Download Lipid resuscitation for local anesthetic toxicity: is it really

Lipid resuscitation for local anesthetic toxicity: is it
really lifesaving?
Ulana Leskiwa and Guy L. Weinberga,b
a
University of Illinois at Chicago College of Medicine
and bJesse Brown VA Medical Center, Chicago, Illinois,
USA
Correspondence to Ulana Leskiw, MD, University of
Illinois at Chicago College of Medicine, 1740 West
Taylor, Suite 3200W, M/C 515, Chicago, IL 60612,
USA
Tel: +1 312 996 4020; fax: +1 312 996 4019;
e-mail: [email protected]
Current Opinion in Anaesthesiology 2009,
22:667–671
Purpose of review
Laboratory studies and clinical reports have led to the acceptance of lipid emulsion
as an effective treatment of local anesthetic-induced cardiac arrest. This review
discusses subsequent clinical reports, relevant laboratory studies and topics for further
research.
Recent findings
Case reports have confirmed the efficacy of lipid resuscitation for local anesthetic
systemic toxicity. Furthermore, lipid emulsion has been used with apparent success
early in the spectrum of local anesthetic systemic toxicity to preempt cardiac arrest. The
role of lipid emulsion has expanded to treatment of cardiac toxicity due to other lipophilic
drugs. This appears to have an acceptable safety profile, although elevated amylase has
been reported. Laboratory investigations in animals suggest that concomitant
hypoxemia hinders resuscitation attempts, and that epinephrine and vasopressin are
more likely to be associated with poor outcomes than lipid.
Summary
Lipid emulsion infusion appears to be an effective treatment for cardiac toxicity induced
by lipophilic medications. Given the difficulties of performing clinical trials, further
laboratory investigation and clinical correlation are needed to better define its role in
resuscitation.
Keywords
lipid emulsion, local anesthetics, resuscitation, toxicity
Curr Opin Anaesthesiol 22:667–671
ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
0952-7907
Introduction
Local anesthetic systemic toxicity (LAST) is a rare but
potentially catastrophic complication of regional anesthesia [1]. Laboratory findings made over the last decade and
recent case reports suggest that lipid emulsion is a potential antidotal treatment and might reduce the morbidity
of this complication. Weinberg et al. [2] first reported in
1998 that lipid emulsion infused during resuscitation
increased the median lethal dose (LD50) of bupivacaine
in rats by 50%. In a subsequent study [3] of bupivacaineinduced cardiac arrest in dogs, treatment with lipid
improved hemodynamics and survival compared with
isotonic saline-treated controls. This review will summarize clinical experience with lipid emulsion, highlight
relevant laboratory studies and address the current status
of this therapy with respect to timing, dose, potential
adverse effects and its overall role in resuscitation.
Clinical experience
In 2006, Rosenblatt et al. [4] and Litz et al. [5] reported
successful clinical use of lipid emulsion to reverse local
0952-7907 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
anesthetic-induced cardiac arrest. In both cases, the
patients failed to respond to standard resuscitation
methods but regained normal hemodynamic parameters
shortly after lipid emulsion infusion. Further clinical
reports [6,7 –10] have provided a growing body of support for use of this therapy. Lipid emulsion has been used
to treat LAST due to bupivacaine, levobupivacaine,
ropivacaine and mepivacaine, alone or in combination.
Lipid preparations other than Intralipid have also been
found to be effective; the successful use of 20% Liposyn
III (Hospira, Inc., Lake Forest, Illinois, USA) [10] and
20% Medialipid (Braun, Kronberg, Germany) [8] has
been reported. In addition to case reports published in
peer-reviewed journals, many cases have been posted at
the educational website www.lipidrescue.org.
Published guidelines
On the basis of initial laboratory studies [2,3] and case
reports [4,5], the Association of Anaesthetists of Great
Britain and Ireland (AAGBI) published guidelines in
2007 for management of severe LAST, which stated that
lipid emulsion should be available in locations where
DOI:10.1097/ACO.0b013e32832eb93f
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668 Regional anaesthesia
potentially toxic doses of local anesthetics are administered; recommended doses were provided (http://www.
aagbi.org/publications/guidelines/docs/latoxicity07.pdf).
In 2008, the American Society of Critical Care Anesthesiologists and the American Society of Anesthesiologists
Committee on Critical Care Medicine as well as the
Resuscitation Council of the UK also published protocols
for treatment of LAST, which incorporated the use of
lipid emulsion (http://www.asahq.org/clinical/Anesthe
siology-CentricACLS.pdf, http://www.resus.org.uk/pages/
caLocalA.htm). Of note, propofol is not a substitute for
lipid emulsion, given its lower lipid content and the known
myocardial depressant effects.
Application to other toxic events
Animal studies have demonstrated efficacy of lipid emulsion in treating verapamil toxicity [11,12], clomipramine
toxicity [13] and propranolol toxicity [14]. Furthermore,
lipid infusion has recently been used by physicians
treating patients for overdoses of other lipophilic toxins.
For instance, Sirianni et al. [15] reported the dramatic
case of a 17-year-old girl with a severe overdose of
bupropion and lamotrigine. She subsequently suffered
a prolonged cardiac arrest refractory to standard advanced
cardiac life support (ACLS), including multiple defibrillations and bolus doses of epinephrine, NaHCO3, amiodarone and ‘wide-open’ infusions of dopamine, norepinephrine and epinephrine. One minute after an infusion
of 100 ml of 20% lipid emulsion, she regained normal
circulation and vital signs. Her hospital course was complicated by acute lung injury (ALI) that was apparent
prior to the lipid infusion, and she was eventually discharged with only minor memory deficits.
As the authors point out, bupivacaine and bupropion
share similar properties, including sodium channel blocking actions and nearly identical octanol : water partition
coefficients. Subsequent reports have described the successful use of lipid rescue in the treatment of circulatory
and neurological symptoms of overdose with sertraline
and quetiapine (coma) [16], sustained-release verapamil
(hypotension) [17] and haldol (torsades de pointes) [18].
An animal study [19] of verapamil overdose indicates that
similar doses of lipid (in terms of total lipid mass) were
necessary as were used to treat bupivacaine-induced asystole in rats.
cases. Although early clinical reports may have been
questioned because recovery might have resulted from
delayed response to conventional treatment rather than
lipid emulsion, the reliably rapid clinical improvement
after administration of lipid in dozens of cases appears to
support its efficacy. Taken together, the growing number
of cases and the highly consistent clinical descriptions of
return of spontaneous circulation strongly support the
usefulness of this therapy. This contrasts with classical
descriptions of refractory cardiac arrests in similar circumstances.
One current challenge is to define the role of lipid
emulsion in the treatment of toxicity induced by lipophilic agents. New information is inevitably followed by
new questions. Issues that remain to be determined
include optimal timing of administration and dose, potential adverse effects and the place of lipid in the scheme
of resuscitation.
Timing of administration
Current protocols from the AAGBI (and www.lipidres
cue.org) recommend lipid emulsion for cardiac arrest in
conjunction with standard basic life support (BLS) and
ACLS practices (http://www.lipidrescue.org, http://www.
aagbi.org/publications/guidelines/docs/latoxicity07.pdf).
However, as lipid therapy has become more accepted,
clinicians have chosen to administer lipid emulsion earlier
in the spectrum of adverse local anesthetic reactions,
preferring to act before refractory cardiac arrest occurs.
For instance, lipid emulsion was used to treat central
nervous system (CNS) toxicity and ventricular ectopy in
an attempt to prevent progression to cardiac arrest [6].
Other examples include a 13-year-old girl who developed
ventricular tachycardia after lumbar plexus block with
a ropivacaine–lidocaine mixture. Lipid emulsion was
administered at the onset of arrhythmia; the electrocardiogram reverted to normal, and surgery was performed
uneventfully [8]. A 91-year-old man became unresponsive with extrasystoles after upper extremity regional
anesthesia with mepivacaine and prilocaine. He received
lipid emulsion, with subsequent restoration of consciousness and resolution of ectopy [9]. Similarly, lipid reversed
CNS symptoms and ventricular tachycardia in an 82-yearold woman after lower extremity nerve block [7]. A
parturient who developed agitation and inability to follow
commands after epidural with bupivacaine was successfully treated with lipid emulsion [20].
Challenges in investigation
The infrequency of severe LAST cases and ethical
considerations preclude randomized clinical trials of lipid
resuscitation. We must, therefore, rely on case reports and
laboratory investigations to inform clinical practice. However, case reports suffer from positive reporting bias and
provide neither a precise numerator nor denominator of
Effective dose
Case reports indicate that currently proposed dose
regimens are efficacious, although it is certainly possible
that there are treatment failures that have not been
reported. For local anesthetic-induced cardiac arrest,
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Lipid resuscitation Leskiw and Weinberg 669
recommendations include a bolus of 20% lipid, 1.5 ml/kg
(http://www.lipidrescue.org, http://www.aagbi.org/publi
cations/guidelines/docs/latoxicity07.pdf, http://www.
resus.org.uk/pages/caLocalA.htm) followed by an infusion of 0.25 ml/kg/min for 20 min (http://www.aagbi.org/
publications/guidelines/docs/latoxicity07.pdf), 30–60 min
(http://www.lipidrescue.org) or until stable rhythm is
restored (http://www.resus.org.uk/pages/caLocalA.htm).
If adequate circulation is not restored, various regimens
have been suggested: bolus doses may be repeated up to
two times (http://www.lipidrescue.org), up to two times at
5 min intervals (http://www.aagbi.org/publications/guide
lines/docs/latoxicity07.pdf) or at 5 min intervals until
stable rhythm is restored (http://www.resus.org.uk/
pages/caLocalA.htm), and the infusion rate may be
increased (http://www.lipidrescue.org) or increased to
0.5 ml/kg/min for 10 min (http://www.aagbi.org/publi
cations/guidelines/docs/latoxicity07.pdf). Marwick et al.
[21] reported recurrence of ventricular ectopy in a
72 kg man who was successfully treated with Intralipid
for bupivacaine-induced cardiac arrest. A 150 ml bolus was
initially administered, followed by 350 ml over the next
30 min. Sinus rhythm and hemodynamic stability were
restored, and surgery proceeded, but 40 min later, ventricular ectopy recurred. They point out that a full 1000 ml of
lipid may be required. On the contrary, in a study [8]
describing lipid treatment of ventricular tachycardia after
nerve block, the bolus dose alone was adequate and infusion was unnecessary.
Adverse effects
There are concerns regarding possible adverse effects of
lipid therapy. The risk–benefit ratio becomes particularly important when lipid emulsion is used in patients
prior to the onset of overt hemodynamic instability and
cardiac arrest. The most serious adverse effect that has
been associated with the use of lipid emulsion for parenteral nutrition is pulmonary injury.
Recently, a single elevated amylase level was reported in
the patient described by Marwick et al. [21] above; the
patient had received a total of 500 ml of Intralipid. No
clinical signs of pancreatitis were noted, and no specific
treatment was needed. Whether other cases of hyperamylasemia have occurred or are underreported is not
known. Notably, no other adverse effects have been
reported with the use of lipid for the treatment of
drug-related toxicity. Again, this may reflect underreporting or positive bias; long-term follow-up may reveal
problems that are not currently apparent.
Laboratory investigations
In order to better define the place of lipid emulsion in
resuscitation, Weinberg et al. [22] studied lipid versus
epinephrine in a rat model of cardiac arrest. Anesthetized
rats received bupivacaine, 20 mg/kg, to induce asystole,
then immediately received cardiopulmonary resuscitation (CPR) with 100% oxygen and either 30% lipid,
5 ml/kg bolus and 0.5 ml/kg/min infusion, epinephrine,
30 mg/kg bolus or normal saline. Bolus doses of medications were repeated at 2.5 and 5 min until the rate
pressure product was above 20% of baseline. At 10 min,
resuscitation rates were 5/5, 4/5 and 0/5 in the lipid group,
epinephrine group and saline group, respectively; pH,
paO2 and saturated venous oxygen (SvO2) were higher
and lactate lower in the lipid group. Notably, an early
increase in blood pressure (BP) with epinephrine was
followed by subsequent decline and pulmonary edema,
not seen in the lipid group. In a similar follow-up study
[23], lipid emulsion was superior to vasopressin and
vasopressin/epinephrine with respect to rate pressure
product, pH, SvO2 and lactate. Results with vasopressin
alone were particularly unfavorable. In a rat model of
bupivacaine-induced asystole, concomitantly administered epinephrine above 10 mg/kg hindered resuscitation
[24]. These data suggest that use of lipid emulsion
earlier in the resuscitative effort and avoidance of pressors may result in better outcomes in this setting. These
are preliminary findings in animals, however, which need
to be investigated further and confirmed prior to extrapolating to the clinical setting.
Of interest, the patient described by Sirianni et al.
[15] above, who received multiple doses of epinephrine
(18 mg total), had postresuscitation pulmonary edema/
ALI. Although pulmonary edema may occur after resuscitation from cardiac arrest treated with standard ACLS
protocols, the consistent pattern of postvasopressor pulmonary edema and worsened recovery in the pressortreated animals in the above-mentioned investigations is
notable. Whether this phenomenon is particular to the rat
model, whether bupivacaine somehow predisposes to
ALI or whether this results from significant myocardial
poisoning by local anesthetic and the vasoconstriction
caused by vasopressin and epinephrine which then overwhelms the weakened ventricle leading to severe failure
remains to be elucidated in further studies.
Despite an apparent general enthusiasm for lipid resuscitation, several reports question its efficacy with respect
to vasopressor treatment. Mayr et al. [25], working with
a porcine model of bupivacaine overdose, reported that
vasopressin combined with epinephrine resulted in higher
coronary perfusion pressure during CPR and better shortterm survival rates than lipid emulsion. In this model,
mechanical ventilation was stopped after anesthetized
animals received 0.5% bupivacaine, 5 ml/kg, then not
resumed until 1 min after asystole occurred, at which time
CPR was initiated and mechanical ventilation resumed.
Animals received either 20% Intralipid (4 ml/kg, followed
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
670 Regional anaesthesia
by infusion of 0.5 ml/kg/min) or vasopressin/epinephrine
(every 5 min in escalating doses, 0.4/45, 0.4/45 and
0.8/200 units/kg and mg/kg). Return of spontaneous circulation, defined as SBP of at least 80 mmHg for at least 5 min,
was obtained in 5/5 of the pressor group but 0/5 of the lipid
group. The authors note that, in this short-term study,
they might have missed survival at a later time among
the lipid group. The design of the study, however, raises
the question of whether the cardiac arrest was bupivacaineinduced or hypoxemia-induced in the context of
bupivacaine toxicity.
In contrast to perioperative occurrences in which the cause
is known, emergency rooms receive patients presenting
with cardiopulmonary and neurologic compromise of
unknown cause. Physicians need to decide whether to
administer lipid without knowing definitively whether the
patient had ingested a lipophilic toxin. It is, therefore,
important to know whether lipid itself interferes with
standard resuscitation. Harvey et al. [26] addressed this
question in a rabbit model of asphyxial cardiac arrest. The
endotracheal tube was cross-clamped to cardiac arrest.
Animals were randomized to normal saline versus 20%
Intralipid, 3 ml/kg. Resuscitation included BLS/ACLS
with defibrillation and epinephrine, 100 mg/kg, repeated
if needed. Lipid emulsion/ACLS resulted in lower coronary perfusion pressure and lower rates of return of spontaneous circulation (1/12 versus 7/11) compared with
ACLS alone. Of interest, however, at 50 min, there was
no difference in survival between groups.
What can we conclude from these conflicting studies?
First of all, the critical importance of prompt airway
management and maintenance of adequate oxygenation
cannot be overstated. The abysmal outcomes in the study
by Harvey et al. [26] reinforce the importance of the ‘A’
and ‘B’ of the ‘ABC’s’ – airway, breathing and circulation.
The reports of successful use of lipid rescue are likely at
least partly predicated on these being ‘witnessed’ events
and the resulting absence of significant hypoxemia as a
contributing factor. These reports generally describe
appropriate airway management at the first sign of CNS
irritability, ventricular ectopy or hemodynamic instability,
with supplemental oxygen, ventilation and intubation
when necessary. The study of Mayr et al. [25] describes
a somewhat different scenario. On the contrary, if documentation of lipophilic toxin ingestion is lacking and
hypoxemia is present, the data by Harvey et al. [26]
would argue against lipid use. Finally, in cases of known
LAST complicated by significant hypoxemia, the data by
Harvey et al. [26] might caution against earlier use of
lipid; however, the poor 50 min survival in both groups
suggests there is still much room for research as the
hypoxemia is likely more damaging than the lipid. The
poor overall survival is consistent with that noted in studies
of out-of-hospital cardiac arrest [27].
Mechanism
Insights into the mechanism of action of lipid emulsion
will aid in optimizing its use. At present, the most likely
theory appears to be that of the lipid ‘sink’ binding the
lipophilic drugs and thereby reducing tissue content of
the toxin. Plasma levels are difficult to obtain during
resuscitation, however, and results so far are inconsistent.
An in-vitro study did indeed demonstrate high solubility
of local anesthetics in lipid emulsions and high binding
capacity of these emulsions; interestingly, Intralipid
appeared about 2.5 times more efficacious than Medialipid and binding was reduced at lower pH [28].
Conclusion
Lipid emulsion has an apparently acceptable safety profile in currently recommended doses and appears to be
effective in the treatment of cardiac arrest resulting
from lipophilic toxins. Clinicians report successful, early
administration of lipid emulsion to preempt cardiac
arrest. Continued diligent observation and reporting by
clinicians as well as appropriate laboratory investigation
will lead to better information and understanding of the
precise role of lipid emulsion in resuscitation.
Acknowledgements
Dr Weinberg has Veterans’ Affairs Merit Funding. Dr Weinberg was
awarded U.S. patent 7 261 903 B1 ‘Lipid emulsion in the treatment of
systemic poisoning’. He does not have equity interest or agreements
with any company or commercial entity related to this method. He has
never received salary or support from any company. He does not
intend to prohibit or restrict the practice of this method on any patient
requiring this treatment. Dr Weinberg also created and maintains
www.lipidrescue.org, an educational, noncommercial website providing information and a forum for discussing the use of lipid emulsion in
treating cardiac toxicity. He derives no salary or support related to
this website.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (p. 696).
1
Albright G. Cardiac arrest following regional anesthesia with etidocaine or
bupivacaine. Anesthesiology 1979; 51:285–287.
2
Weinberg G, VadeBoncouer T, Ramaraju G, et al. Pretreatment or resuscitation with a lipid infusion shifts the dose-response to bupivacaine-induced
asystole in rats. Anesthesiology 1998; 88:1071–1075.
3
Weinberg G, Ripper R, Feinstein D, Hoffman W. Lipid emulsion infusion
rescues dogs from bupivacaine-induced cardiac toxicity. Reg Anesth Pain
Med 2003; 28:198–202.
4
Rosenblatt MA, Abel M, Fischer GW, et al. Successful use of a 20% lipid
emulsion to resuscitate a patient after a presumed bupivacaine-related
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5
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ropivacaine-induced asystole after axillary plexus block using lipid infusion.
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6
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cardiovascular collapse treated with Intralipid. Anaesthesia 2007; 62:516–
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7
McCutchen T, Gerancher JC. Early Intralipid therapy may have prevented
bupivacaine-associated cardiac arrest. Reg Anesth Pain Med 2008; 33:178–
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This study describes use of lipid emulsion to successfully treat CNS signs and
ventricular tachycardia with a pulse in a patient after nerve block.
19 Perez E, Bania TC, Medlej K, Chu J. Determining the optimal dose of
intravenous fat emulsion for the treatment of severe verapamil toxicity in a
rodent model. Acad Emerg Med 2008; 15:1284–1289.
In this animal study of treatment of verapamil toxicity, the optimal dose of lipid was
approximately 18 ml/kg.
Ludot H, Tharin JY, Belouadah M, et al. Successful resuscitation after
ropivacaine and lidocaine-induced ventricular arrhythmia following posterior
lumbar plexus block in a child. Anesth Analg 2008; 106:1572–1574.
This study describes the successful use of Medialipid to treat a 13-year-old girl
who developed ventricular tachycardia after lumbar plexus block with ropivacaine.
20 Spence A. Lipid reversal of central nervous system symptoms of bupivacaine
toxicity (letter). Anesthesiology 2007; 107:516–517.
8
Litz RJ, Roessel T, Heller AR, Stehr S. Reversal of central nervous system and
cardiac toxicity after local anesthetic intoxication by lipid emulsion injection.
Anesth Analg 2008; 106:1575–1577.
This study describes the successful use of lipid emulsion to reverse CNS signs and
treat ventricular ectopy in a patient who received brachial plexus block.
9
10 Warren J, Thoma RB, Georgescu A, Saurin S. Intravenous lipid infusion in the
successful resuscitation of local anesthetic-induced cardiovascular collapse
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1580.
This study describes the successful use of Liposyn III to treat cardiac arrest after
brachial plexus block.
11 Tebbutt S, Harvey M, Nicholson T, Cave G. Intralipid prolongs survival in a rat
model of verapamil toxicity. Acad Emerg Med 2006; 13:134–139.
12 Bania TC. Hemodynamic effects of intravenous fat emulsion in an animal
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normal saline. Acad Emerg Med 2007; 14:105–111.
13 Harvey M, Cave G. Intralipid outperforms sodium bicarbonate in a rabbit
model of clomipramine toxicity. Ann Emerg Med 2007; 49:178–185.
14 Harvey MG, Cave GR. Intralipid infusion ameliorates propranolol-induced
hypotension in rabbits. J Med Toxicol 2008; 4:71–76.
15 Sirianni AJ, Osterhoudt KC, Callelo DP, et al. Use of lipid emulsion in the
resuscitation of a patient with prolonged cardiovascular collapse after
overdose of bupropion and lamotrigine. Ann Emerg Med 2008; 51:412–
415.
This study describes the first clinical use of lipid emulsion to treat a patient with
toxicity due to lipophilic medications other than local anesthetics.
16 Finn SDH, Uncles DR, Willers J, Sable N. Early treatment of quetiapine and
sertraline overdose with Intralipid. Anaesthesia 2009; 64:191–194.
This study describes the use of lipid emulsion to reverse coma in a patient with
drug overdose.
21 Marwick PC, Levin AI, Coetzee AR. Recurrence of bupivacaine toxicity after
lipid rescue from bupivacaine-induced cardiac arrest. Anesth Analg 2009;
108:1344–1346.
This study describes a patient who developed recurrence of ventricular ectopy
40 min after successful resuscitation from cardiac arrest with lipid. Amylase was
elevated postoperatively, but no signs of pancreatitis were noted.
22 Weinberg G, DiGregorio G, Ripper R, et al. Resuscitation with lipid versus
epinephrine in a rat model of bupivacaine overdose. Anesthesiology 2008;
108:907–913.
This study of bupivacaine-induced cardiac arrest in a rat model found that lipid was
superior to epinephrine with respect to resuscitation rates and metabolic parameters.
23 Di Gregorio G, Schwartz D, Ripper R, et al. Lipid emulsion is superior to
vasopressin in a rodent model of resuscitation from toxin-induced cardiac
arrest. Crit Care Med 2009; 37:993–999.
This study in a rat model found that lipid was superior to vasopressin and
vasopressin/epinephrine for resuscitation of bupivacaine-induced cardiac arrest.
24 Hiller D, Di Gregorio G, Ripper R, et al. Epinephrine impairs lipid resuscitation
from bupivacaine overdose: a threshold effect. Anesthesiology (in press).
In this study of bupivacaine-induced cardiac arrest in a rat model, epinephrine more
than 10 mg/kg hindered resuscitation.
25 Mayr VD, Mitterschiftthaler L, Neurater A, et al. Comparison of the combination
of epinephrine and vasopressin with lipid emulsion in a porcine model of
asphyxial cardiac arrest after intravenous injection of bupivacaine. Anesth
Analg 2008; 106:1566–1571.
In this study of bupivacaine toxicity in a porcine asphyxial model, vasopressin/
epinephrine resulted in a better short-term survival than lipid emulsion.
26 Harvey M, Cave G, Kazemi A. Intralipid infusion diminishes return of sponta neous circulation after hypoxic cardiac arrest in rabbits. Anesth Analg 2009;
108:1163–1168.
In this study, in a rabbit asphyxial model of cardiac arrest without lipophilic toxins,
ACLS alone resulted in better return of spontaneous circulation than ACLS/lipid
emulsion.
17 Young AC, Velez LI, Kleinschmidt KC. Intravenous fat emulsion therapy
for intentional sustained-release verapamil overdose. Resuscitation 2009;
80:591–593.
This study describes the use of lipid emulsion to treat hypotension due to overdose
of sustained-release verapamil.
27 Gueugniaud PY, David JS, Chanzy E, et al. Vasopressin and epinephrine vs.
epinephrine alone in cardiopulmonary resuscitation. N Engl J Med 2008;
359:21–30.
In this large study of epinephrine/vasopressin versus epinephrine alone for out-ofhospital cardiac arrest, there were no significant differences between groups in
survival to hospital admission (approximately 21%) or survival to hospital discharge
(approximately 2%).
18 Weinberg G, Di Gregorio G, Hiller G, et al. Lipid emulsion reversal of
haloperidol-induced cardiac arrest. Ann Intern Med 2009; 150:737–738.
This study describes the successful use of lipid emulsion to treat pulseless
multiform ventricular tachycardia resulting from administration of haldol.
28 Mazoit JX, Le Guen R, Beloeil H, Benhamou D. Binding of long-lasting local
anesthetics to lipid emulsions. Anesthesiology 2008; 106:1333–1336.
This in-vitro study demonstrated high solubility of local anesthetics in lipid emulsion
and high binding capacity of lipid emulsions.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.