Keywords
awake craniotomy - scalp block - ptosis - ropivacaine
Case Report
A 14-year-old, 55-kg girl with a known case of epilepsy with complex partial seizures
was electively admitted for a right craniectomy and electrocorticography (ECoG) electrode
insertion. She was diagnosed with epilepsy secondary to a right temporal dysembryoplastic
neuroepithelial tumor (DNET). On preoperative assessment, she was asymptomatic and
had been free from seizure episodes for approximately 1 month with oral carbamazepine
300 mg OM and 400 mg ON. On examination, the patient was fully alert, conscious, and
cooperative, with normal higher mental function. There were no cranial nerve palsies
or other focal neurologic signs. The assessment of the motor, sensory, and cerebellar
systems was also unremarkable.
The patient underwent two consecutive phases of surgeries. The first surgery, for
the right temporoparietal craniectomy and the insertion of ECoG electrodes, was performed
under general anesthesia. The surgery was uneventful, and the patient was extubated
immediately after surgery. The second surgery, for reopening of the scalp, ECoG electrode
removal, lesionectomy, and cranioplasty were performed 3 days after the first operation,
under awake craniotomy with monitored anesthesia care (MAC) and a scalp block.
The scalp block was performed using ropivacaine 0.75% with 5 µg/mL adrenaline. A volume
of 2.5 to 3.0 mL of ropivacaine 0.75% was infiltrated at each nerve that innervated
the bilateral scalp—the supratrochlear, supraorbital, zygomaticotemporal, auriculotemporal,
lesser occipital, and greater occipital nerves—making up a total volume of 30 mL of
ropivacaine 0.75% for 12 sites of infiltration bilaterally. The block of left supraorbital
nerve was performed subcutaneously at left supraorbital notch with the needle pointed
perpendicularly during 2.5 to 3.0 mL injection of local anesthesia. After that, the
needle was directed medially along the orbital wall border as far as the bridge of
the nose to block left supratrochlear nerve with another 2.5 to 3.0 mL of local anesthesia
given as a subcutaneous sausage. The total local anesthetic dose given for the whole
block did not exceed the maximum allowable dose of 4 mg/kg.
A loading dose of intravenous (IV) dexmedetomidine at 1 µg/kg over 10 minutes was
administered while performing the scalp block infiltration, with subsequent maintenance
of 0.7 µg/kg/h (B. Braun Perfusor Space, Firma Braun, Melsungen, Germany), combined
with an IV infusion of remifentanil at 0.05 to 0.1 µg/kg/min (B. Braun Perfusor Space)
and a target-controlled infusion of propofol at 1.5 µg/mL (Alaris PK pump, Paedfusor
model, CareFusion, Yorba Linda, California, United States). The BIS (bispectral index
monitor) was kept around 70 to 100 throughout the operation. After head pinning and
positioning, sedation was maintained only by a low dose of dexmedetomidine (0.2 µg/kg/h)
to achieve an adequate conscious sedation effect.
Intraoperatively, the patient was comfortable, cooperative, and arousable, but complete
left eye ptosis began to be noticed during the operation. The left eye ptosis gradually
worsened and complete ptosis was observed approximately 30 minutes after the injection
of the scalp block. However, there were no associated airway obstructive symptoms,
and the vital signs were normal. There was no focal neurological deficit nor any intraoperative
episode of fit. The surgery ended after 5 hours, and the patient did not complain
of any pain during or after the operation.
Postoperatively, the full neurological assessment was repeated. There was no associated
diplopia, and the extraocular muscle movements were intact. The visual field and visual
acuity were normal as well. The pupillary size was equal and reactive in both the
eyes, and there was no other cranial nerve abnormality detected. The motor function
of muscles for facial expression was normal. The higher mental functions, as well
as the motor, sensory, and cerebellar systems, were otherwise intact following the
operation. The patient was subsequently monitored in the neurocritical care unit,
and a referral to the ophthalmology team was made. Reassurance was given to the patient,
and no steroid was prescribed.
The complete left eye ptosis gradually improved to 75% ptosis after day 1, and total
resolution of the ptosis was seen on day 2. A diagnosis of complete left eye mechanical
ptosis secondary to local anesthetic injection was made. The patient was reassured,
and she was subsequently discharged on the fourth day after the operation.
Discussion
Awake craniotomy is the favored technique of neurosurgery for certain procedures such
as tumor excision near the eloquent cortex, epilepsy surgery, and deep brain stimulation
surgery. The MAC technique with a scalp block as locoregional analgesia is one of
the anesthetic options for this surgery, aside from the asleep-awake-asleep technique.
A scalp block offers adequate analgesia during an awake craniotomy for smoothness
of intraoperative cortical mapping and neurological assessment; at the same time,
it provides hemodynamic stability and stress response reduction.[1] A scalp block using adrenaline containing local anesthetic of ropivacaine and levobupivacaine,
with the dosage up to 3.6 mg/kg and 2.5 mg/kg, respectively, has been proven to be
safe, despite the rapid increase in the plasma level.[2] The local anesthetic is infiltrated into the auriculotemporal nerve, zygomaticotemporal
nerve, supratrochlear nerve, supraorbital nerve, the great auricular nerve, and the
greater and lesser occipital nerves. Targeted infiltration of 2 to 3 mL of local anesthetic
at multiple sites with a 23- to 25-gauge needle is commonly used during the scalp
block.[3] Alternatively, a superficial cervical plexus block may reduce the amount of local
infiltration of the scalp block.[4] A combination of remifentanil and dexmedetomidine infusions is used to provide rapid-onset,
rapid-offset, and good analgesia with anxiolysis and conscious sedation. Complications
of awake craniotomies include seizures, bleeding, nausea, vomiting, obstructive apnea,
hypertension, air embolisms, hypoventilation, tachycardia, and loss of patient cooperation.
The trigeminocardiac reflex can be a result of a scalp block or manipulation of the
dura.[5]
[6] This reflex is caused by afferent fibers arising from sensory branches of the trigeminal
nerve causing stimulation of cardiac branches of the vagus nerve. The rapid infiltration
of the local anesthetic on the supratrochlear nerve may induce compression and stretching
in the nerve and provoke the reflex.[6] An incident of transient facial nerve palsy due to direct injury to auriculotemporal
nerve block has also been reported.[7] Nevertheless, the incidence of unilateral complete ptosis has been extremely low.
Mechanical ptosis can be caused by excessive local anesthetic infiltration causing
injury or edema in the muscles responsible for eyelid retraction. In contrast, facial
nerve palsy secondary to auriculotemporal nerve injury leads to depression of the
eyebrow due to dysfunction of the frontalis muscle. The levator palpebrae superioris,
Müller's muscle, and frontalis muscle are responsible for eyelid retraction. The former,
which is the predominant muscle, originates from the lesser wing of the sphenoid bone
and traverses the orbit; it may be injured due to local anesthetic infiltration. In
this case, the absence of Horner's syndrome and the presence of normal extraocular
muscle movements exclude a diagnosis of neurogenic ptosis. Aponeurotic ptosis was
also impossible because the area of surgery, clamping, and skin incision was distant
from the orbit and the eyelid.
Although the incidence of local anesthetic toxicity is extremely low, caution should
always be used during a scalp block because the scalp is highly vascular and potential
adverse cardiovascular and central nervous system side effects can occur as early
as 5 minutes after infiltration. In practice, most clinicians use 3 to 5 mL of local
anesthetic volume at each nerve.[3]
[7]
[8] However, the volume of local infiltrates in pediatric patients should be revised.
Costello and Cormack[9] suggested a maximum volume of 40 mL of ropivacaine 0.75% with adrenaline 1:200,000
dilution for a 70- to 90-kg adult. As a wide therapeutic window between clinical efficacy
and adverse reaction is seen in both levobupivacaine and ropivacaine, these drugs
were preferentially used over bupivacaine for scalp blocks.[2]
In conclusion, attention to the anatomical landmarks and correct techniques during
local anesthetic injections on the supratrochlear and supraorbital nerve, together
with a judiciously chosen volume of infiltrates, is crucial to prevent iatrogenic
ptosis.
