2. INTRODUCTION
• Diagnostic angiographic procedures have been supplanted by noninvasive
imaging
• Therapeutic procedures have become more Complex.
• The safest endovascular procedure is the one that can be avoided by performing
noninvasive imaging.
6. NEUROLOGICAL COMPLICATION
Ischemic stroke / TIA (Most common Neurological complication)
Thrombosis within the catheter with subsequent embolization.
Mechanical disruption of aortic or supra-aortic vessel plaque.
Dissection of the catheterized vessel with subsequent thrombosis and
embolization secondary to wire or catheter manipulation.
Air embolism
7. Transient Global Amnesia and Cortical Blindness
Aneurysmal Rupture During Angiography
8.
9. RISK FACTORS
• For complications in the first 24 hours after cerebral angiography include
Patients who are referred because of stroke or transient ischemic attacks.
Patients whose angiograms demonstrate greater than 50% to 70% stenotic
disease of the cerebral vessels.
10. RISK FACTORS
Patients older than age 70.
Patients whose angiograms require a higher volume of contrast.
Patients whose angiograms last more than 60 to 90 minutes or require multiple
catheters.
Patients whose angiogram was performed by a fellow alone.
11. RISK FACTORS
Patients with systemic hypertension or renal impairment.
Patients referred for subarachnoid haemorrhage or who are immediately
postoperative.
12. DISEASE RELATED COMPLICATION
• In analysis of three prospective studies
Permanent and transient complications was significantly lower in patients with
SAH compared to TIA or stroke (1.8% versus 3.7%).
Aneurysm/AVM without SAH compared with TIA or stroke (0.3% versus
3.7%).
13. ASYMPTOMATIC ISCHEMIC EVENTS
• Asymptomatic ischemic events (detected on DWMRI) during cerebral
angiography have gained more attention.
• Long vs short procedure.
• With risk factors vs without risk factors.
• Experienced vs trainee
14.
15.
16. MINIMUM STANDARD
• American Society of Neuroradiology and allied societies in the neurovascular field issued a joint
statement in 2004 suggesting that a case log of 100 patients become the minimum standard for
establishing adequate training in diagnostic cervicocerebral angiography.
17. MICROEMBOLI AND MICROBUBBLES
• Emboli may represent dislodged
1. Atheromatous material
2. Thrombus from the catheter
3. Air bubbles.
• Transcranial Doppler (TCD) - reveal much about cerebrovascular physiology and
intraprocedural events.
22. Treatment
• If large enough to be detected fluoroscopically, and the vessel is easily
accessible, aspirate using microcatheter and flush the vessel with heparinized
saline to break up the remaining bubbles.
• Quick and readily available (though unproven) methods
1. Use of transcranial Doppler (to agitate and break up bubbles),
2. Heparinization (to prevent clot from forming in vessels stagnating from the air)
3. Administration of oxygen and induction of hypertension
23. • If available, hyperbaric oxygen chambers have shown good outcomes.
Started within 6 hours / After 6 hours - Outcome 67% / 35%.
• When in doubt, a variety of methods can be used simultaneously, including
hyperbaric oxygen plus induction of barbiturate coma to attempt to protect the
brain.
• The most important thing is to recognize that air emboli have occurred and then
use whatever treatment modalities that are available.
24. CATHETER RELATED THROMBOSIS
Catheter Flushing
• Continuous irrigation system
• Intermittently double flushing the catheter with syringes every 90 seconds
25.
26.
27. 65/M DSA evaluation for Posterior fossa Dural AVM.
Thrombus formation in the catheter obliterating
superior division of Rt MCA artery.
28. Treatment
• Arterial pressure should be raised.
• Visible thrombus may be treated by mechanical lysis using a guide wire.
• Thrombolytic agent – tPA. Recanalisation rate-44%.
• Antiplatelets before procedure.
29. Catheter related vasospasm
• Prevents adequate positioning of catheter.
• Also cause vasospasm induced cerebral hypoperfusion.
• Rx – intraarterial 2% lidocaine (20mg diluted in 10 ml saline)
• Nicardipine (1 mg in 10 ml saline)
30. 44/F . Case of coil embolization for unruptured aneurysm had
bronchospasm on repeated catheterization.
31. TRANSIENT GLOBAL AMNESIAAND
CORTICAL BLINDNESS
• Transient global amnesia after cerebral angiography – reported rare but not so
rare.
• Some of these appear to be idiosyncratic to the patient, for instance, direct
toxicity in the setting of compromise of the blood–brain barrier resulting in
clinical onset of cortical blindness, hemiballismus, or bilateral cochlear deafness.
32. • Usually occurs in the absence of other neurologic signs.
• Patients invariably recover without specific intervention within 24 to 72 hours.
• Effect on the posterior circulation with particular reference to the medial
temporal lobes.
• Seen in patients with atherosclerotic vertebrobasilar disease. The possibilities of
atheromatous emboli and particulate contamination of contrast are possible
explanations.
33. ANEURYSMAL RUPTURE DURING ANGIOGRAPHY
• Most severe neurologic event - rebleeding of a freshly ruptured aneurysm, with
a mortality upto 79%.
• Rebleeding was considered coincidental.
• Power injections of standard rates accompanied by an increase in intravascular
pressure.
34. • Studies intracarotid contrast injection may cause a reflex bradycardia and
mild hypotension, there is an initial 1- to 2-second period of elevated intracarotid
pressure, which declines over approximately 2 to 10 seconds.
• Koenig et al. reported on 10 cases of aneurysmal rupture during angiography and
reviewed the literature. They observed a 100% mortality rate in their patients.
• They advised that consideration be given to a reduction in contrast injection rates
to about 4 mL/s in patients with recent subarachnoid haemorrhage.
35. • Komiyama et al. conducted an extensive review and found a rate of 79%
mortality associated with aneurysmal rupture during angiography.
• Occurred in approximately 3% of all patients referred for angiography for SAH.
• More likely when cerebral angiography was undertaken within 6 hours of the
initial bleed.
• Hand injection can occasionally be more provocative than power injector.
36. • Intraprocedural rupture may not always be seen on the angiographic images.
• Warning signals - vital signs, subjective complaints, and deterioration in
neurologic status.
• Should be monitored after each angiographic run.
• Initial increase in flow followed by a marked reduction in flow.
37. • With a sudden increase in ICP , diminished runoff of contrast in the internal
carotid artery may be seen.
• Occluding embolus / sudden sustained elevation of ICP can cause similar
stagnation and poor runoff of contrast.
• Nornes et al. reported data on the changes in internal carotid artery blood flow
and pressure associated with intraoperative aneurysmal rupture.
38.
39. Treatment
• Packing the defect with coils.
• Emergency craniotomy and clipping may be required
• Acute hydrocephalus due to SAH – ventricular drainage
40. NONNEUROLOGIC COMPLICATIONS
OF CEREBRAL ANGIOGRAPHY
• Hematoma formation at the arterial puncture site.
• Reported as high as 10.7% for femoral puncture sites depending on sheath size
and use of heparinization.
• Higher hematoma rates for carotid and brachial sites have been reported at 25.3%
and 15.7%, respectively.
41. • The pulse is more difficult to control in the brachial areas during compression.
• Dion et al. reported that patients older than age 70 had a hematoma rate of 18%
after transfemoral cerebral angiography, of whom one third needed fluid
replacement or surgical repair.
• Rx - Compression. Protamine sulfate
42. • Femoral artery pseudoaneurysms are rare – Incidence 0.05% to 0.55%.
• Other nonneurologic complications with an incidence of less than 1% to 2%,
which constitute serious problems, include MI, allergic reactions.
• Minor complications include nausea or vomiting, benign bradycardia or
extrasystoles, fainting, or delayed hematoma formation after discharge.
43. • There should also be a lucid set of orders for patient immobilization, groin and pulse precautions,
and intravenous fluids to continue over the following 4 to 8 hours.
44. CONTRAST-INDUCED NEPHROPATHY
• Acute contrast-induced AKI is defined as a rise in serum creatinine of >25%
above baseline or a rise of 0.5 mg/ dL within 48 hours of a contrast-based
procedure.
• A marker for significantly increased in-hospital mortality - 22% compared
with 1.5% in nonaffected patients
• Occurrence of contrast-induced dialysis is associated with an in-hospital
mortality rate of 35%
45. • Accounts for as much as 10% of hospital-acquired renal failure.
• May be seen in as many as 14.5% of coronary catheterization patients.
• In up to 40% of diabetic patients undergoing angiography.
• Even higher proportions in patients with established severe renal impairment.
• Usually transient and requires long-term dialysis in less that 1% of cases.
46. • Diabetic patients, and particularly those with (GFR) <60 mL/min, will need to
discontinue using metformin for at least 48 hours following a procedure.
• Adequate hydration in preparation for the procedure + use of a bicarbonate
infusion protocol, discussed below.
• Premedication with N-acetylcysteine.
• Use of nonionic contrast agents, particularly iodixanol.
47. • A meta-analysis of trials suggests that use of iodixanol can reduce the likelihood
of AKI from 3.5% to 1.4% in an at-risk patient, or by even more in higher-risk
groups.
48. CONTRAST REACTION
• Previous episode of anaphylactoid reaction to contrast - 17% - 35% risk
• Prednisone 50 mg every 6 hours for 3 doses ending 1 hour before the procedure
and diphenhydramine 50 mg intramuscularly (IM) 1 hour before the procedure
• For emergency patients, hydrocortisone 200 mg IV stat and repeated every 4
hours during the procedure.
• MPS 32 mg PO during the 24 hours before an angiogram and repeated 2 hours
before the procedure.
50. REFERENCES
• Pearse Morris, Practical Neuroangiography T h i r d E d i t i o n
• Complications of Diagnostic Cerebral Angiography, Timothy J. Kaufmann et al., Radiology:
Volume 243: Number 3—June 2007
• Textbook of Interventional Neurology by Adnan I. Qureshi
• Complications of Intravenous Digital Subtraction Angiography, ball et al., Arch Neurol
1985;42:969-972
A somewhat difficult-looking elongated aneurysm of the basilar apex is illustrated in this elective case. The patient had a clipping of a previous aneurysm in the anterior circulation complicated by ischemic complications and was keen to avoid similar complications. The right vertebral artery injection AP plane (A) and lateral plane (B) shows the aneurysm to be wide at its base and associated with a second smaller aneurysm (small arrow in A) lodged between the left posterior cerebral artery and the left superior cerebellar artery. Overlapping dimes on the patient’s head (18 mm) are used for external sizing reference. Both vertebral arteries were catheterized and a microcatheter advanced via the left vertebral artery was jailed into the aneurysm by a neuroform stent extending from the midbasilar artery to the right P1 segmentImages immediately after the stent deployment (C and D) showed a sizeable bubble (arrow) bobbing anteriorly in the aneurysm, most likely having escaped from the stent catheter. Suction was applied (vigorously) to the aneurysm microcatheter and as a result of these efforts or the solvent properties of the flowing blood, the bubble disappeared and was gone when the next run wasperformed. No clinical sequelae were evident after the case, and many valuable lessons were learned by all.
Importance of prompt recognition of complications.
A 65-year-old male undergoing angiographic evaluation of a posterior fossa dural AVM.
A right internal carotid artery PA injection (A) demonstrates stump-like density (arrow in A) off the middle cerebral artery. Although there appears to be an adequate number of middle cerebral artery branches on the PA view, the lateral view (B) demonstrates lucency in the window formed under the pericallosal branch of the anterior cerebral artery due to occlusion of the superior division of the right middle cerebral artery. The branches of the inferior division are present (arrows in B).
This represents a procedural complication probably due to The patient was heparinized immediately, and the systolic blood pressure was elevated to 160 mm Hg.
A common carotid arteriogram (C, D) done minutes later in anticipation of emergency thrombolysis demonstrated reopening of the superior division (arrow in C).
Compare the lateral appearance after reopening (D) with the appearance during occlusion (B), demonstrating the sensitivity of the lateral view to branch occlusion of the middle cerebral artery.
The patient recovered from this complication without clinical or imaging evidence of a related deficit.
Pathologic opacification of veins in the posterior fossa is seen due to the dural AVM in the region of the foramen magnum.