the characteristics of the
aneurysm itself such as neck size, diameter, lobular appearance, fusiform shape, and soforth.
Cerebral AVMs present with acute intracranial hemorrhage or with seizures, focal neurological decits, headache,
or hydrocephalus. e presence of multiple intracranial
AVMs should raise the suspicion of hereditary hemorrhagic
telangiectasia (HHT). e AVMs are graded using the
aneurysms, they are typically stabilized over 1– 2 days,
with EVDs for control of ICP, management of hypertension, and evaluation of clinically signicant cardiac dysfunction or other coexisting illnesses. e ICP should be
monitored and treated, avoiding sudden drainage of large
volumes of CSF, which can cause rebleeding. e intensivists should initiate correction of uid, electrolyte, and glucose derangements. Patients with neurogenic pulmonary
Spetzler- Martin system based on the size, pattern of venous
drainage, and neurological eloquence of the adjacent brain.6
Although most patients undergo preoperative endovascular embolization to decrease the vascularity of the AVM,
the anesthesiologist should be prepared for intraoperative
bleeding requiring transfusion. Another major concern is
the risk of hyperemic complications leading to hemorrhage
and edema aer resection ofAVM.
edema may require mechanical ventilation.
Electrocardiogram abnormalities such as ST segment
depression, T- wave inversion, appearance of U- waves, and
prolonged QT interval occur commonly aer SAH and
are usually of neurogenic rather than cardiogenic origin.5
Severe myocardial dysfunction with regional wall motion
abnormalities (neurogenic stress cardiomyopathy) are relatively uncommon but well- known cardiac sequelae asso-
ANESTHETIC MANAGEMENT
Proper case management requires an understanding of the
nuances of care to be delivered during a variety of circumstances ranging from induction and emergence to intraoperative intracranial hemorrhage and aneurysm clipping,
each of which is discussedbelow.
ciated with SAH. Cardiac troponin Ilevels and 12- lead
ECGs may be useful to detect cardiac ischemia in this setting. In rare cases, patients with severe cardiac dysfunction
may not be suitable candidates for craniotomy and may
instead undergo endovascular coiling of the aneurysm.
Induction ofAnesthesia/ Emergent Intubation
Anesthesiologists may be called to the emergency room
(ER) or intensive care unit (ICU) to intubate patients
who have suered an SAH for airway protection, airway
TABLE63.2 THE WORLD FEDERATION OFNEUROLOGICAL
SURGEONS (WFNS) GRADING SCALE FORINTRACRANIAL
ANEURYSMS
WFNS Grade
3
Glasgow Coma Scale (GCS) score
1 15 −
2 13–14 −
Motor Decits
obstruction, or hypoxemia from aspiration or ash pulmonary edema. Aer standard preparation for an emergent
intubation, preoxygenation should be managed carefully
to avoid agitation and a hypertensive response. e biggest
concern during laryngoscopy and intubation is the avoidance of hypertension, as it can cause an increase in the transmural pressure across the aneurysm wall and precipitate
rebleeding. Likewise, it may cause bleeding from an AVM
3 13–14 +
4 7–12 +/ −
5 3–6 +/ -
although the risk may be lower. Ahypertensive response to
intubation can be attenuated using opioids, lidocaine, beta
blockers, or calcium channel blockers. e eect of succinylcholine on ICP is oen debated, though it has been
NONTRAUMATIC INTRACRANIAL HEMORRHAGE 457
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shown to have no detrimental eect on ICP and anesthesiologists should not hesitate to use it if anticipating a dicult airway.1 Placement of an arterial line prior to induction
of anesthesia for surgery allows close monitoring of blood
pressure and can guide rapid treatment if needed. As always,
hypoxia, hypercarbia, and hypotension should be avoided,
as they can precipitate or worsen cerebral ischemia.
vasodilation, it is oen preferred in situations with elevated
ICP, with more modest use of hyperventilation.
e eect of anesthetics on evoked potential signal
quality should be considered while selecting the anesthetic
agent. While the inhalational agents cause dose- dependent
increases in latency and decreases in amplitude of somatosensory evoked potentials (SSEPs), less than 1.0 MAC concentration is usually compatible with monitoring of cortical
Choice ofAnesthetic Agents and Evoked Potential
Monitoring
e choice of intravenous or inhaled anesthetic agents is
based on the patient’s neurological condition, proposed
procedure, coexisting diseases, and planned neurophysiological monitoring. Volatile anesthetic agents decrease the
cerebral metabolic rate (CMR), but also cause direct cerebral vasodilation and increased cerebral blood ow (CBF),
particularly at concentrations greater than 1.0 MAC (minimum alveolar concentration). In patients with reduced
intracranial compliance, this “luxury perfusion” can cause
further increases in ICP and brain swelling, making surgical
exposure dicult (Box 63.1). ough the cerebral vasodila-
SSEPs. Propofol anesthesia has a minimal eect on SSEPs
and is occasionally preferred in situations where the SSEPs
may be impaired at baseline and are critical to the surgical
procedure.7 If motor evoked potentials (MEPs) are monitored, propofol anesthesia is frequently preferred, especially
in patients with preexisting neurological decits, because it
aects MEP amplitude and latency signicantly less than
volatile anesthetics. For patients without preexisting neurological decits, desurane used in concentrations less than
0.5 MAC is also compatible with MEP monitoring in most
patients.8 Monitoring MEPs also precludes the use of neuromuscular blocking agents aer intubation. Volatile anesthetic agents may be used with brainstem evoked potentials,
as they have very little eect on these signals.
tory eect of inhalational agents may be oset by hyperventilation, it is dicult to estimate the exact PaCO2 needed
to avoid cerebral ischemia without specialized monitoring. Because propofol does not cause direct cerebral
Monitoring
Besides the standard ASA monitors, an arterial line should
be placed for continuous blood pressure monitoring, for
sampling PaCO2, glucose levels, and electrolytes as well as
BOX 63.1 INTRACRANIAL PRESSURE MANAGEMENT AND
BRAIN RELAXATION
for measuring pulse pressure variability to guide uid status.
Acentral venous line may be placed to supplement vascular
access, facilitate infusion of total intravenous anesthesia
The strategies for ICP control and brain relaxation include:
• Maintenance of adequate depth of anesthesia and
analgesia
• Optimal positioning (slight head elevation and avoiding
excessive neck exion or rotation) to maximize
intracranial venous outow.
(TIVA) and medications such as hypertonic saline, phenytoin, or vasoactive infusions. e EVD should be used
to monitor ICP and to drain CSF at the specic request of
the surgeon. Specialized monitoring such as jugular venous
oximetry, electroencephalogram (EEG), SSEPs, and MEPs,
may be used to guide determination of blood pressure and
PaCO2 targets to minimize the risk of cerebral ischemia.9
• Selection of volatile versus propofol anesthetics
based on assessment of intracranial compliance.
• Administration of mannitol or hypertonicsaline
e EEG may also be used to titrate anesthetic doses for
burst suppression during temporary clipping of aneurysms.
Monitoring SSEPs and MEPs guides maintenance of adequate perfusion to the “at- risk” brain, particularly during
• Controlled hyperventilation (aggressive hyperventilation
should not be instituted before dural opening because
the resulting decrease in the transmural pressure can
cause rebleeding)
temporary clipping.
Temporary Clipping forAneurysms
• CSF Drainage (should be used cautiously considering
the potential risk of rebleeding with rapid CSF
drainage, particularly before dural opening)
458 SECTION A. CEREBRAL ORIGIN
e treatment of aneurysms may involve the placement
of a temporary clip to occlude the parent vessel proximal
to the aneurysm. e temporary clip reduces blood ow
through the aneurysm, allowing for the dissection and
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459
accurate placement of a permanent clip without the risk of
catastrophic bleeding. Hypotension and excessive hyperventilation should be avoided during temporary clipping.
e blood pressure is typically increased to 10%– 20%
above baseline during temporary clipping to recruit collateral blood ow to the territory at risk of ischemia. Another
strategy to avoid cerebral ischemia during temporary clipping is to decrease the CMR by administration of a bolus
by normal perfusion pressure breakthrough (NPPB).13
High- ow AVMs have very low resistance, causing impaired
autoregulation that is shied leward. Following removal
of the low- resistance AVM, the capillary beds and arterioles
in the “normal” parenchyma are now subjected to a much
higher resistance that may exceed their ability to vasoconstrict to prevent excessive increases in blood ow, even at
normal perfusion pressures.
13
dose of anesthetic agent (propofol or etomidate) to induce
burst suppression on EEG. e reduction in CMR may
Immediate Postoperative Management
prolong the tolerance of reduced blood ow, although the
eectiveness of this technique is questionable.1 Induced
hypothermia has not been shown to be benecial and cannot be recommended for neuroprotection in patients with
good gradeSAH.
10
Postoperatively, the patients should be closely monitored
for adequacy of oxygenation and ventilation, hemodynamic stability, pain control, and neurological recovery.
Opioids should be used judiciously for postoperative pain
management, avoiding overdose- related adverse eects
Intraoperative Intracranial Hemorrhage
Eective communication between the neurosurgeon,
anesthesiologist, and the operating room sta is critical
while dealing with ongoing blood loss. If there is acute
bleeding from the aneurysm during surgery and proximal control is not achieved, the surgeon may request a
short period of induced hypotension. Short- acting agents
such as nicardipine and esmolol are best suited for such
situations, and the depth of anesthesia may be increased
such as respiratory depression, carbon dioxide retention,
increased CBF, and ICP. Other alternatives include intraoperative local anesthetic scalp inltration, and intravenous paracetamol. Selective serotonin (5- HT3) receptor
antagonists are the rst- choice drugs for prophylaxis of
postoperative nausea and vomiting (PONV) because of
their favorable safety prole. For rescue of PONV metoclopramide, droperidol, or scopolamine may be used.
Postoperative hypertension is undesirable particularly in
patients withAVMs.
by administration of a propofol bolus to cause burst
suppression before such interventions. In select cases, a
CASE- BASED LEARNING DISCUSSION
brief cardiac standstill may be induced using adenosine.
Circulatory arrest induced by adenosine allows the surgeon to place a temporary clip to control the bleeding
and has been found to be safe and eective to facilitate
the management of intraoperative aneurysmal rupture.11
A dose of 0.3– 0.4 mg/ kg ideal body weight provides
approximately 45 seconds of profound systemic hypotension.12 Assessment of estimated blood loss, maintenance
of euvolemia, and avoidance of excessive hyperventilation
are important to provide adequate cerebral perfusion.
Previous blood pressure goals should be restored as soon
1. What is this patient’s modied Hunt and Hess grade,
and what are the implications for outcome and
management?
2. e ECG shows ST segment depression in leads II and
aVL, and the patient is requiring vasoactive medications
to maintain a mean arterial pressure of 70mmHg.
What is the implication? Will you proceed with the
anesthetic or ask for further investigations? Why/ why
not? If yes, what investigations?Why?
as the bleeding is controlled.
3. e patient who takes chronic high- dose opioids
Hemodynamic Management During Emergence
Hypertension is undesirable before the aneurysm is clipped
because it can precipitate rebleeding. Once, the aneurysm
is secured, the blood pressure can be normalized. However,
patients with AVMs dier from patients with aneurysms in
that blood pressure needs to be kept below the preoperative
baseline even aer the AVM has been resected to prevent
hyperemic complications (hemorrhage and edema) caused
for back pain arrives to the operating room without
a functioning arterial line. Will you proceed with
anesthesia induction without an arterial line? How will
you prevent hemodynamic responses to laryngoscopy
and intubation?
4. Prior to dural opening, the surgeon complains that
she cannot do the operation because the brain is
bulging. What options do you have to maximize brain
relaxation?
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5. e surgeon reports that she anticipates this aneurysm
will be dicult to clip and that she will be using
temporary clips. How will you minimize the risk of
cerebral ischemia during temporary clipping? Will
BOX 63.2 PREDISPOSING FACTORS FORPITUITARY TUMOR
APOPLEXY
• Traumatic braininjury
you consider hypothermia for brain protection? Why/
whynot?
• Uncontrolled high or low blood pressures
6. During dissection and before temporary clips are
placed, the aneurysm ruptures and the blood pressure
increases to 189/ 105mmHg. What is your rst
response? What medications can you use to lower
the blood pressure? What is the role of adenosineinduced temporary ow arrest in the control of
intraoperative intracerebral hemorrhage? What are the
contraindications to the use of adenosine?
PITUITARY APOPLEXY
CLINICALCASE
A 60- year- old male presented to the emergency department
with sudden onset of headache, ptosis, and blurred vision in
the le eye. Neurologic examination revealed that he was
confused and had visual loss in the le eye and le occulo-
• Major surgery (coronary artery bypass or stenting)
• Anticoagulation therapy
• Estrogen or dopamine agonist therapy
• Dynamic pituitary function testing
• Radiotherapy
• Pregnancy
and electrolyte abnormalities such as hyponatremia.
yrotropin and gonadotropin deciencies occur in
50%– 75% of patients.15 Occasionally, low prolactin levels
or diabetes insipidus may be present. Pituitary apoplexy is
a neurosurgical emergency, and urgent decompression is
usually necessary to save vision and prevent catastrophic
hypopituitarism. Box 63.2 lists the potential factors pre-
disposing to apoplexy.
motor nerve palsy. An emergency MRI conrmed pituitary
adenoma with acute hemorrhage and compression of the
optic chiasm. Adecision to proceed with endoscopic endonasal tumor decompression wasmade.
MANAGEMENT
Urgent transsphenoidal decompression of the optic chiasm
and adjacent neuronal tissues is the mainstay of therapy.
PATHOPHYSIOLOGY OFTHE DISEASESTATE
However, in stable patients, a conservative pharmacological
approach with steroids and hormonal supplements and rigPituitary apoplexy results from sudden enlargement of the
sellar gland caused by spontaneous hemorrhage or infarction into a pituitary tumor. e clinical manifestation is
oen dramatic and is characterized by severe headache,
orous management of uid and electrolyte balance is oen
favored. Studies have failed to show a dierence in the long-
term outcomes of conservatively and surgically managed
patients.
16
nausea, occulomotor nerve palsy (diplopia), altered mental status, and hypopituitarism.14 e expanding pituitary
tumor causes direct compression on the adjacent tissue
with an interruption of its blood supply. Aprecipitous
ANESTHETIC MANAGEMENT
Preoperative Preparation
rise in the contents of the sella yields to an abrupt increase
in the intrapituitary pressure, which triggers the neurological and endocrine manifestations. Alarge tumor can
surpass its vascular supply, leading to hemorrhage or ischemia of the pituitary. Visual eld decits are related to
the compression of the optic chiasm or optic nerves from
an increase in the tumor mass or hematoma. Apoplexy is
associated with hypopituitarism in more than 80% of the
cases.15 e most serious decit involves ACTH (adrenocorticotrophic hormone), causing severe hypotension
In addition to the standard evaluation of a neurosurgical
patient, preoperative screening should include assessment
of hormone deciencies, electrolyte imbalance, and signs
and symptoms of raised ICP (Box 63.3). Intravenous treat-
ment with hydrocortisone should be initiated in order to
avoid hemodynamic instability and acute adrenal insu-
ciency. Some patients may have acromegaly from the pitu-
itary tumor, which may complicate airway management.
Any delays in surgery must be avoided.
460 SECTION A. CEREBRAL ORIGIN
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461
Strategies to facilitate smooth emergence include low- dose
BOX 63.3 GOALS OFANESTHETIC MANAGEMENT
FORSURGERY FORPITUITARY APOPLEXY
1. Correct uid and electrolyte imbalances and administer
hydrocortisone.
2. Maintain cerebral perfusion.
remifentanil infusion, intravenous lidocaine, or incorporating dexmedetomedine in the anesthetic regimen.18 e
hemodynamic responses associated with emergence should
be rapidly treated with a short- acting agent such as esmolol
and/ or nicardipine.
3. Ensure patient immobility to avoid inadvertent injury to
the internal carotid arter y or the cavernoussinus.
POSTOPERATIVE CONCERNS
Postoperative complications may occur immediately aer
4. Avoid inadvertent hypocapnia and hypothermia.
5. Facilitate early emergence for assessment of vision with
avoidance of coughing/ straining
pituitary tumor decompression or may be delayed. Early
complications include CSF leak, hemorrhage, DI, and
visual loss. Late complications include endocrine decits,
electrolyte and water imbalance (SIADH), and infections.
Anesthetic Technique
CASE- BASED LEARNING DISCUSSION
In addition to the standard American Society of
Anesthesiologists (ASA) monitors, an arterial line is also
recommended to closely manage hemodynamics and continue to evaluate and treat any electrolyte imbalances.
Intravenous access with at least two large bore lines is essential. Rapid sequence induction may be needed, because
the patient may not be fasting and ICP may be raised.
Following intubation, a throat pack is oen inserted to
prevent the entry of blood and secretions into the stomach,
which may cause postoperative vomiting. Both intravenous
1. Describe the important components of preoperative
evaluation of a patient with pituitary apoplexy.
2. Aer uneventful induction of anesthesia, the surgeon
topicalized the nasal mucosa with bupivacaine 0.25%
and epinephrine 1:200,000. is led to hypertension
with blood pressure of 180/ 110mmHg and a heart rate
of 40 bpm. What is happening? How will you manage
the situation?
and inhalational anesthetic agents may be used to achieve
the anesthetic goals described above. Typically, short- acting
anesthetic agents are selected, such as remifentanil and
propofol, or a combination of remifentanil with inhaled
anesthetics with low blood solubility, for example, sevourane or desurane. A prospective study comparing the
combination of TIVA with remifentanil/ propofol to remifentanil/ sevourane showed no major dierences regarding
hemodynamic stability, however recovery was signicantly
3. At the end of tumor resection a CSF leak is detected.
e surgeon seals it with an abdominal fat gra and
requests deep extubation. How will you emerge the
patient? What techniques can be used for an awake,
otherwise smooth extubation?
4. Eight hours postoperatively, you nd out that the
patient’s urine output has been 300 mL/ hour, and he is
hypotensive and tachycardic. How will you proceed?
longer with TIVA than with remifentanil/ sevourane.17
Hypotension should be rapidly treated, and normocapnia
should be targeted. Inadvertent hyperventilation may result
in loss of brain bulk and make any suprasellar extension of
REFERENCES
the tumor less accessible surgically. Electrolyte levels and
urine output should be carefully monitored to diagnose
diabetes insipidus(DI).
Emergence
Smooth emergence from anesthesia is particularly important because straining or coughing on the endotracheal
tube may cause bleeding or dislodge a previously implanted
fat gra and cause a CSF leak and potential infection.
1. Sharma D, Wright D. Cerebrovascular surgery. In: Mashour G,
Engelhard K, eds., Oxford Textbook of Perioperative Neuroscience
and Neuroanaesthesia. 1st ed. Oxford University Press. (InPress)
2. Hunt WE, Hess RM. Surgical risk as related to time of intervention
in the repair of intracranial aneurysms. Journal of Neurosurgery.
1968;28:14– 20.
3. Report of World Federation of Neurological Surgeons Committee
on a Universal Subarachnoid Hemorrhage Grading Scale. Journal of
Neurosurgery. 1988;68:985– 6.
4. Fisher, CM, Kistler, JP, Davis, JM. Relation of cerebral vasospasm to
subarachnoid hemorrhage visualized by CT scanning. Neurosurgery.
1980;6:1– 9.
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5. Manninen PH, Ayra B, Gelb AW, etal. Association between electrocardiographic abnormalities and intracranial blood in patients
following acute subarachnoid hemorrhage. Journal of Neurosurgical
Anesthesiology. 1995;7:12– 6.
6. Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. Journal of Neurosurgery. 1986;65:476– 83.
7. Boisseau N, Madany M, Staccini P, etal. Comparison of the eects
of sevourane and propofol on cortical somatosensory evoked
potentials. British Journal of Anaesthesia. 2002;88:785– 9.
8. Sloan TB, Toleikis JR, Toleikis SC, etal. Intraoperative neurophysiological monitoring during spine surgery with total intravenous
anesthesia or balanced anesthesia with 3% desurane. Journal of
Clinical Monitoring and Computing. 2015;29:77– 85.
9. Sharma D, Siriussawakul A, Dooney N, etal. Clinical experience
with intraoperative jugular venous oximetry during pediatric intracranial neurosurgery. Pediatric Anaesthesia. 2013;23:84– 90.
10. Todd MM, Hindman BJ, Clarke WR, et al; Intraoperative
Hypothermia for Aneurysm Surgery Trial (IHAST) Investigators.
Mild intraoperative hypothermia during surgery for intracranial
aneurysm. New England Journal of Medicine. 2005;352:135– 45.
11. Lee SH, Kwun BD, Kim JU, etal. Adenosine- induced transient asystole during intracranial aneurysm surgery:indications, dosing, ecacy, and risks. Acta Neurochirurgica (Wien). 2015;157:1879– 86.
12. Bebawy JF, Gupta DK, Bendok BR, et al. Adenosine- induced
ow arrest to facilitate intracranial aneurysm clip ligation: doseresponse data and safety prole. Anesthesia and Analgesia.
2010;110:1406– 11.
13. Spetzler RF, Wilson CB, Weinstein P, etal. Normal perfusion pressure breakthrough theory. Clinical Neurosurgery. 1978;25:651– 72.
14. Verrees M, Arafah BM, Selman WR. Pituitary tumor apoplexy: characteristics, treatment, and outcomes. Neurosurgery
Focus. 2004;16:E6.
15. Johnston PC, Hamrahian AH. Pituitary tumor apoplexy. Journal of
Clinical Neuroscience. 2015;22:939– 944.
16. Singh TD, Valizadeh N, Meyer FB, etal. Management and outcomes
of pituitary apoplexy. Journal of Neurosurgery. 2015;122:1450– 7.
17. Caero T, Cavallo LM, Frangiosa A, et al. Clinical comparison
of remifentanil– sevourane vs. remifentanil– propofol for endoscopic endonasal transphenoidal surgery. European Journal of
Anaesthesiology. 2007;24:441– 6.
18. G opalakrishna KN, Dash PK, Chatterjee N, eta l. Dexmedetomidine
as an anesthetic adjuvant in patients undergoing transsphenoidal resection of pituitary tumor. Journal of Neurosurgical
Anesthesiology. 2015;27:209– 15.
462 SECTION A. CEREBRAL ORIGIN
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64.
ACUTESTROKE
Laurel E.Moore
CLINICALCASE
brillation is a major cause of embolic stroke and, given
our aging patient population, increasingly contributory to
Patient PS is a 75- year- old woman with a history of wellcontrolled hypertension and paroxysmal atrial brillation
scheduled for an elective hip replacement. General anesthesia is planned because of a past surgical history of extensive
lumbar fusion surgery and patient preference.
stroke etiology.
In 1995 the NINDS trial3 supported the administration of recombinant tissue plasminogen activator (IV
rtPA) within 3 hours of stroke onset to reduce infarct size
and improve patient outcomes. For the rst time, eective
treatment for AIS was available. Trials over time have con-
INTRODUCTION
tinued to support the use of thrombolytic therapy for AIS,
extending the window of eligibility for treatment from 3 to
4.5 hours in 2005,11 although FDA approval for this exten-
Stroke is the leading cause of disability in the United States,1
and in terms of mortality is second only to ischemic heart
disease worldwide.2 Medical management for acute ischemic stroke (AIS) has advanced from supportive care for
decades to therapeutic care since 1995 with thrombolysis.3
In the past 3years, four major articles have been published
in support of endovascular intervention for AIS,
4– 7
making
this a central focus of this chapter. Other related topics for
this chapter include the timing of elective surgery following
stroke, how to assess perioperative risk for patients having
a history of remote stroke, and implications for postoperative morbidity and mortality associated with perioperative
stroke in noncardiac surgery.
8
sion is still lacking. ere are specic patient subsets, however, for whom thrombolysis may have limited eectiveness.
Patients with large- vessel or “proximal” arterial occlusion
(Figure 64.1, 64.2, ) may be poorly responsive to rtPA due
to the size and density of the occluding clot. ere are also
patients for whom systemic thrombolysis may be contraindicated, for example patients with catastrophic strokes
beyond the window of eligibility (and at risk for hemorrhagic conversion) or patients suering perioperative stroke
placing them at risk for operative site hemorrhage. For these
selected patients, mechanical thrombectomy may provide
benet, although clear evidence for endovascular intervention for AIS was mixed until late 2014. Since then, four large
randomized trials comparing mechanical retrieval with a
ACUTE ISCHEMICSTROKE
stent retriever device versus medical management have been
published and strongly support endovascular intervention
for proximal vessel occlusion, typically in conjunction with
Acute ischemic stroke is dened as the occlusion of
arterial blood ow to a xed distribution of brain
(Figures64.1, 64.2,). e phrase “Time is Brain!” is frequently used, as patients suering stroke lose up to 2million neurons per minute,9 and patient outcomes are clearly
improved with early intervention.1 e central tenet for
AIS management is that there is brain at risk for infarction which is potentially salvageable with emergent intervention. Because most strokes are ischemic in origin,10
this subset is the topic of interest for this chapter. Atrial
4– 7
rtPA .
In an editorial discussing the signicance of these
four trials, Grotta and Hacke12 summarized their ndings
by concluding that endovascular intervention for AIS is a
“potently” eective treatment for proximal vessel occlusion,
particularly for patients undergoing thrombolytic therapy
prior to intervention. ey further conclude that outcomes
are improved when intervention is performed at a stroke
center, when time to recanalization is minimized and when
stent retriever devices are employed. Finally, they add that
outcomes are improved when general anesthesia is avoided.
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associated with GA during endovascular intervention is particularly critical to patient outcome and, second, whether it
is possible that GA is inherently neurotoxic and thus negatively aecting outcomes in patients with AIS. Neither of
these questions can be answered at present, but it certainly
seems reasonable to evaluate each patient independently
and when CS is deemed safe, proceed with CS. Conscious
sedation can consist of no sedative agents and simple verbal
reassurance (as we frequently do at our institution) to lowdose propofol infusion. Box 64.1 lists considerations when
making this determination for an individual patient. e
determination of anesthetic technique based on individual
patient factors is supported by the Society for Neuroscience
in Anesthesiology and Critical Care (SNACC) in their
Figure 64.1 Occlusion of middle cerebral artery. SOURCE: Courtesy of Dr. Aditya
Pandey, University of Michigan.
2014 consensus statement onAIS.
Evidence to guide the medical management of patients
13
during endovascular intervention is surprisingly limited.
is nal statement, compared to their other conclusions,
is less clearly supported. While there is overwhelming evidence in the existing literature that patients receiving conscious sedation (CS) during endovascular intervention for
AIS have better outcomes than patients receiving general
anesthesia (GA), all studies are signicantly weakened by
selection bias (i.e., there are no studies controlled for presenting neurologic condition, and patients receiving GA are
uniformly sicker), they are almost all small and retrospective,
there are no studies controlling for blood pressure and other
physiologic variables, and nally, practice patterns over
time favor CS but interventional techniques and patient
processes have also improved over time, further confusing
any conclusions regarding CS superiority. Despite these
weaknesses, given the sheer volume of studies supporting
CS, it seems reasonable to ask, rst, whether hypotension
ere are recommendations such as those oered by the
SNACC consensus statement,13 but hard evidence is lacking. One of the most important clinical determinations is
at what level to maintain patient blood pressure during the
periprocedural period. Arterial access is benecial in this
setting, but whenever possible, placement of an arterial line
should not delay groin puncture but occur simultaneously
(or slave o of the sheath). If GA is required, the anesthesia team may appropriately choose to place an arterial line
prior to induction of anesthesia for close hemodynamic
control. As regards blood pressure goals, the relationship
between patient blood pressure and survival is U- shaped,14
meaning those stroke patients presenting with severe
hypertension or hypotension generally have worse outcomes. Given the upper limit of 185/ 105 mmHg to qualify
for rtPA administration15 (and many patients undergoing
endovascular therapy have received rtPA), these seem like
reasonable upper limits. As for the lower acceptable limit
for blood pressure, SNACC recommends maintaining
systolic pressure above 140 mmHg13 in order to optimize
collateral ow to the ischemic penumbra. Blood pressures
below this level should be aggressively treated. Other management goals include normoglycemia, normocapnia, and
oxygen saturation greater than 92%.13 Although hypothermia is neuroprotective for focal ischemia in animal models,16 as yet there is no evidence in human trials to support
hypothermia for AIS.
It is notable that between the years of 2008 and 2012
only 8% of hospitals treating stroke oered mechanical
thrombectomy as a treatment option.17 Clearly, from a
public health standpoint, we have work to do to facili-
Figure64.2 Successful endovascular recanalization for same patient as Figure
64.1. SOURCE:Cour tesy of Dr.Aditya Pandey, University of Michigan.
tate the rapid recognition and treatment of patients suffering AIS. Given the recent data strongly supporting
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465
Furthermore, perioperative stroke has a two- to threefold
BOX 64.1 CLINICAL CONSIDERATIONS FORDETERMINING
ANESTHETIC TECHNIQUE FORAIS INTERVENTION
greater mortality than strokes occurring in the nonoperative setting.19 While clinically evident stroke following
noncardiac and nonneurosurgical procedures is rare with
Considerations inFavor ofGeneral Anesthesia
1. Procedure may be painful, and patients may react
unpredictably
an incidence of 1:1000, with ve or more patient risk factors (see Box 64.2) this incidence becomes 2%,8 a striking incidence for procedures considered to be “low risk.”
Stroke in the perioperative setting is dicult to recognize
2. Patients with dominant MCA occlusion may be aphasic
and unable to cooperate with directions
3. Posterior circulation strokes may limit patient ability to
protectairway
4. Improved control of oxygenation and ventilation
clinically for many reasons including residual anesthetic
BOX 64.2 PERIOPERATIVE ASSOCIATIONS
WITHPERIOPERATIVESTROKE
Considerations inFavor ofConscious Sedation
1. Better cerebral perfusion pressure to ischemic brain and
collateral circulation
2. More rapid “door to clot”times
3. Real- time neurologic assessment
4. Patient comorbidities may place them at riskforGA
endovascular intervention for large- vessel occlusion, it
seems reasonable to expect increasing volumes of patients
presenting for emergent anesthetic management, particularly as the US population ages. Systematic problems for
anesthesiologists include the fact that these patients are
inherently sick with multiple medical comorbidities, they
present with little to no medical information pertaining
to their comorbidities, and they are truly emergent procedures, severely limiting our ability to gather medical
information. Given the unpredictable timing of stroke
presentation, stang for these procedures also presents
issues for anesthesiology departments at stroke centers
performing endovascular intervention. Despite these
issues, the fact that we can now oer eective therapy to
improve outcomes in patients suering AIS is true progress and provides hope for further improvements in outcome for this patient population.
Patient Comorbidities
1. Age
2. h/ o TIA orstroke
3. h/ o renal disease
4. Femalesex
5. Cardiac disease
6. Hypertension
7. Smoking
Representative Risk Based onSurgical Procedure
1. Noncardiac nonneurosurgical0.1%
2. Noncarotid vascular1%
3. Coronary arter y bypass2%– 4%
4. Double- triple valve replacements10%
Perioperative Events That May Be Associated
withIncreased Risk ofPerioperativeStroke
1. Hypotension
2. Atrial brillation
3. Beta- blocker administration (particularly nonselective)
PERIOPERATIVESTROKE
Perioperative stroke, generally dened as stroke within
30days of surgery, is a devastating complication of surgery
and anesthesia that is clearly associated with an increased
risk for perioperative mortality and morbidity.
ACUTESTROKE 465
8,18
4. Anemia
5. General anesthesia (specic to total jointsonly)
6. Prothrombotic state associated with surgery
7. Anticoagulant or antiplatelet cessation
8. Statin cessation
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