1) Traumatic vascular injuries of the brain include arteriovenous fistulas, traumatic aneurysms, and traumatic dissections of extracranial and intracranial vessels.
2) Arteriovenous fistulas are abnormal connections between arteries and veins that can cause headaches and bleeding in the brain if left untreated. One type is carotid cavernous fistulas.
3) Carotid cavernous fistulas result from an abnormal connection between the carotid artery and cavernous sinus and can cause eye bulging and vision loss if not treated. Endovascular treatment is the preferred treatment option.
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Traumatic vascular injuries of brain
1. Traumatic Vascular Injuries
of Brain
Dr. Avinash KM
MS, MRCS Ed(UK), Mch (KEM, Mumbai), FINR(Switzerland), FMINS(Germany),
• Interventional & Neurovascular surgeon and Stroke specialist,
• Endoscopic Neuro and Spine surgeon,
• Minimally invasive Neuro and Spine surgeon (FMINS).
mob: 9740866228, E mail: doc_avin@hotmail.com
website: www.stroke-surgeon.com
Consultant Neurosurgeon and Neurointerventionist
Columbia Asia Hospital, Bangalore.
2. What are the types of vascular
injuries of brain?
Vascular injuries of brain are common in young
population due to sporting activities and road traffic
accidents
Types of vascular injuries are:
• Arterio venous fistulas
– carotid fistula: carotic cavernous fistula
– vertibro-vertibral fistula:
• Traumatic aneurysms
• extracranial aneurysms:
• intracranial aneurysms:
• Traumatic dissection-
– extra cranial vescular dissections:
– Intracranial vescular dissections:
3. Arteriovenous fistulas
Abnormal connection between arteries and veins
of the brain.
This results in transformation of arterial pressure into the
vein resulting in their dilatation, tortuousities, abnormal
venous aneurysms, venous outflow obstructions,
venous hypertension resulting in headaches, vomiting,
unconsciousness if untreated, bleeding in the brain,
seizures.
Types of Arterio venous fistulas are
– carotid fistula: carotic cavernous fistula
– vertibro-vertibral fistula:
4. Carotico cavernous fistulas
A carotid-cavernous fistula (CCF) results from an
abnormal communication between the arterial and
venous systems within the cavernous sinus in the
skull.
As arterial blood under high pressure enters the
cavernous sinus, the normal venous return to the
cavernous sinus is impeded and this causes
engorgement of the draining veins, manifesting most
dramatically as a sudden engorgement and redness of
the eye of the same side.
Watch following Videos for better understanding:
• http://www.youtube.com/watch?v=M_4hnamUkFM&feature=channel&list=UL
• http://www.youtube.com/watch?v=M_4hnamUkFM
6. What are the types of
caroticocavernous fistulas?
Type A: direct fistula between the intracavernous ICA and cavernous sinus.
Type B fistulas: have dural ICA branches to the cavernous sinus.
Type C fistulas: have dural ECA branches to the cavernous sinus.
Type D fistulas have dural ICA and ECA branches to the cavernous sinus.
7. What are the clinical featurs of CCF?
While CCF is not a lethal disease, its symptoms can be
disabling and include
• bruit (a humming sound within the skull due to high blood flow
through the arteriovenous fistula),
• progressive visual loss.
• pulsatile proptosis or progressive bulging of the eye due to
dilatation of the veins draining the eye.
• Pain is the symptoms that patients often find the most difficult to
tolerate.
Patients usually present with sudden or insidious onset
of redness in one eye, associated with progressive
proptosis or bulging.
8. Management of CCF?
Endovascular treatment is the treatment of choice in
these cases. Surgery is rarely needed for failed
endovascular cases.
9. Vertebro-vertebral Fistula
It is similar to carotico cavernous fistula, where an artery opens
into the vein leading to some problems
Fistulous connection
Normal Vertebral Artery
10. Traumatic Dissections of vessels:
Dissections occurs when a tear in the intima(inner layer
of the blood vessel) allows blood to enter between the
layers of the vessel wall, thus forming an hematoma
inside the wall.
Exposure of the intima(inner layer of vessel) and the
presence of an intimal flap lead to increased blood
clotting and stroke may result from embolization or
flow-limiting stenosis of the vessel’s true lumen.
Early detection and treatment are important as the
recurrence of stroke is highest during the first month
following the event.
Watch video to understand what is dissection---
http://www.youtube.com/watch?v=97Lkl52LI-g&feature=related
http://www.youtube.com/watch?v=KrNJ-Byuwm4
11. Dissection of the vessels
Carotid artery dissections affects all age groups, but
there is a predilection for younger individuals. It
accounted for 25%–30% of all the strokes in patients
younger than 45 years.
The higher susceptibility to trauma of some arterial
segments may be explained by their relation to
adjacent bony structures.
Dissection is more common in the extracranial than
in the intracranial vessels, possibly due to the higher
mobility and greater vulnerability of extracranial
arteries to torsional stress. The internal carotid artery
is mobile from its origin at the bifurcation to its
entrance in the skull. Its most vulnerable region is
at the junction between the mobile (cervical) and
relatively fixed (petrous) segments where
susceptibility to torsion stress is increased.
In the vertebral arteries, the segment after the exit
from the vertebral transverse foramina between the
C1 and C2 levels and prior to entering the skull base
(V3 segment) is mobile and highly prone to stretch
injury.
12. What are the causes of dissections?
Causes of dissections:
• Neck trauma is the most common cause. Direct trauma to the artery, a
torsional or stretching force that induces shear stress to the intima, or injury
against surrounding bony structures may be the causative factors.
• Spontaneous CAD has been related to minor events, such as sneezing,
coughing, vomiting, flexion/extension/rotation movements of the neck (as in
chiropractic manipulation or endotracheal intubation), swimming, or
yoga. It is estimated that CAD occurs in 1 out of 20 000 neck
manipulations.
• Another factor predisposing to CAD are inherent defects of the arterial
wall. Diseases such as Marfan’s syndrome, Ehlers–Danlos syndrome type
IV, fibromuscular dysplasia, cystic medial necrosis, alpha 1 antitrypsin
deficiency, polycystic kidney disease, osteogenesis imperfecta type I among
others are associated with higher occurrence of CAD.
14. how do you treat dissections?
Management:
Conservative medical management:
• Current practice guidelines from the American Heart Association/American Stroke
Association Council on Stroke state that:
• “for patients with ischemic stroke or TIA and extracranial arterial dissection, use of
warfarin for 3 to 6 months or use of antiplatelet agents is reasonable (Class IIa, Level
of Evidence B).
• Beyond 3 to 6 months, long-term antiplatelet therapy is reasonable for most stroke or
TIA patients. Anticoagulant therapy beyond 3 to 6 months may be considered among
patients with recurrent ischemic events (Class IIb, Level of Evidence C).”
• In patients with intracranial dissection anticoagulation is contraindicated given the
higher risk of pseudoaneurysm formation and SAH.
Endovascular management:
• The American Heart Association/American Stroke Association Council on Stroke
recommends consideration of endovascular treatment for patients who fail or are not
candidates for endovascular therapy (Class IIb, Level of Evidence C).
• While no randomized controlled trials exist, medical therapy with antiplatelet or
anticoagulant treatment is first-line therapy, with the majority of patients
demonstrating no recurrent ischemic symptoms and healing of the artery on
follow-up.
• Endovascular therapy with stenting has been reported in several small case
series, and is generally considered for patients who fail medical therapy.
15. Comments: In my personal opinion
• For extracranial dissections: first line of treatment for
extracranial dissections is medical . Endovascular
should be considered only when medical therapy fails(
recurrant stroke or when patient develops
hemodynamic compromise)
• For intracranial dissections: with NO subarachnoid
hemorrhage medical line can be attempted if there is
no hemodynamic compromise. If there is
hemodynamic compromise, then either stenting or
surgical bypass should be considered. If there is
subarachnoid hemorrhage associated with dissection,
trapping with bypass should be first option, next being
stenting( as it will need double anticoagulation in a
ruptured vessel). If there is good collateral circulation
parent artery sacrifice can be done.