Keywords
bradycardia - cranial fixation - depressed skull fracture - extradural hematoma -
pediatric - pin-site complications - posterior fossa
Introduction
Mayfield skull clamp (Cincinnati, Ohio, United States) is routinely used during neurosurgeries.
A plethora of complications following this method of three-point cranial fixation
has been reported. Pin-site depressed skull fracture and extradural hematoma are infrequent
complications associated with the use of this device.[1]
[2]
[3]
[4]
[5]
[6]
[7] In most cases, intraoperative brain swelling[2]
[3]
[4] or postoperative neurological deterioration[5]
[6]
[7] alerts the neurosurgeon to investigate further for these complications.
We report a case of depressed skull fracture and extradural hematoma following posterior
fossa tumor excision in a child on whom Mayfield skull clamp was applied. Sudden bradycardia
at the end of surgery was the only clinical sign that prompted the anesthesiologist
to insist on computed tomographic (CT) scan of the head for further investigation.
Such a predictor for this pin-site complication in a child undergoing posterior fossa
craniotomy has not been reported earlier. Etiopathogenesis of sudden occurrence of
bradycardia has also been discussed.
Written informed consent was obtained from the parent of the patient prior to writing
this report.
Case Report
A 4-year-old boy, weighing 25 kg, with history of intermittent headache for 6 months
and gait imbalance for 1 month, was diagnosed with a posterior fossa mass. His contrast-enhanced
magnetic resonance imaging (MRI) scan of the brain showed a posterior fossa mass (5.2
cm × 5.1 cm × 4.9 cm) with moderate obstructive hydrocephalus with no midline shift
([Fig. 1]). A midline suboccipital craniotomy for tumor decompression was planned. Clinical
examination of the child did not reveal any abnormality. His biochemical and hematological
investigations were within normal limits.
Fig. 1 Contrast-enhanced MRI scan of brain showing posterior fossa mass (5.2 cm × 5.1 cm
× 4.9 cm) with moderate obstructive hydrocephalus with no midline shift. MRI, magnetic
resonance imaging.
Anesthesia was induced with sevoflurane 8% in a nitrous oxide and oxygen mixture (50:50).
Intravenous (IV) access was secured. Propofol 50 mg was administered. Fentanyl 40
μg was used for analgesia. Rocuronium 25 mg was administered to facilitate orotracheal
intubation with a 5.5-mm internal diameter cuffed oral endotracheal tube. Left radial
artery was cannulated. Continuous monitoring of electrocardiogram (ECG), SaO2, intra-arterial blood pressure, end-tidal CO2 (ETCO2), core temperature, and urine output was performed. Anesthesia was maintained with
sevoflurane in air and oxygen (50:50), fentanyl, rocuronium, and intermittent positive-pressure
ventilation. ETCO2 was maintained around 30 mm Hg.
The child was secured in the prone position with his head placed in a three-point
skull fixation device (Mayfield) using pediatric pins tightened to 40 lb. A single
pin on the right parietal bone and a pin each on left temporal and left occipital
bones were applied. Near-total excision of the tumor was accomplished in 7 hours.
The patient remained hemodynamically stable and normothermic throughout the surgery.
Blood loss was estimated to be approximately 600 mL. The child received 1,500 mL of
Ringer's lactate and 1,500 mL of normal saline, as well as 250 mL of packed cells.
Urine output was 1,000 mL. Intraoperative arterial blood gas (ABG) (pH 7.4/PO2 197.6/PCO2 36.2/HCO3
− 22.4/base deficit −1.2) showed no abnormalities. At the end of surgery, to remove
the Mayfield headrest, the right parietal cranial pin was first unfastened. A spurt
of blood was noted at this site. It was partially controlled with pressure, and the
remaining two pins along with the Mayfield head rest were removed. The patient was
immediately turned supine, and the pin-site bleeding was finally stopped with a suture.
The patient seemed to be awakening normally from anesthesia with no apparent neurological
deficits. Prior to reversal of residual neuromuscular blockade, the patient's heart
rate suddenly dropped from 102 to 58 beats/min, accompanied by a systolic blood pressure
of 120 to 130 mm Hg. Anticholinergic drugs were not administered as blood pressure
remained stable. Pupils were normal and reacting to light. In view of persistent bradycardia,
the anesthesiologist urged the neurosurgeon to undertake an emergency CT scan of the
head. The CT revealed an evolving large right parietal extradural hematoma with an
overlying depressed fracture of the right parietal bone ([Fig. 2]). There was approximately 15 mm midline shift to the left side. The patient immediately
underwent right temporoparietal craniotomy for evacuation of the extradural hematoma.
Anesthetic induction was done with propofol 30 mg, fentanyl 20 µg, and rocuronium
5 mg. Sevoflurane 2 to 3% in oxygen and air was used for maintenance. Intermittent
positive-pressure ventilation maintained ETCO2 in the range of 30 to 35 mm Hg. Blood loss was approximately 200 mL. Crystalloids
(1,000 mL) and packed cells (100 mL) were transfused. Urine output was approximately
500 mL during the 2-hour procedure. Levetiracetam 500 mg was administered for seizure
prophylaxis. Bradycardia persisted until craniotomy was achieved approximately 40
minutes after the initial drop in heart rate. Thereafter, heart rate stabilized at
100 to 110 beats/min. The child was electively ventilated till the first postoperative
day and extubated on second postoperative day with no neurological deficit. He was
discharged from the hospital in a stable neurological state 1 week after the surgery.
Fig. 2 (A) Postoperative emergent noncontrast computed tomographic scan of the head revealed
an evolving large right parietal extradural hematoma, with (B) underlying depressed fracture of the right parietal bone (where the pin had been
placed).
Discussion
Acute extradural hematoma following head-pin fixation is an infrequent but serious
complication following neurosurgery.[1]
[2]
[3]
[4]
[5]
[6]
[7] Early detection and timely management play a vital for ensuring complete functional
recovery of the patient.
In this case, a sudden spurt of blood from the right parietal pin site alerted us
to the possibility of vascular injury or intracranial hematoma. However, it was the
sudden and persistent bradycardia that led us to further investigation. Lo and behold,
a depressed fracture of the right parietal bone and a large evolving right parietal
extradural hematoma was revealed. This case is unique because it highlights sudden
and persistent bradycardia as the sole, on-table indicator of an evolving extradural
hematoma in a child on whom Mayfield three-point skull clamp was used. In previous
reports of pin-site extradural hematoma, either acute intraoperative brain swelling,[2]
[3]
[4] postoperative neurological deterioration, or onset of new neurological deficits[5]
[6]
[7] has led to the diagnosis.
Deciphering the etiopathogenesis of the bradycardia in this case was intriguing. Bradycardia
may have been due to (1) Cushing's reflex as a result of intracranial hypertension
caused by increasing mass effect of the extradural hematoma or (2) an unusual manifestation
of the trigeminocardiac reflex (TCR) following stretch and compression of the dura
by the expanding hematoma volume. Sensory innervation of supratentorial dura mater
is mainly by meningeal branches of the trigeminal nerve. Stimulation of this nerve
anywhere along its course may cause reflex bradycardia for as long as the stimulation
persists.[8] By most definitions of TCR, the bradycardia is accompanied by sudden hypotension.
This was not observed in our patient. Instead, the blood pressure remained stable
and slightly in the higher range. More significantly, once the intracranial hypertension
was relieved by craniotomy, the heart rate normalized. Therefore, the most plausible
explanation for the bradycardia observed in our patient is Cushing's reflex.
Depressed skull fracture and extradural hematoma are potentially fatal complications
of skull pin fixation in children undergoing craniotomy. Isolated, sudden, and persistent
bradycardia at the end of posterior fossa surgery may serve as an immediate on-table
warning sign. It is imperative that the anesthesiologist maintains vigilance and effective
communication with surgical colleagues.
