Local anesthetic system toxicity following brachial plexus anesthesia is severe complication of regional block. We reported a case of central nervous system toxicity following brachial plexus anesthesia, who was rescued successfully with intravenous lipid emulsion.
Trang 1CASE REPORT: INTRAVENOUS LIPID EMULSION FOR
TREATMENT OF LOCAL ANESTHETIC TOXICITY FOLLOWING
BRACHIAL PLEXUS ANESTHESIA
Vo Van Hien*; Nguyen Trung Kien*
SUMMARY
Local anesthetic system toxicity following brachial plexus anesthesia is severe complication
of regional block We reported a case of central nervous system toxicity following brachial
plexus anesthesia, who was rescued successfully with intravenous lipid emulsion
* Key words: Local anesthetic system toxicity; Lipid emulsion
INTRODUCTION
Local anesthetic system toxicity (LAST)
is a recognized complication of major
conduction anesthesia The estimate of
clinically important local anesthetic toxicity
is from 7.5 to 20 occurrences per 10,000
peripheral nerve blocks [6] The incidence
of toxicity is greater with brachial plexus
techniques than most others, because larger
than usual doses of local anesthetics are
used and the injections are made in and
around large vascular channels in the head,
neck and axillary regions LAST includes
two major types: central nervous system
toxicity and cardiovascular system toxicity
that can be treated with lipid emulsion [1]
CASE REPORT
A 73 years old man, 164 cm tall, 50 kg
of weight, was admitted with right hand
injury due to labour accident which required
an emergency for wound resection and
reformed index and middle finger amputation
under supraclavicular approach anesthesia
on Monday 27 of June, 2016
- Biochemical test: glucose 7.5 mmol/L, ure 7.1 mmol/L, creatinine 76 µmol/L, GOT
122 U/L, GPT 117 U/L, K+ 3.8 mmol/L,
Na+ 136 mmol/L; ECG was normal at rate
of 67/min,sinus rythm
- Blood test: red blood cell 3.48 Tera/L, hemoglobin 101 g/L, hematocrit 0.32 l/L, platelet 100 G/L
- Continuously monitored of ECG, heart rate, oxygen saturation (SpO2) Blood pressure was monitored in 2.5 mins interval;
oxygen was given via facemask at a rate
of 3 L/min Blood pressure was 132/73 mmHg; respiratory rate 18 per minute
- In the operating room: an IV 18G was placed After given IV 100 µg of fentanyl and 20 mg of propofol, ultrasound guided supraclavicular approach anesthetizes was done with 300 mg of lidocaine in 25 mL (6 mg/kg) and 50 mg of ropivacaine (1 mg/kg) The patient was awake during the block No blood or paresthesias was seen during procedure The patient felt numbness in his arm 3 minutes after brachial block, motor block was assessed
by Bromage score at level 2
* 103 Hospital
Corresponding author: Nguyen Trung Kien (drkien103@gmail.com)
Trang 2- Approximately 10 minutes after the
needle removement, patient became confused
and unconscious, stopped breathing, SpO2
decreased from 100% to 50%
- Supported ventilation through facemask
with 100% oxygen for 5 minutes and SpO2
recovered in normal range 98 - 100%,
hemodynamic was stable pattern during
that time Spontaneous respiratory rate
recovered at rate of 18 per minute but
consciousness was still not recovered and
the patient did not response to verbal
commands as well as deep pain
stimulation any more Pupils were in
normal size and responded well with light
- Monitoring closely and surgeons
started procedure
unconciousness, lipid emulsion (10%)
therapy was started with bolus dose of
3 mL/kg (150 mL) intravenously over
1 minute
- The patient opened his eyes and
responded well to verbal commands and
got full recovery immediately from finishing
bolus dose
- We did not use continuous infusion
and operation finished at 64 minutes after
brachial plexus anesthesia The patient
was transfered to postoperative care unit
with normal parameter of hemodynamic
and respiratory He was discharged after
7 days of treatments
DISCUSSION
Some reasons of unconsciousness and
stopped breathing in this patient might be
caused by injecting 100 µg of fentanyl
and 20 mg of propofol before brachial
plexus anesthesia However, stopped
breathing and unconsciousness due to fentanyl and propofol effects could be excluded because the patient was still awake during and after taking ultrasound guided supraclavicular approach block Small dose of propofol just brought a sedation meaning and could not bring general anesthesia effect in this situation
He also felt numbness in his arm 3 minutes and motor block at level 2 according to Bromage score after brachial plexus block Thus, unconsciousness and stopped breathing could not have been blaimed for fentanyl or propofol effects
Local anesthetic toxicity happened in this patient may be due to high dose
of lidocaine (6 mg/kg) combined with ropivacaine (1 mg/kg) without combination with epinephrine Some authors indicated that toxicity occured most frequently following accidental intravascular injections and rarely following absorption of injected solutions from peripheral sites [2, 3] However, absorption was thought as a crucial reason in this patient because ultrasound guided for brachial block with inplane technique was performed Thus, doctor could see the needle as well as the tip of the needle clearly before injecting local anesthetics Further more, negative aspiration test was confirmed before injection local anesthetics
Local anesthetics are widely and commonly used for regional anesthesia Although it is rare for patients to manifest serious adverse effects or experience complications secondary to local anesthetic administration, adverse events can occur, even it is taken under ultrasound guided, let alone take blind techniques These range from the mild symptoms that may
Trang 3follow systemic absorption of local
anesthetics from a correctly sited and
appropriately dosed regional anesthetic
procedure to major central nervous
system (CNS) and/or cardiac toxicity
(most often from unintentional intravascular
injection) that can result in disability or
death [2]
A variety of factors influence the
likelihood and severity of local anesthetic
systemic toxicity (LAST), including individual
patient risk factors, concurrent medications,
location and technique of block, specific
local anesthetic compound, total local
anesthetic dose (concentration, volume),
timeliness of detection, and adequacy of
treatment Although the patient had a
higher GOT and GPT than normal level,
that was not reason for this complication
Slight anemia may have been a contributive
factor for making higher free level
concentration of local anesthetics in
plasma That is the reason this patient
was diagnosed central nervous system
toxicity in a typical type and lipid emulsion
was transfused after that
Local anesthetic dose is very important
factor to evoke the LAST According to
Felice [5], maximal dose of lidocaine is
6 - 8 mg/kg But, in this patient, brachial
plexus block was done with medium dose
(6 mg/kg of lidocaine and 1 mg/kg
ropivacaine) without combination with
epinephrine Moreover, elderly patient
with low level of protein (55 g/L) could
make a higher free concentration of local
anesthetics (LA) in plasma In fact that
one confounder in the interpretation of
serum concentrations of LA is protein
binding, which generally decreases with
increasing drug concentrations In the clinical setting of probable LA toxicity, an elevated total drug concentration may be reflective of a high free drug concentration
It is noted that, the serum concentration
of LA may correlate with clinical signs and symptoms of toxicity Lidocaine administration in regional blocks usually results in a serum concentration of
3 - 5 µg/mL and therapeutic plasma concentrations of lidocaine are 1 to
5 µg/mL when used for ventricular arrhythmias Symptoms of toxicity may occur at concentrations 6 µg/mL, convulsions may occur at concentrations 10 µg/mL, and cardiovascular collapse with levels
30 µg/mL [7] Our patient did not have symptoms of cardiac toxicity
The commercial products of intravenous lipid emulsion (IVLE) are available in various concentrations The 20% formulation of IVLE contains 20% soybean oil, 1.2% egg yolk phospholipids, 2.25% glycerin, and the remainder is water The osmolality of IVLE is approximately 350 mOsm/kg water and 260 mOsm/kg lipid emulsion In this case, it was not available of IVLE 20%
and IVLE 10% was injected with double volume in compare with guidline [7]
There are multiple theories about the mechanism of action of IVLE in LA toxicity
One theory is that IVLE serves as a “lipid sink,” providing a large lipid phase in the serum that is able to extract LAs from the plasma This may be true at the tissue level, as well Another theory is that IVLE has metabolic effects by inhibiting mitochondrial metabolism of lipids, reducing tissue acidosis and decreasing carbon dioxide production during times of myocardial
Trang 4ischemia Also, as LAs may impair fatty
acid delivery to the mitochondria, IVLE
may work to saturate this impaired fatty
acid delivery to enable further energy
production Additionally, fatty acids, as
found in IVLE, have been shown to activate
calcium and potassium channels, which
have been associated with LA-induced
cardiotoxicity [4]
Treatment of central nervous system
(CNS) complications and toxicity remains
controversial Seizures have been treated
successfully with benzodiazepines or
barbiturates (eg, phenobarbital) However,
Weinberg [7] recommended that lipid
infusion should be considered early, and
the treating physician should be familiar
with this method He also recommends
avoiding vasopressin and using epinephrine
only in small dose Obviously, vigilance,
preparedness, and quick action will improve
outcomes of this dreaded complication In
this case, we used lipid emulsion (10%)
therapy and the bolus dose was started
with of 3 mL/kg (150 mL) intravenously
and obtained good outcomes
According to Weinberg [7], if LAST
happended, we should use intralipid
emulsion and follow protocol for recovering
includes: bolus 1.5 mL/kg (lean body mass)
intravenously over 1 minute (~100 mL)
Then, continuous infusion 0.25 mL/kg/min
(~18 mL/min; adjust by roller clamp);
repeat bolus once or twice for persistent
cardiovascular collapse Double the infusion
rate to 0.5 mL/kg/min if blood pressure
remains low; continue infusion for at least
10 minutes after attaining circulatory
stability and recommended upper limit:
approximately 10 mL/kg lipid emulsion over the first 30 minutes Thus, plan for management of this complication should
be established, and a Local Anesthetic Toxicity Kit and posting instructions should be ready to use
CONCLUSIONS
Intravenous lipid emulsion infusion provided a good effective treatment for central nervous system toxicity due to complication of regional anesthesia
REFERENCES
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3 Dillane D, Finucane BT Local anesthetic
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brachial plexus anesthesia, complications of regional anesthesia Springer Science + Business Media, LLC: USA 2007, pp.121-144
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