hemorrhagic stroke

Question 1

Epidural hemorrhage location, shape

Answer 1

occurs between the skull and the dura, typically from an artery, especially the middle meningeal artery. These collect in a convex, or lemon shaped hematoma

Question 2

Subdural hemorrhage location, shape

Answer 2

occurs between the dura and the thin arachnoid layer covering the brain, typically from a torn or ruptured bridging vein between the dura and the cortex. This layers like a banana (i.e. concave).

Question 3

Subarachnoid hemorrhages location, causes

Answer 3

occur right next to the brain, underneath the arachnoid layer. Trauma is the most common cause, but everyone is more concerned with the spontaneous (i.e. non-traumatic) version from aneurysms, Arterio Venous Malformation, or other causes. An unusual occurrence, Cortical Subarachnoid Hemorrhage (cSAH) can show up with vasospasm, migraine, ischemia or without obvious cause.

Question 4

Intra-parenchymal hemorrhages location

Answer 4

are formed blood clots which dissect into the brain. These can be anywhere. Most common in basal ganglia (putamen)

Question 5

Intra Ventricular Hemorrhage

Answer 5

Any Hemorrhage can find it’s way into the Ventricular system

Question 6

Hemorrhagic transformation

Answer 6

Hemorrhagic transformation of ischemic stroke beds occurs with large vessel cortical strokes. This can be asymptomatic if mild ‘bruising’ or fatal if a large formed hematoma

Question 7

Intra-parenchymal hemorrhages causes and brain location

Answer 7

Caused by HTN, age, coagulation dz or therapeutic anticoagulation. Typical locations in Putaman, Thalamus, Pons and Cerebellum deep grey matter. Atypical locations include deep white matter, which can be from age/HTN or AVMs, aneurysm, vasculitis, bleeding disorders or hemorrhage into tumors.

Question 8

Deep vs lobar intracerebral hemorrhage locations, risk factors, outcomes

Answer 8

Deep: aka ganglionic, putamenal, striatocapsular, hypertensive. Risk factors are HTN (2/3) and age, and non whites have higher risk. Poor outcome. Charcot-bouchard aneurysm. Lobar: frontal > parietal > occipital > temporal. Congophilic or amyloid angiopathy. Risk factors are aage, dementia, coagulation problems, HTN (1/3), whites/Asians higher risk. Tolerated well

Question 9

Amyloid Angiopathy

Answer 9

Type of intra-parenchymal hemorrhage where patients get recurrent lobar hemorrhages that lead to progressive dementia and disability. Amyloid deposition is found in the vessels. Tolerated well by many

Question 10

Subdural hemorrhage progression

Answer 10

The Subdural space easily tears bridging veins and causes a lower pressure, slower bleeding process. Spontaneous Subdural Hemorrhage can be relatively asymptomatic, and progress to a “Chronic Subdual Hemorrhage” which enlarges over days to months.

Question 11

Epidural hemorrhage progression

Answer 11

The Epidural contains the Middle Meningeal Artery, which often will tear from a skull fracture creating the Epidural Hematoma. Since this is arterial or high pressure bleed, the progression can be rapid

Question 12

Subarachnoid hemorrhage non-traumatic causes

Answer 12

aneurysmal rupture (80%), or to arteriovenous malformation (15%). Some people have “benign” peri-mesencephalic SAH that is curiously unassociated with aneurysm or AVM

Question 13

Subarachnoid and intra-parenchymal hemorrhages common presentation

Answer 13

sudden onset of neurological deficits, but typically have associated headache, nausea, and vomiting along with a depressed level of consciousness.

Question 14

non-traumatic subarachnoid hemorrhage presentation

Answer 14

Severe headache (“worst headache of their life”), sudden death in 1/3 ( from acute hydrocephalus or sympathetic surge and cardiac arrhythmia), Cranial nerve palsy (III), hemiparesis

Question 15

Risk factors for aneurysmal hemorrhage

Answer 15

Genetics and smoking. NOT HTN

Question 16

Intraparenchymal hematomas presentation

Answer 16

begin with a mild headache, deficit, maybe some nausea, and progress over a few minutes to hours adding decreased level of consciousness. hemiparesis steadily progressing into hemiplegia and a level of consciousness that steadily deteriorates into coma.

Question 17

Intraparenchymal Hemorrhage risk factors

Answer 17

Aging, HTN, stimulant use. More common than ischemic stroke in china and Asia

Question 18

Cerebral Amyloid Angiopathy risk factors

Answer 18

age

Question 19

Cerebral Amyloid Angiopathy - how are amyloid crystals detected

Answer 19

birefringence lens- amyloid crystals seen in vessel walls

Question 20

Classification of subarachnoid hemorrhages

Answer 20

Grade 1: asymptomatic or minimal headache, slight nuchal rigidity. Grade 2: moderate to severe headache, nuchal rigidity, no neurological deficity apart from cranial nerve palsy. Grade 3: drowsiness, confusion, mild focal deficit. Grade 4: stupor, moderate to severe hemiparesis, possible early decerebrate posturing. Grade 5: deep coma, decerebrate posturing

Question 21

Hemorrhage management

Answer 21

1. control BP: includes smoking cessation. 2. anti-platelet or anticoagulants: if hemorrhagic transformation is the cause. 3. Control intracranial pressure: diuresis and reduction of blood pCO2. Mannitol or loop diuretics

Question 22

Subarachnoid hemorrhage treatment

Answer 22

1. physical intervention to repair aneurysm or AVM: surgery, catheter ablation, etc. 2. Sedation. 3. Relative hypotension: reduce risk of re bleeding before surgery. 4. Nimodipine and statins: reduce ischemic damage from vasospasm from irritation of vessels by blood in subarachnoid space. 5. after surgery, hypervolemic hypertensive hemodilution (HHH), angioplasty, vasodilator meds, and other therapies can be used to reduce the effects of vasospasm.

Question 23

Subdural/epidural hemorrhage treatment

Answer 23

Surgical decompression often needed in addition to general management of hemorrhages