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60.
LOCAL ANESTHETIC SYSTEMIC TOXICITY INPREGNANCY
Brian F.S.Allen
CLINICALCASE
lead to dierences seen in LAST presentation and severity.4
Dysrhythmia is a more prominent feature of bupivacaine
A 27- year- old pregnant female at 39 weeks estimated gestational age presents in labor. She has had two previous
uncomplicated vaginal deliveries. e anesthetic plan is to
provide labor analgesia with a lumbar epidural.
toxicity, whereas with lidocaine, myocardial depression is
reported to predominate.4 Potent, long- acting anesthetics
such as bupivacaine (and to a lesser extent ropivacaine and
levobupivacaine) bind to cardiac sodium channels more
avidly than do short- acting anesthetics, producing more
PATHOPHYSIOLOGY OFDISEASESTATE
MECHANISM
Local anesthetic systemic toxicity (LAST) is a set of neurologic and cardiovascular signs and symptoms resulting from
elevated plasma levels of local anesthetic (LA). Neurologic
sequelae range in severity, and might reect central nervous
system (CNS) excitation or depression, or might be nonspecic. Potential signs and symptoms include perioral numbness, tinnitus, drowsiness, disorientation, agitation, seizure,
or loss of consciousness.
1,2
Cardiovascular morbidity results
from electrophysiological abnormalities (dysrhythmia) or
depressed cardiac contractility.
1,3,4
Presentation of cardiovascular toxicity is highly variable, with bradycardia, tachycardia,
hypotension, hypertension, ventricular tachycardia, ectopy,
and asystole having been reported as possible manifestations.
Local anesthetics function through binding to voltagegated sodium channels, blocking the sodium ion ow
across cell membranes required for nerve depolarization to
prevent action potential propagation, causing the clinical
eect of nerve blockade. is activity is systemic and is not
limited to neuronal cells. Cardiac toxicity occurs when cardiac myocytes are exposed to elevated plasma levels of LAs.4
is usually results from inadvertent intravascular injection, but can also occur with excessive perineural administration of LAs with vascular uptake.
1,5
Cardiac sodium channels, as well as other voltage- gated
channels, are inhibited, leading to conduction disturbances
and myocardial depression. Heterogeneity among dierent
LAs in binding anity for sodium channel isoforms may
severe toxicity, which can be refractory to therapy.
potent LAs, such as lidocaine, CNS signs and symptoms
oen precede cardiac toxicity, serving as a potential warning sign. Long- acting LAs are less likely to show symptom
progression; cardiovascular toxicity may occur alone or in
quick succession with neurologic toxicity.
RISK
1,4
Risk of LAST is increased with hypercapnia, hypoxia,
changes in protein binding, acidosis, and— for several
reasons— pregnancy.
5,7
e vulnerability to LAST in pregnancy results from (1)increased susceptibility to toxic LA
eects, (2)higher levels of unbound free drug in the plasma,
and (3) more frequent epidural catheter misplacement.
Increased susceptibility to LA during pregnancy derives
from hormonal changes that sensitize myocardial cells to
1
dysrhythmia as well as neuronal changes that may lower the
seizure threshold.7 Increased free LA in the plasma results
from pregnancy- related decreases in protein binding and
rapid epidural drug uptake secondary to increased maternal cardiac output and epidural vein dilation. Increased risk
of intravascular epidural catheter placement or migration is
also related to epidural vein dilation.
Choice of LA aects risk of toxicity and of refractory
or fatal LAST. Bupivacaine is the causative agent in >50%
of reported LAST cases, with ropivacaine implicated in
30% and other LAs accounting for the remainder.1 is
distribution may reect patterns of use and not increased
likelihood of toxicity. However, if cardiac arrest occurs, successful resuscitation with return of spontaneous circulation
(ROSC) has been shown to be less likely with bupivacaine
4,6
For less
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than other agents.
duce fatal LAST than bupivacaine, is more deadly than
lidocaine LAST in animal studies.6 e reasons for this
discrepancy may relate to LA avidity for cardiac receptors
and/ or dierences in sodium channel isoform binding, as
described previously.
6,8
Ropivacaine, though less likely to pro-
ventricular brillation, premature ventricular contractions
(PVC), wide complex rhythms, and ST changes are all possible.1 No single dysrhythmia is predominant in reported
LASTcases.
Due to the variable presentation of LAST— 40% of
cases report an “atypical presentation”— any patient receiving LAs who manifests neurologic or cardiovascular signs or
ASSESSMENT OFTHE PATIENT:PRESENTING
SIGNS AND SYMPTOMS
symptoms should be carefully evaluated for having LAST.
Although it remains a rare complication during labor and
delivery, a high index of suspicion for LAST in parturients
1,9
with this spectrum of symptoms is warranted, since preg-
Most cases of LAST occur aer a single injection, though
15% of reported cases occur during continuous infusion.1
Inadvertent intravascular injection of local anesthetics usually results in rapid onset of symptoms. Most published cases
of LAST aer a single injection occur within 5 minutes of
LA administration, with a median onset of slightly less than
1 minute.
1,9
Aquarter of toxicity events may occur 5 minutes or more aer a LA single injection, with delayed events
up to an hour aer administration.
1,9
With continuous LA
infusion, toxicity occurs hours or days aer initiation.
Central nervous system (CNS) toxicity is present in
89% of reported cases, with cardiovascular (CV) toxic-
nancy increases the risk of toxicity. e top 15 causes of
peripartum cardiac arrest do not include LAST.10 But other
causes of maternal morbidity such as eclampsia, amniotic
uid embolism, magnesium toxicity, myocardial infarction, heart failure, and anaphylaxis can also present with
dysrhythmia or neurologic signs. erefore, LAST should
remain in the dierential diagnosis of a patient with these
signs and symptoms. In many cases, an epidural catheter
with LAs infusing is present when parturients suer one of
the above disease processes. Since LAST therapy is unique
and not appropriate for other pathophysiologic conditions,
distinguishing among causes is of critical importance.
ity aecting 55% (Figure 60.1). Combined CNS and CV
signs are seen in 44% of patients. Isolated CV signs are far
less common (11% of cases) as compared to isolated CNS
signs (45% of cases).1 Seizure, agitation, and loss of consciousness (LOC) are the most common presenting CNS
signs. Milder symptoms such as dizziness, tinnitus, or perioral paresthesia may be initial symptoms and may presage
more serious signs. Cardiovascular toxicity is more variable.
Hyperdynamic changes (tachycardia, hypertension) are
possible and can precede CV collapse. Conduction abnormalities and dysrhythmias such as bradycardia, asystole,
MANAGEMENT OFTHE PATIENT
Prevention is the key to LAST. Careful catheter aspiration
to assess for intravascular placement should be performed.
Test dosing of epidural catheters upon placement, rst
studied in 1981, can help rule out intravascular catheter
placement.
9,11
Asmall dose of LA, commonly lidocaine 45
mg, can produce low- grade symptoms of systemic toxicity
if injected through an inadvertent intravascular catheter.
A perceived auditory rushing or ringing, perioral numbness, and metallic taste are commonly reported symptoms
of a positive (intravascular) test dose. Intravascular epineph-
45%
Neurologic Toxicity
rine 10– 15 mcg, administered with lidocaine in the test
dose, produces a rapid rise in heart rate (HR) of >10 beats
and Cardiac Toxicity
Cardiac Toxicity
44%
per minute and/ or a systolic blood pressure (SBP) rise of
≥15mmHg.
9,12,13
Apositive test dose indicates intravascular
catheter location, which should prompt catheter removal
and replacement. Anegative test dose also usually rules out
intrathecal catheter misplacement, which would present
11%
with rapid onset of spinal anesthesia and motorblock.
Both HR and SBP responses, and thus the sensitiv-
Figur e6 0.1 Diagram showing the presentations of published cases of LAST
from 1979 to 2009:45% showed isolated neurologic toxicity, 44% combined
neurologic and cardiac toxicity, and only 11% showing isolated cardiac
toxicity. SOURCE:Adapted from data in Di Gregorio G, Neal JM, Rosenquist RW, Weinberg
GL. Clinical presentation of local anesthetic systemic toxicity. Regional Anesthesia and Pain
Medicine. 2010;35(2):181– 7. doi:10.1097/ AAP.0b013e3181d2310b.
ity and specicity of the medications administered as an
epidural test dose, can be confounded by beta blockade,
advanced age, or uterine contractions.
11,12
Additionally,
uterine contractions can cause SBP and HR elevations due
LOCAL ANESTHETIC SYSTEMIC TOXICITY IN PREGNANCY 437
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to pain. Falls in SBP and HR may accompany resolution
of a contraction. Giving a test dose at the start or end of a
contraction can lead to false positive or false negative test
doses, respectively. erefore, timing administration to the
period between contractions is critical.
A negative test dose may instill condence that a
catheter is not intravascular, but no one intervention can
completely prevent LAST. Dose reduction— minimizing
the volume and concentration of LAs administered— is
another crucial step in prevention of toxicity.
9,11
Providers
should note overall local anesthetic dose when administering a large epidural bolus to stay below toxic thresholds. An
initially epidural catheter can migrate into the intravascular
space, causing toxicity with subsequent dosing. Incremental
dosing when bolusing an epidural catheter with aspiration
prior to each dose may help identify a catheter that is newly
located within a vascular space. Spinal anesthesia in the
absence of other administered local anesthetics does not
involve enough local anesthetic to causeLAST.
preferentially with benzodiazepines— propofol is not recommended, because although it can ablate seizures, this
drug may worsen hemodynamic changes.
2,18
As with all treatment algorithms of cardiac arrest, proper
management LAST requires high- quality CPR, including
rapid chest compressions (>100 per minute) with minimal
interruption and debrillation when appropriate. Supine
positioning with le uterine displacement if the uterus is
palpable or visible is recommended in maternal arrest.
7,14,19
However, the pharmacologic therapy for LAST diers from
standard ACLS (Box 60.1) in that dose reduction of epinephrine (or avoidance) is recommended. Timing of epinephrine
administration should mimic the ACLS algorithm, but with
doses adjusted to 10– 100 mcg IV, keeping individual doses
to <1 mcg/ kg.2 is replaces the epinephrine 1 mg IV dose
typically administered as part of ACLS. Animal models of
LAST demonstrating poor outcome with resuscitation when
higher doses of epinephrine are used serve as the basis for this
dosing change.
4,7,18,20
Vasopressin, calcium channel block-
ers, and beta adrenergic blockers can also worsen outcomes
INITIAL TREATMENTSTEPS
Clear algorithms exist for patients experiencing LAST or
and hemodynamic status and should be avoided. Lidocaine
should not be administered if LAST is suspected. In the parturient, magnesium therapy should be stopped, if present.
maternal cardiac arrest, both of which dier in important
ways from standard advanced cardiovascular life support
(ACLS).
2,14
ough a combined maternal LAST protocol
does not exist, key points are clear. Patients experiencing
neurologic or cardiovascular signs and symptoms, including
SUBSEQUENT TREATMENTSTEPS
Administration of intralipid in LAST marks a variation
from traditional ACLS. e use of intralipid as therapy for
seizure, loss of consciousness, dysrhythmia, or cardiovascular collapse should receive immediate Basic Life Support.
is includes multiple calls for help— call for an “OB code,”
the neonatal team, intralipid, and cardiopulmonary bypass
equipment and personnel when LAST is suspected.
2,14
Use of a checklist tool in either physical or electronic
BOX 60.1 LOCAL ANESTHETIC SYSTEMIC TOXICITY (LAST)—
DIFFERENCES FROMACLS
Medications toAvoid:
form has been shown to improve adherence to management guidelines for LAST.
15,16
A designated reader who
relays sequential management steps from the checklist to
Calcium channel blockers
Beta- adrenergic blockers
the medical team but does not actively participate in resuscitation is recommended. In simulated LAST scenarios,
adherence to the guideline is improved both by a checklist
and designated reader.
15,16
In the case of maternal LAST,
a maternal cardiac arrest algorithm should also be present
and referenced during management.
Vasopressin
Lidocaine
Propofol
Additional Interventions:
Airway management is a crucial rst step in management, both for aspiration prevention and to minimize the
hypoxia and acidosis that worsen LAST.
4,9,17
Ventilation
Lipid emulsion therapy for severe LAST (see Table2)
Cardiopulmonary bypass for refractoryLAST
with 100% oxygen is recommended. Pregnant patients
should be considered to have a full stomach and consideration given to intubation for aspiration prevention
Changes in Medication Dosage:
Epinephrine dose reduced to <1mcg/ kg
should seizure or LOC occur. Seizures should be treated
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439
LAST was described in animal models starting in 1998.21
Human case reports of 20% lipid emulsion therapy began
in 2006.22 In multiple subsequent cases, case series, and
animal studies, intralipid administration has demonstrated
ecacy in terminating LAST, facilitating ROSC, and
decreasing mortality. Several proposed mechanisms for
these eects exist. e “lipid sink” theory suggests the lipid
emulsion serves as a reservoir, pulling LA molecules out of
the plasma, from myocardial cells, and into micelles that
are later cleared by the liver.
4,7,9,23
Improvements in cardiac
mitochondrial metabolism and elevations in myocyte calcium levels are other proposed mechanisms.
4
Current guidelines recommend lipid emulsion (20%)
administration during cases of LAST where refractory seizure, severe dysrhythmias, and/ or hemodynamic instability
occur. Dosing recommendations are detailed in Box 60.2. An
initial intralipid bolus of 1.5 mL/ kg based on lean body mass
should be rapidly administered.2 For ease of administration,
approximately 100 mL can be administered. Subsequently,
an infusion of 0.25 mL/ kg/ min, approximately 18 mL/ min,
BOX 60.2 INTRALIPID THERAPY
For suspected LAST (ventricular ectopy, tinnitus,
paresthesias, confusion, seizure):
Call for intralipid (20% lipid emulsion) to bedside
Consider intralipid therapy as below based on severity and
symptom progression
For severe LAST (intractable seizure, hemodynamic
instability, severe dysrhythmia):
Bolus 1.5 mL/ kg by lean bodymass
should continue until ROSC and hemodynamic stability
are noted. If toxicity does not abate with these initial steps,
additional boluses may be administered and the infusion rate
should be doubled to 0.5 mL/ kg/ min. e recommended
maximum dose of intralipid in the initial 30 minutes of
therapy is 10 mL/ kg. Asurvey in 2011 showed that 95% of
academic anesthesiology programs had intralipid available
on their obstetric units.24 Ideally this should be located on
the unit “crashcart.”
Controversy exists regarding when to initiate intralipid
therapy. Current guidelines recommend therapy when
severe neurologic or cardiovascular signs and symptoms
consistent with LAST occur. Forgoing therapy until ACLS
fails is not acceptable practice, because of the minimal risk
of intralipid therapy. Yet, intralipid is best avoided when
symptoms are mild or LAST is unlikely. e guidance is
to consider the severity and speed of progression of LAST
when initiating intralipid.
of starting intralipid likely outweigh the risks.
2,25
When in doubt, the benets
7,25
Similar to other causes of maternal cardiac arrest,
perimortem cesarean delivery (PMCD) should occur for
patients at >20– 24 weeks estimated gestational age (recommendations vary) if ROSC does not occur aer 4 minutes
of resuscitative eorts.
14,19
e goal is fetal delivery within
5 minutes of the start of resuscitation. is intervention is
therapeutic for a viable fetus, which may be rescued, as well
as for the mother. Relief of aortocaval compression in the
mother may improve venous return, pulmonary mechanics, and cardiac output while decreasing oxygen requirements.14 ese benets lead to improved maternal and fetal
outcome. Perimortem cesarean delivery should occur at the
location of arrest, since patient transport increases the time
to surgical intervention and worsens the quality of ACLS.
26
Infuse 0.25 mL/ kg/ min
Continue infusion until hemodynamically stable for
10minutes
For refractory LAST (continued instability after initial
intralipid bolus and infusion):
Bolus an additional 1.5mL/ kg
Increase infusion to 0.5 mL/ kg/ min
Max dose:10 mL/ kg in 30 minutes
Continue infusion until hemodynamically stable for
10minutes
Initiate cardiopulmonary bypass if instability persists
LOCAL ANESTHETIC SYSTEMIC TOXICITY IN PREGNANCY 439
REFRACTORY/ RECURRENT LOCAL ANESTHETIC
TOXICITY
Hemodynamic instability with LAST, especially when
bupivacaine is the culprit, is oen refractory to therapy
and may require prolonged ACLS. Even with ROSC, lipid
emulsion infusion should continue for at least 10 minutes
following the achievement of hemodynamic stability (i.e.,
no further requirement of inotrope/ vasopressor support).2
Recurrent cardiotoxicity has been reported, so the patient
should be closely monitored for 12 hours following successful LAST therapy.
2,27
If ACLS, PMCD, and stepwise escalation of lipid emulsion therapy fail to resolve cardiovascular toxicity, cardiopulmonary bypass (CPB) is indicated.
2,14
At facilities that
possess the capability to perform emergency CPB, it should
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be requested early— ideally at the onset of severe LAST.
is allows time to muster personnel and equipment and
in the case of a pregnant patient, to likely transport the
patient from labor and delivery to the main operating room
suite. Where CPB is not feasible, refractory LAST should
prompt patient transport to a nearby facility capable of
CPB. is is of special consideration in the young mother
who can likely survive without serious complication as long
as adequate perfusion can be maintained with high- quality
CPR and CPB when needed.
asystole 1 minute later. You call for additional
assistance. What personnel, equipment, and
medications are important to have for treatment of
this patient? How do you proceed with resuscitation
in the rst minutes aer this arrest? What medications
should be given? What interventions performed?
How should the patient be positioned?
6. Aer 4 minutes of high quality CPR, the patient has
not returned to spontaneous circulation. Acolleague
recommends moving to the operating room for
emergency cesarean section. What should bedone?
FOLLOW- UP
Reports of LAST should be reported to www.lipidrescue.
org. Use of intralipid should be reported to www.lipidregistry.org.
7. Intralipid becomes available during resuscitation
eorts. How should it be administered and dosed? If
cardiovascular instability does not respond to initial
intralipid use, how should the dosing be adjusted?
What should be done if the maximum dose of intralipid
CASE- BASED LEARNING DISCUSSION
is reached and arrest continues?
8. With prolonged therapy, the patient returns to
a rhythm adequate for perfusion and regains
1. Alumbar epidural catheter is placed for labor
analgesia. How is the catheter tested for intravascular
consciousness. What should be done with the intralipid
infusion? How long should the patient be observed?
or intrathecal placement? What medications are
administered in the test dose? What signs and
symptoms indicate a positive testdose?
2. Aer a negative test dose, the epidural is secured and
REFERENCES
LA is bolused through the catheter, establishing an
analgesic block covering the T10 to S2 dermatomes.
One hour later, despite use of an epidural infusion
with patient controlled bolus, the patient complains of
return of pain with contractions. Assessment reveals
regression of analgesic block. What are some potential
causes of block regression? What could be done to
improve the patient’s pain control and reestablish the
block? What medication(s) would you administer?
3. You administer bupivacaine 0.25% via the epidural
catheter in two 5- mL aliquots, separated by 5 minutes.
Immediately on completion of the second bolus, the
patient complains of a metallic taste in her mouth and
becomes agitated and confused. What is the likely
diagnosis? How should these symptoms be managed?
4. e patient loses consciousness, aer which her arm and
leg muscles tense for several seconds and then begin to
contract and relax rapidly. What should be donenow?
5. e seizure abates with treatment. Aer initial
elevated HR and SBP, the patient becomes
bradycardic and hypotensive. is progresses to
1. Di Gregorio G, Neal JM, Rosenquist RW, Weinberg GL. Clinical
presentation of local anesthetic systemic toxicity. Regional
Anesthesia and Pain Medicine. 2010;35:181– 7.
2. Neal JM, Mulroy MF, Weinberg GL. American society of regional
anesthesia and pain medicine checklist for managing local anesthetic systemic toxicity:2012 version. Regional Anesthesia and Pain
Medicine. 2012;37:16– 18.
3. Butterworth JF. Models and mechanisms of local anesthetic cardiac toxicity: a review. Regional Anesthesia and Pain Medicine.
2010;35:167– 76.
4. Wolfe JW, Butterworth JF. Local anesthetic systemic toxicity: update on mechanisms and treatment. Current Opinions in
Anaesthesiology. 2011;24:561– 6.
5. Rosenberg P, Veering B, Urmey W. Maximum recommended doses
of local anesthetics:a multifactorial concept. Regional Anesthesia
and Pain Medicine. 2004;29:564– 75.
6. Casati A, Putzu M. Bupivacaine, levobupivacaine and ropivacaine: are they clinically dierent? Best Practice and Research in
Clinical Anaesthesiology. 2005;19:247– 68.
7. Bern S, Weinberg G. Local anesthetic toxicity and lipid resuscitation in pregnancy. Current Opinions in Anaesthesiology.
2011;24:262– 7.
8. Groban L, Deal DD, Vernon JC, James RL, Butterworth J. Cardiac
resuscitation aer incremental overdosage with lidocaine, bupivacaine, levobupivacaine, and ropivacaine in anesthetized dogs.
Anesthesia & Analgesia. 2001;92:37– 43.
9. Neal JM, Bernards CM, Butterworth JF IV, etal. ASRA practice
advisory on local anesthetic systemic toxicity. Regional Anesthesia
and Pain Medicine. 2010;35:152– 61.
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10. Mhyre JM, Tsen LC, Einav S, Kuklina EV, Leert LR, Bateman
BT. Cardiac arrest during hospitalization for delivery in the United
States, 1998– 2011. Anesthesiology. 2014;120:810– 18.
11. Mulroy MF, Hejtmanek MR . Prevention of local anesthetic systemic
toxicity. Regional Anesthesia and Pain Medicine. 2010;35:177– 80.
12. Moore DC, Batra MS. e components of an eective test dose
prior to epidural block. Anesthesiology. 1981;55:693– 6.
13. Colonna- Romano P, Lingaraju N, Godfrey SD, Braitman LE.
Epidural test dose and intravascular injection in obstetrics:sensitivity, specicity, and lowest eective dose. Anesthesia & Analgesia.
1992;75:372– 6.
14. Lipman S, Cohen S, Jeejeebhoy F, etal. e Society for Obstetric
Anesthesia and Perinatology consensus statement on the management of cardiac arrest in pregnancy. Anesthesia & Analgesia.
2014;118:1003– 16.
15. Neal JM, Hsiung RL, Mulroy MF, Halpern BB, Dragnich AD,
Slee AE. ASRA checklist improves trainee performance during
a simulated episode of local anesthetic systemic toxicity. Regional
Anesthesia and Pain Medicine. 2012;37:8– 15.
16. McEvoy MD, Hand WR, Stoll WD, Furse CM, Nietert PJ.
Adherence to guidelines for the management of local anesthetic
systemic toxicity is improved by an electronic decision support tool
and designated “reader.” Regional Anesthesia and Pain Medicine.
2014;39:299– 305.
17. Porter JM, Markos F, Snow HM, Shorten GD. Eects of respiratory
and metabolic pH changes and hypoxia on ropivacaine- induced cardiotoxicity in dogs. British Journal of Anaesthesia. 2000;84:92– 94.
18. Toledo P. e role of lipid emulsion during advanced cardiac life support for local anesthetic toxicity. International Journal of Obstetric
Anesthesia. 2011;20:60– 63.
19. Drukker L, Hants Y, Sharon E, Sela HY, Grisaru- Granovsky S.
Perimortem cesarean section for maternal and fetal salvage:concise
review and protocol. Acta Obstetrics and Gynecology Scandanavia.
2014;93:965– 72.
20. Hiller DB, Gregorio GD, Ripper R, et al. Epinephrine impairs
lipid resuscitation from bupivacaine overdose: a threshold eect.
Anesthesiology. 2009;111:498– 505.
21. Weinberg GL, VadeBoncouer T, Ramaraju GA, Garcia- Amaro
MF, Cwik MJ. Pretreatment or resuscitation with a lipid infusion
shis the dose- response to bupivacaine- induced asystole in rats.
Anesthesiology. 1998;88:1071– 75.
22. Rosenblatt MA, Abel M, Fischer GW, Itzkovich CJ, Eisenkra
JB. Successful use of a 20% lipid emulsion to resuscitate a patient
aer a presumed bupivacaine- related cardiac arrest. Anesthesiology.
2006;105:217– 18.
23. Kuo I, Akpa BS. Validity of the lipid sink as a mechanism for the
reversal of local anesthetic systemic toxicity:a physiologically based
pharmacokinetic model study. Anesthesiology. 2013;118:1350– 61.
24. Toledo P, Nixon HC, Mhyre JM, Weinberg G. Availability of lipid
emulsion in United States obstetric units. Anesthesia & Analgesia.
2013;116(2):406– 8.
25. McCutchen T, Gerancher JC. Early intralipid therapy may have prevented bupivacaine- associated cardiac arrest. Reg Anesth Pain Med.
2008;33(2):178– 80.
26. Lipman SS, Wong JY, Arafeh J, Cohen SE, Carvalho B. Transport
decreases the quality of cardiopulmonary resuscitation during simulated maternal cardiac arrest. Anesthesia & Analgesia.
2013;116:162– 7.
27. Marwick PC, Levin AI, Coetzee AR. Recurrence of cardiotoxicity aer lipid rescue from bupivacaine- induced cardiac arrest.
Anesthesia & Analgesia. 2009;108:1344– 6.
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PARTVII.
NEUROLOGIC CRISES
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61.
INTRODUCTION TOACUTE NEUROLOGIC EVENTS INTHE
PERIOPERATIVEPERIOD
LorriA.Lee
APPROACH TOTHE PATIENT WITHAN ACUTE
NEUROLOGICEVENT
step along with assessing the patient’s airway, ventilation,
and circulation. Hypoxia, hypercarbia, and severe hypo-
tension can aect mental status, or conversely, neurologic
Anesthesiologists may encounter patients with acute neurologic events at various stages in their workup, diagnosis, and
treatment. e urgency of diagnosis, workup, and denitive treatment falls on a spectrum from minutes to days
to weeks, depending on the clinical scenario. Patients may
present as a known surgical emergency with a reasonably
complete workup, such as an acute ischemic stroke patient
who is boarded emergently for the operating room for intracranial thrombus retrieval. Alternatively, patients may have
unexpected neurologic events that occur perioperatively,
such as new- onset seizures or intracranial hemorrhage that
rst requires prompt recognition that an acute neurologic
process is occurring followed by a rapid workup and treatment. Less emergent conditions, such as delirium or cerebral salt wasting, do not require immediate assessment and
treatment within minutes, but nonetheless require appropriate workup and treatment, as early intervention is associated with better perioperative outcomes. Finally, patients
may also have less urgent neurologic complications, such as
perioperative nerve injuries from positioning, that can be
evaluated on a nonurgent basis depending on the clinical
setting but nonetheless require a thorough understanding
of how to address these problems that are very important to
overall patient outcomes. is section deals primarily with
the emergent/ urgent acute neurologic events where time to
treatment is paramount to a good neurological outcome.
Acute neurologic events in the perioperative period
may occur in the preoperative, intraoperative or postoperative settings at numerous locations including the emergency room, intensive care unit, operating room, oor,
and various imaging sites such as the CT scanner. ese
events are oen life threatening and can result in disastrous debilitating outcomes for patients. Recognition that
a neurologic problem may be occurring is the rst critical
complications can aect a patient’s ability to maintain a
patent airway or respiratory drive, or result in severe bradycardia and hypertension with Cushing’s reex from raised
intracranial pressure. Aer assessing these basic functions
and whether a patient requires emergent intubation or
vasoactive medications, one should obtain a neurology or
neurosurgical consultation and assess whether the patient is
stable enough to undergo diagnostic imaging or other therapeutic interventions. Basic knowledge of the presentations
and dierential diagnoses of various neurologic complications along with early therapeutic interventions can make
the dierence between a reasonable quality of life or complete dependence on caregivers for patients. Concern for an
acute perioperative stroke for patients who have undergone
nonneurosurgical procedures should prompt an emergent
stroke alert to maximize the chances of a prompt diagnostic workup and treatment. ese stroke alert systems are
specically designed within hospitals to maximize ecient
workup and treatment for acute strokes. Clinicians should
not take it on themselves to attempt these stroke evaluations
outside of these systems when available in their institution.
Emergent operative treatment of known acute neurologic events include procedures such as retrieval of
thrombus from acute stroke patients, decompressive
craniectomy for left middle cerebral artery stroke, evacuation of an acute subdural or epidural hematoma, and
decompression of a rapidly evolving spinal cord injury
caused by compression. These operations require rapid
anesthetic preparation, as time to restoring normal cerebral and spinal cord perfusion are directly related to
outcomes. Discussion with the neurosurgeon regarding the surgical plans, need for mannitol or hypertonic
saline, and hemodynamic and ventilation goals is helpful so that there is clear communication and agreement
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