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European Review for Medical and Pharmacological Sciences
2011; 15: 211-213
Effect of anesthesia in a patient with
pre-existing anisocoria
P. ACETO, V. PERILLI, F. VITALE, L. SOLLAZZI
Department of Anaesthesiology and Intensive Care, Catholic University of the Sacred Heart,
Rome (Italy)
Abstract. – In this case report, we describe an accentuation of a pre-existing anisocoria shortly after tracheal intubation in a patient
undergoing thyroidectomy.
A 45-yr-old female patient with unequal pupillary diameter (right 2 mm > than left) and decreased light reflex in the right eye – due to a previous eye trauma – was scheduled for thyroidectomy because of multinodular goiter. Anesthesia
was induced with propofol 2,5 mg/kg, fentanyl 3
mcg/kg and cisatracurium 0.15 mcg/kg. Immediately after tracheal intubation, examination of the
right eye revealed a markedly dilated pupil (8 mm)
which was nonreactive to direct and consensual
light reflex. The left pupil was 2 mm, and normally
reactive to light. An increase in heart rate was also registered (> 20% of baseline) with spontaneous return to baseline within 2 minutes. The
right pupil returned to preoperative size within
approximately one hour after awakening.
From this case report, it emerges that a preexisting anisocoria may be exacerbated during
anesthesia probably due to incomplete abolition
of response to painful stimulus, such as tracheal
intubation, provided by anesthetic drugs in the
affected eye. The main contributing factor for accentuation of anisocoria could be sympathetic
dominance in the pupil with pre-existing mechanical interruption in compensatory parasympathetic mechanisms.
Key Words:
Finding of anisocoria during anaesthesia is a
disturbing and unusual sign and may indicate serious neurological conditions. Previous reports
have documented unilateral mydriasis occurring
as a result of accidental direct or indirect exposure of papillary muscles to mydriatic (alphaadrenergic or anticholinergic) agents before or
during surgery3-7. Sometimes, ciliary ganglion
may be unintentionally anaesthetized by the
spread of local anaesthetics8,9. Other possible
causes may be mechanical ones, such as eye
trauma during intubation or dislocation of an unstable cervical spine resulting in Horner’s syndrome, or asymmetric impaired venous return
from head and neck resulting in anisocoria with
concurrent exophthalmos2. In case of hypertension after intubation, an acute intracranial hemorrhagic event (e.g. undiagnosed intracranial
aneurysm) should be suspected3.
Evidence supporting effects of anaesthetic
drugs has been discussed10, but cases of exacerbated pre-existing unilateral mydriasis in patients
undergoing general anaesthesia have never been
described.
In the present case report, we describe an accentuation of a pre-existing anisocoria shortly after tracheal intubation in a patient undergoing
thyroidectomy.
Anaesthesia, Anisocoria, Sympathetic system.
Introduction
Pupillary function is controlled by a balance of
sympathetic (dilator) and parasympathetic (constrictor) neural pathways. Pharmacologic or mechanical disruption of these pathways may result
in anisocoria1,2. A variety of potential causes for
anisocoria exists, ranging from normal to life
threatening variation1.
Case Report
An ASA I, 65 kg, 168 cm, 45-yr-old female
patient was scheduled for thyroidectomy because
of multinodular goiter.
When she was 20 years old, she had an eye
trauma resulting in the damage of iris sphincter
muscle. Preoperative neurologic examination revealed unequal pupillary diameter (right 2 mm >
than left) and decreased light reflex in the affected eye with normal visual function. The vital
signs and results of laboratory tests were normal.
Corresponding Author: Paola Aceto, MD; e-mail: [email protected]
211
P. Aceto, V. Perilli, F. Vitale, L. Sollazzi
Patient did not receive anaesthetic premedication. At the patient’s arrival in the operating
room, electrocardiogram, peripheral oxygen saturation, non invasive blood pressure, expired
carbon dioxide and bispectral index were monitored. Anaesthesia was induced with propofol
2,5 mg/kg and fentanyl 3 mcg/kg. Cisatracurium 0.15 mcg/kg was administered to facilitate
tracheal intubation.
Immediately after tracheal intubation, examination of the right eye revealed a markedly dilated pupil (8 mm) which was non-reactive to
direct and consensual light reflex. The left pupil
was 2 mm, and normally reactive to light. Neither eye was oedematous or showed signs of
pressure or traumatic injury. We also registered
an increase in heart rate (>20% of baseline)
with spontaneous return to baseline within 2
minutes. Systemic blood pressure was preserved. We felt that surgery could proceed because of her history of anisocoria.
Desflurane in an air-oxygen mixture was
used for maintenance of anaesthesia. No supplementary doses of fentanyl or cisatracurium were
required. Ventilation was adjusted to maintain
normocapnia (end-Tidal partial pressure of carbon dioxide range, 35-40 mmHg).
At the end of the procedure, which lasted 50
minutes, neuromuscular blockade was reversed
with neostigmine (2.5 mg) and atropine (1 mg).
After establishing recover of a spontaneous diaphragmatic breathing with adequate Tidal volume, the tracheal tube was removed. The right
pupil returned to preoperative size within approximately one hour after awakening. The 24hr postoperative course was uneventful.
Discussion
In the present case, we find an exacerbation
of preexisting anisocoria in a patient undergoing general anaesthesia. In the first instance, we
theorized that this phenomenon was due to the
parasympathetic dominance caused by sympathicolysis as a result of concomitant use of
propofol and fentanyl. However, the parasympathetic-dominant status would induce a rapid
constriction in the normal eye, but much slower
constriction in the tonic pupil, resulting in
marked differences in the two pupillary diameters. In our patient, we did not find a constric212
tion in the normal eye but only an evident accentuation of anisocoria in the affected eye
which appeared immediately after intubation
and was associated with a brief increase in heart
rate. This reaction is suggestive of a sympathetic dominance due to a disruption of the sympathetic-parasympathetic balance and may reflect
an abnormal response to a painful stimulus,
such as tracheal intubation, leading to suppose
that administered anaesthetic drugs provided
unaccomplished sympathicolysis.
Sympathetic block induced by thoracic
epidural in presence of anaesthetics such as
propofol and sevoflurane was previously pointed out to determine anisocoria in a patient without preoperative papillary abnormalities10. The
Authors concluded that the parasympatheticdominant status was the main contributing factor for the Adie pupil to appear. In fact, anisocoria associated with an Adie pupil is believed
to originate from a peripheral mechanism involving parasympathetic postganglionic fibers,
arising by a damaged ciliary ganglion that innervate the iris sphincter muscle, responsible
for pupillary constriction. The accentuation of
anisocoria in our patient probably resulted from
just the opposite process. As a possible proof of
sympathetic status dominance, the iris dilator
muscle – responsible for pupillary dilation and
receiving sympathetic input from the superior
cervical sympathetic ganglion via the long ciliary nerve of the trigeminal nerve’s ophthalmic
branch – was not or was weakly affected by
anaesthetic drugs. The role of painful stimulus,
such as tracheal intubation, remains undetermined.
It must be taken into account that, when
anisocoria occurs in patients under general
anaesthesia, the cause can be difficult to diagnose as convergence response and neurological
symptoms cannot be confirmed without a wakeup test3. The pilocarpine test, which is effective
even in a vegetative state, also appears to be
useful to rapidly differentiate neurogenic from
phenylephrine-induced mydriasis11. In the patient of this case report, neither phenylephrine
or wake-up test were performed because of her
known medical history of unilateral dilated
pupil due to a lesion of iris sphincter muscle
caused by a previous direct eye trauma. In the
absence of the patient’s history of anisocoria,
we believe that intraoperative wake-up test or
the more rapid pilocarpine test would have been
indicated.
Effect of anesthesia in a patient with pre-existing anisocoria
From literature, it emerges that unilateral mydriasis under anaesthesia may reflect alterations
in either sympathetic or parasympathetic autonomic tone, triggered by either a disturbance in
cranial nerve function or a pharmacological alteration in autonomic nerve transmission.
Anisocoria during anaesthesia has previously
resulted from accidental direct or indirect eye
exposure to phenylephrine4,5, submucosal infiltration with epinephrine6 or lidocaine plus epinephrine 8 or as a result of cocaine spread
(nasociliary ganglion block)9. Anisocoria has also been described after airway topical anaesthesia with lidocaine and phenylephrine provided
by an oxygen driven face mask nebulizer 3 .
Anisocoria may be also caused by impaired ocular blood flow. In a child showing anisocoria
during renal transplantation probably due to a
retinal hypoperfusion, mydriasis slowly developed on both eyes, but was more pronounced
for the left pupil and was associated with concurrent bilateral congiuntival chemosis. Evidence of impaired ocular blood flow was obtained by cranial ultrasound. The pupil size returned to normal with administration of norepinephrine12.
Therefore, the assessment of perioperative
unilateral mydriasis should always include consideration of accidental exposure of mydriatic
agents before or during surgery. As neurologic
assessment by physical examination is often
difficult under general anaesthesia, in absence
of any history of anisocoria or certain causes of
anisocoria, the diagnosis of any intracranial
pathology to rapidly exclude life-threatening
neurologic events requires a cranial computed
tomography scan.
In conclusion, from this case report, it emerges
that a pre-existing anisocoria may be exacerbated
probably because of the uncompleted abolition of
response to painful stimulus, such as tracheal intubation, provided by anaesthetic drugs in the affected eye. The main contributing factor could be
sympathetic dominance in a pupil with pre-existing mechanical interruption in compensatory
parasympathetic mechanisms.
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Acknowledgements
We would like to acknowledge Jacqueline Melvin for
her careful revision of the manuscript language.
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