Keywords
intracranial aneurysm - coarctation of aorta - aneurysm coiling
Introduction
The estimated incidence of intracranial aneurysms (IA) is generally 2% of the general
western population.[1]
[2] Coarctation of aorta (CoA) is an evident major risk factor for IA formation. CoA
accounts for 5% of all cardiac defects.[3] The coincidence of IAs with CoA ranges from 2% to as high as 50%.[4] The estimated incidence of CoA in patients with IAs is low (0.19–1.9%).[5]
[6] We present our experience of successful anesthetic management of a 26-year-old male
diagnosed with CoA and posted for endovascular coiling of an unruptured internal carotid
artery (ICA) aneurysm.
Case Report
A young male, smoker, and known hypertensive for last 3 months on three antihypertensives
(prescribed by a local pharmacist) presented to this hospital with sudden onset weakness
of right upper and lower limb, headache, and multiple episodes of vomiting. His computed
tomography (CT) scan head was performed on emergent basis which showed left basal
ganglia bleed. It was decided to manage the basal ganglia bleed conservatively. His
CT angiography revealed an unruptured partially thrombosed saccular aneurysm measuring
5.9 × 4.5 mm with neck measuring 4.9 mm arising from the dorsal wall of left supra
clinoid ICA. As the location of the aneurysm had a difficult surgical access, the
patient was subsequently advised coiling of the unruptured aneurysm.
The patient was referred to us for preanesthetic check-up (PAC) where the patient
was restless, having severe headache. His muscle power was 5/5 on right side and 0/5
on left side. His blood pressure (BP) was 220/130 mm Hg and patient was being prescribed
amlodipine 10 mg (tablet), telmisartan (40 mg, tablet), hydrochlorothiazide (12.5
mg) and metoprolol (tablet) extended release 20 mg once daily along with Labetalol
injection on SOS basis. We found that his lower pulses were feeble, and when we examined
his BP in lower limb, it was 112/80 mm Hg. On auscultation of the heart, there was
a systolic murmur heard on the precordium. Electrocardiography was suggestive of left
ventricular hypertrophy (LVH) ([Fig. 1]). Upon suspicion of CoA, it was advised that the patient gets a chest CT angiogram
and cardiac workup. Diagnostic digital subtraction angiography (DSA) confirmed the
CoA distal to the origin of left subclavian artery ([Fig. 2]) with very prominent collaterals. The morphology of ICA aneurysm was also confirmed
and the coiling was deferred till cardiac evaluation of the patient.
Fig.1 Electrocardiogram suggestive of left ventricular hypertrophy.
Fig. 2 Coarctation of aorta as seen during digital subtraction angiography.
The patient was subsequently examined by cardiology team and echocardiogram (echo)
test revealed concentric LVH with normal left ventricular systolic function and an
ejection fraction of 82%. Cardiologist opined that the ICA aneurysm be coiled before
correction of CoA keeping in view the hemodynamic fluctuations that may occur during
correction of coarctation (predisposing to aneurysm rupture). We subsequently reviewed
the patient for coiling under general anesthesia with high cardiac risk.
On the day of surgery, patient was shifted to DSA suite and baseline monitors were
attached. The patient was drowsy preoperatively. His left radial artery was cannulated
under local anesthesia and invasive BP transduced, which was 187/97 mm Hg. Noninvasive
BP cuff was attached in left calf and cycled at 1 min and was found to be 118/78 mm
Hg.
Our intraoperative aim was to prevent wide fluctuations in the hemodynamics and prevent
hyperemia of the cerebral circulation and regions above the level of coarctation and
also in the same time prevent ischemia below the coarctation. The patient was induced
with morphine 15 mg injection, fentanyl 100 µg injection, and thiopentone 175 mg injection.
After ensuring adequate mask ventilation, vecuronium 6 mg injection intravenously
was given followed by lignocaine injection (preservative free) 60 mg and esmolol 30
mg and patient intubated with size 8.5-mm internal diameter (ID) endotracheal tube.
Thereafter, balanced anesthesia was administered to the patient with oxygen and nitrous
oxide in the ratio 1:1 and sevoflurane to attain a minimum alveolar concentration
(MAC) of 0.8 to 1.0. We then placed an arterial cannula in left dorsalis pedis artery
and transduced it to measure BP distal to the coarctation. A central venous catheter
was placed aseptically in right subclavian. Thereafter, the patient was handed over
to the neuroradiologist for endovascular coiling.
The intervention proceeded uneventfully and patient's BP in lower limb was kept above
a mean arterial pressure (MAP) above 70 mm Hg throughout the procedure. The MAP in
the left radial artery remained around 110 mm Hg during the procedure. The urine output
was monitored hourly. Postoperatively, patient was shifted to neuro-intensive care
unit unreversed and electively ventilated. He was slowly weaned off the ventilator
and extubated smoothly with a Glasgow Coma Scale of E4V5M6.
Two weeks post coiling of IA, the patient underwent correction of coarctation by balloon
angioplasty uneventfully. He was discharged from the hospital with a residual weakness
of 2/5 on left side of body.
Discussion
The presence of the CoA (post ductal) is responsible for hyper tension and subsequent
formation of intracerebral aneurysms. The cause of the basal ganglia bleed was in
all probability a hypertensive bleed. As pressure in the precoarctation segment of
the aorta increases, there is a significant elevation in the aortocerebral blood flow
and coupled with the increased resistance of the cerebral circulation, the dilatation
of the cervicocephalic arteries takes place.[7] This scenario was very evident in our case.
In our patient, as the aortocranial pressure difference increased (due to coarctation)
and with the presence of dilated cerebral as well as cervicocephalic arteries, the
blood flow was increased proximally. In the distal segment however, the stenosis of
the coarctation was responsible for decreased flow in the lower extremities leading
to lower BP distal to the coarctation.
Our aim was to administer general anesthesia with aggressive hemodynamic monitoring
to prevent any perioperative aneurysmal rupture and at the same time prevent any ischemia
distal to the aneurysm. The obtundation of the sympathetic response was achieved by
high opiate preinduction dose and administration of preservative free lignocaine and
esmolol. Extubation of such patients also requires to be done in a controlled environment
as any bucking can prove to be detrimental.
The DSA suite itself is a challenging place to administer anesthesia. The lack of
space coupled with absence of expert assistance due to remoteness of the place gives
us added challenges.
Our take-home messages while presenting this report is to stress on the following
issues:
-
Any trivial finding during PAC must be thoroughly investigated, as the management
of cases can completely change.
-
Understanding the altered physiology in patients of CoA needs to be understood while
caring for these patients perioperatively.
