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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: [email protected] website: www.stroke-surgeon.com Consultant Neurosurgeon and Neurointerventionist Columbia Asia Hospital, Bangalore.

Traumatic vascular injuries of brain

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Dr Avinash.KM is a Neurosurgeon with advanced training in Interventional vascular Neurosurgery(FINR) from Zurich, Switzerland, and FMINS-Fellowship in minimally invasive and Endoscopic Neurosurgery from Germany. He is presently working in Columbia asia hospitals, Bangalore. His main areas of interest are Vascular Neurosurgery, Stroke specialist, interventional neuroradiology, Endovascular Neurosurgery, Endoscopic and minimally invasive Neurosurgery, Endoscopic spine surgery.He has advanced training in both Brain Aneurysm coiling and clipping, Brain AVM embolizations and its surgical removal, carotid artery stenting and carotid endarterectomy. Since he is trained both in open microvascular Neurosurgery and in Interventional Neurosurgery he helps patients in choosing the right treatment options for brain vascular diseases with out any bias of one treatment over the other.

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Page 1: Traumatic vascular injuries of brain

Traumatic Vascular Injuries of Brain

Dr. Avinash KMMS, 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: [email protected]: www.stroke-surgeon.com

Consultant Neurosurgeon and Neurointerventionist

Columbia Asia Hospital, Bangalore.

Page 2: Traumatic vascular injuries of brain

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:

Page 3: Traumatic vascular injuries of brain

Arteriovenous fistulasAbnormal 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:

Page 4: Traumatic vascular injuries of brain

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

Page 5: Traumatic vascular injuries of brain

Caroticocavernous fistula

Causes:

•Trauma, •intracavernous aneurysms, •collagen vascular diseases, •infections,

Page 6: Traumatic vascular injuries of brain

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.

Page 7: Traumatic vascular injuries of brain

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.

Page 8: Traumatic vascular injuries of brain

Management of CCF?Endovascular treatment is the treatment of choice in

these cases. Surgery is rarely needed for failed endovascular cases.

Page 9: Traumatic vascular injuries of brain

Vertebro-vertebral FistulaIt is similar to carotico cavernous fistula, where an artery opens

into the vein leading to some problems

Fistulous connectionNormal Vertebral Artery

Page 10: Traumatic vascular injuries of brain

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

Page 11: Traumatic vascular injuries of brain

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.

Page 12: Traumatic vascular injuries of brain

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.

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What are the clinical features of dissections?

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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.

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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.