A Case - DergiPark

The New Journal of Medicine 2013;30:199-201
Case report
Pulmonary Edema Triggered By Prilocaine
Induced Methemoglobinemia After Local
Anesthesia: A Case
(Lokal anestezi sonrasÕ prilokainin indükledi÷i methemoglobinemi tarafÕndan tetiklenen pulmoner ödem:
Bir olgu)
øbrahim DUVAN 1, Murat KURTOöLU 1, Burak Emre ONUK 1, Sanser ATEù 1, Beyhan BAKKALOöLU 2,
Y. Halidun KARAGÖZ 1
1
2
Güven Hospital Department of Cardiac Surgery, ANKARA
Güven Hospital Department of Cardiac Anaesthesiology, ANKARA
ÖZET
Methemoglobinemi, hemoglobin sentez ve metabolizmasÕndaki konjenital de÷iúikliklere veya bazÕ kimyasal
ajanlar tarafÕndan indüklenen oksidasyon ve redüksiyon
tepkimelerinde
akut
dengesizliklere
ba÷lÕ
oluúan
methemoglobin kan düzeylerindeki artÕúÕn neden oldu÷u
klinik bir sendromdur.
Prilokain tüm di÷er lokal anestezik ajanlarla karúÕlaútÕrÕldÕ÷Õnda, en düúük sistemik toksisiteye sahip oldu÷u
halde, MetHb oluúumunda artÕúa neden olabilir. Sa÷lÕklÕ
bireylerde daha yüksek MetHb düzeyleri sÕklÕkla kolayca
tolere edilebilirken, kardiopulmoner kapasiteleri kÕsÕtlÕ ve
anemik hastalarda oksijen sunumu azalabilir.
Bu yazÕ 80 yaúÕnda, sÕnÕrda ejeksiyon fraksiyonu olan bir
hasta ve prilokain adlÕ lokal anestezik ajanÕn indükledi÷i
methemoglobineminin bu hastadaki etkileri hakkÕnda bir
vaka sunumudur.
Anahtar Kelimeler: Prilokain; methemoglobinemi; atriyal
fibrilasyon; pulmoner ödem
ABSTRACT
Methemoglobinemia (MetHba) is a clinical syndrome
caused by an increase in the blood levels of
methemoglobin (MetHb)1 secondary to both congenital
changes in hemoglobin (Hb) synthesis or metabolism or
acquired reasons such as acute imbalances in reduction
and oxidation reactions induced by several chemical
agents.
Prilocaine, in comparison with all other local anesthetics,
has the lowest direct systemic toxicity, but may lead to
an increased formation of MetHb2. Whereas in healthy
individuals, higher concentrations of MetHb are usually
well tolerated, it may endanger oxygen supply in
patients with diminished cardiopulmonary reserves or
anemia3.
This paper is a case report of an 80 year old man with a
borderline ejection fraction and the effects of MetHba
induced by a local anesthesic agent prilocaine on him.
Key Words: Prilocaine; methemoglobinemia;
fibrillation; pulmonary edema
atrial
CASE REPORT
An 80 year old male patient with a stent
implantation history about 6 months ago had still
dyspneic symptoms and rhythm problems and
applied to our clinic for coronary artery bypass
graft (CABG) operation after a coronary angiography. Hypertension, diabetes mellitus, carotid
stenosis and family history were the major risk
factors of diffuse atherosclerosis for him. At the
time of acceptance the patient had a normal sinus
rhythm proven by the preoperative electrocardiogram whereas he had the signs of inferior
myocardial infarction resulted with akinesia in
posterior basal and inferior segments. During one
of his dyspneic periods he was proven to have an
attack of atrial fibrillation.
Correspondence:
Ibrahim Duvan, M.D.
Guven Hospital Department of Cardiac Surgery, Ankara
e-mail: [email protected]
Arrival date
: 02.01.2013
Acceptance date
: 11.02.2013
The patient was given a successful operation of
beating heart CABGx4 and was discharged on the
5th day. He never had another attack of atrial
fibrillation postoperatively.
Twenty one days after the discharge, infectious
sternal incision was detected on the lower half and
following a thorough examination, deep sternal
wound infection was ruled. Coagulase (-),
Methicillin-sensitive Staphylococcus aureus was
detected and treated by 3x500 mg Stafine (Koçak
Farma ølaç) tablet. The patient was reoperated for
this purpose and postoperatively he received a
treatment via vacuum-assisted closure (VAC)
therapy for about 2 months as an outpatient until
there was no sign or symptom of infection.
The patient who had a very low threshold of
pain was given a minor flap surgery by our Plastic
and Reconstructive Department for the sternal
incision and during this intervention 60 ml (1200
mg) dose of prilocaine (Citanest®) was administered locally. 30 minutes later, heavy dyspneic
199
ø. Duvan et al.
symptoms occurred, irregular heart beats, cyanosis,
excessive sweating and anxiety were seen, then
the patient was accepted to the intensive care unit
(ICU) and atrial fibrillation came out once again.
Pulmonary edema signs were seen also in the
patient’s chest X-Ray, too (Figure 1). Blood gas
analysis (Radiometer ABL 725) proved that the
patient had hypoxia (SO2 70.5%) with acidosis
and MetHb level was 30%. He was intubated and
recovered after the appropriate treatment of atrial
fibrillation, pulmonary edema depending on
congestive heart failure and oxygenation. Clinical
cyanotic signs disappeared in 2 hours via these
supporting treatment strategies, additionally
MetHb level turned back to 2% without a
treatment by methylene blue, thionine or ascorbic
acid after 8 hours (Figure 2).
Figure 1. Chest X-Ray of the patient during the dyspneic attack just after the prilocaine injection. (Signs of
pulmonary edema; Kerley B lines and increased vascular
shadowing in the perihiler regions are clearly seen)
Figure 2. Chest X-Ray of the patient after intubation and
appropriate treatment. (Regressions of the pulmonary
edema signs are apparently seen)
DISCUSSION
The molecule of hemoglobin (Hb) is a tetramer
composed of alpha, beta, gamma, or delta chains.
Each Hb chain is formed by a globin polypeptide
linked to a heme group, which is formed by a
200
complex of a protoporfirin IX ring and one atom of
ferrous iron (Fe+2). So, each Hb molecule has four
atoms of iron. Each Fe+2 can reversibly bind one
O2 molecule, for a total of four molecules of O2
transported by each Hb molecule4.
Methemoglobinemia (MetHba) is a clinical
syndrome caused by an increase in the blood
levels of MetHb secondary to both congenital
changes or acute imbalances in reduction and
oxidation reactions induced by the exposure to
several
chemical
agents1.
Hemoglobin
is
constantly being oxidized and MetHb occurs; then
it is converted back to hemoglobin by cytochromeb5 reductase which is an enzyme responsible for
the endogenous reduction of MetHb. MetHb levels
are maintained less than the level of 2% by the
help of this enzyme system4. An abnormally high
level of MetHb will occur when the production
exceeds the capacity of the MetHb reduction
processes. This may occur after exposure to
various toxic substances and drugs. The most
commonly used drugs that cause MetHba are
benzocaine, lidocaine, prilocaine, dapsone, amyl
nitrate, isobutyl nitrate, nitroglycerin, nitroprusside,
primaquine, sulfonamides and phenazopyridine5.
Four types of local anesthetics have been
reported as possibly causing methemoglobinemia:
prilocaine, benzocaine, lidocaine, and tetracaine.
Prilocaine, in comparison with all other local
anesthetics, has the lowest direct systemic
toxicity, but may lead to an increased formation of
MetHb2.
MetHb represents a dyshemoglobin, a type of
hemoglobin that can not bind O2. Besides the
inability to bind O2, MetHb shifts the dissociation
curve of partially oxidized Hb to the left, hindering
the release of O2 in the tissues. Tissue hypoxia
caused by MetHba is secondary to a reduction in
free Hb to transport O2 and the difficulty to
release O2 in the tissues6.
Whereas
in
healthy
individuals
higher
concentrations of MetHb are usually well tolerated,
it may endanger oxygen supply in patients with
diminished cardiopulmonary reserves or anemia3.
Clinical signs and the symptoms generally
demonstrate the decrease in the transport of O2,
leading tissue hypoxia. MetHb level of 15% means
grayish skin but nothing more, 15-30% will be a
reason of a chocolate-brown blood accompanying
with cyanosis. Heavy neurologic and cardiovascular symptoms are commonly present with the
increasing levels of MetHb. Levels of MetHb above
70% are usually fatal.
Our patient was an 80 year old man who had a
decreased capacity of cardiac contractility and just
recovered from a seriously deep sternal wound
ø. Duvan et al.
infection prone to be affected from a prilocaine
injection triggering MetHba.
He got well after intubation and supportive
treatment of the symptoms without any
methylene blue, thionine or ascorbic acid whereas
it is recommended to receive methylene blue for
whom had a level of MetHb > 20%7. Treatment of
patients with MetHba should be guided, primarily,
by the severity of the disorder. Blood levels of
MetHb represent a secondary parameter in the
definition of the treatment. In the patient
described, the cyanosis and MetHb level improved
rapidly after intubation. We chose not to
administer an antidote because Guay J pointed out
a different view that 53 cases of 242 MetHba
related to local anesthetics were not given any
antidotes and the time to disappearance of clinical
cyanosis varied from 0.25 to 9 h in those who
received methylene blue, thionine or ascorbic acid
and from 2 to 19.8 h in those who received no
treatment8. We also aimed to protect our patient
from the side effects of methylene blue because of
his intolerable physical condition7.
As a conclusion high dose of a local anesthetic
agent prilocaine, caused MetHba in this patient
similar to the examples in the literature. In our
patient prilocaine triggered atrial fibrillation due to
the affects of MetHba and hypoxia. Since the
patient had a borderline ejection fraction,
pulmonary edema was developed and became the
major reason of the clinical signs and symptoms
but
acute
respiratory
distress
syndrome,
pneumonia, pulmonary embolism etc. may also be
considered as the other alternative diagnostic
subjects in this case.
Finally, one should keep in mind that local
anesthetic agents administered to CABG patients
having a borderline ejection fraction and history of
atrial fibrillation attacks are prone to redevelope
atrial fibrillation and pulmonary edema as a result
of the left ventricular failure due to the affects of
MetHba and hypoxia inspite of a successful
surgical intervention.
Confinct of interest statement none declared.
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