Hemorrhagic stroke in NS practice Flashcards
Etiology of Spontaneous Intracerebral hematoma
1- Hypertension: either acute hypertension or in chronic hypertension patients.
2- Coagulopathies (patients with thrombocytopenia or patients on anticoagulant or antiplatelet medications)
3- Ruptured of cerebral vascular anomalies (AVM- AneurysmCavrnous hemangioma- capillary telangectashia)
4- Hemorrhagic brain tumors
5- Artriopathies , also called small cerebral vessel disease ( cerebral amyloid angiopathy is the commonest)
C/P of spontaneous intracerebral hematoma
1- Acute deterioration of conscious level
2- localizing signs, Hemiplegia or hemiparesis, Aphasia, homnomous hemianopia Seizures.
3- Increases ICP symptoms: headache and vomiting
Hemorrhage expansion occurs usually during first 3 to 6 hours up to 24 hours after onset of hemorrhage, which requires repeat of brain CT brain routinely or at any clinical deterioration.
So delayed clinical deterioration maybe due to expansion of hemorrhage, hydrocephalus, increased brain edema or onset of clinical seizure
Types of brain aneurysm on location
1- Anterior communicating aneurysms (commonest)
2- Posterior communicating internal carotid artery aneurysms
3- Middle cerebral artery aneurysms
4- Vertebro-basliar aneurysms
types of aneurysm according to etiology
1- congenital
2- Flow-related: generally at branch points (biforcations) of arteries, usually due to shear forces at these locations.
3- Mycotic due to infection
4- Posttraumatic
5- Conditions with abnormalities of blood vessels, including: autosomal dominant polycystic kidney disease (ADPKD) or connective tissue disorders (Marfan syndrome, Ehlers-Danlos…)
6- Dissecting aneurysm: results from a tear in the arterial lining which allows blood to enter the arterial wall. Usually traumatically induced.
7- Pseudo aneurysm (false aneurysm): a blood clot adjacent to a rent in the arterial wall.
Clinical picture of Subarachnoid hemorrhage + Neurological complications
- Sudden onset of severe headache with vomiting, syncope, neck pain and photophobia
- May occur with lost consciousness and with subsequent recovery.
- Focal cranial nerve deficits may occur
- During examination, Meningismus (Nuchal rigidity), hypertension, focal neurologic deficit and different degrees of coma.
- Ocular hemorrhage can occur in three patterns: subhyaloid hemorrhage, retinal hemorrhage and vitreous hemorrhage (Terson syndrome)
1- Re-bleeding from aneurysm due to persistent hypertension or delayed aneurysm treatment
2- Vasospasm or delayed cerebral ischemia causing clinical deterioration on top of cerebral hypo perfusion
3- Hydrocephalus either obstructive hydrocephalus by blood blocking ventricles or communicating post hemorrhagic hydrocephalus
Clinical grading scale was described to categorize SAH patient called Hunt and Hess grade, Draw it.
Grade 1: Asymptomatic or mild headache and slight nuchal rigidity.
Grade 2: Cranial N. palsy (e.g., III, VI), moderate to severe headache and nuchal rigidity.
Grade 3: Mild focal deficit, lethargy, or confusion.
Grade 4: Stupor, moderate to severe hemiparesis, early decerebrate rigidity
Grade 5: Deep coma, decerebrate rigidity, moribund appearance
ttt of Subarachnoid hmg
- Nimodipin ( a calcium channel blocker ) is highly effect in preventing cerebral vasospam in SAH.
- Close monitoring in ICU is essential to properly discover and manage the systemic complications of SAH such as hyponatermia, cardiac complications or thromboembolic events
ttt of brain aneurysm
1- Surgical treatment (microsurgical clipping techniques – parent vessel occlusion with bypass surgery- wrapping of aneurysm)
2- Endovascular coiling procedure using platinum coils ( with or without stent or balloon)
3- Endovascular flow diverter stent in cases of giant fusiform aneurysm
Name Vascular malformations in the brain with their percentages
1- arteriovenous malformation (AVM): represents 45–60%
2- cavernous malformation represents 19– 31%
3- capillary telangiectasia represents 4–12 %
4- other categories include developmental venous anomaly (DVA), Dural A/V
Presentation of AVM
1- Hemorrhage (most common): 58%, quoted annual risk is 2% to 4%, Previous rupture. The strongest Prognostic for future hemorrhage is more common was
smaller size AVM,
2- Seizures: 34%
3- Mass effect: e.g., trigeminal neuralgia due to CPA AVM
4- Ischemia: by steal feeding arteries and draining veins
5- Headache. AVMs may occasionally be associated with migraines. bruit: especially with dural AVMs
6- Increased ICP, which is findings limited almost exclusively to pediatrics, usually with large midline AVMs that drain into an enlarged vein of Galen (“vein of Galen malformation” which results in hydrocephalus with macrocephaly or congestive heart failure with cardiomegaly
Diagnosis of AVM
1- Unenhanced brain CT is the best study to rule out acute hemorrhage (> 90% sensitivity). It can miss some AVMs, but can demonstrate calcifications within the lesion or increased density of the nidus. Adding a contrast CT will show enhancement within the vessels, and can delineate the nidus
2- CT angiography (CTA) with IV contrast : helps to study vessels and arteriovenous anatomy of AVM
3- MRI brain: can detect the AVM by detecting flow void pattern in tortuous vessels , also detects hemorrhage ,adding contrast will help to understand the vascular anatomy
4- Magnetic resonance angiography (MRA): can be done without IV contrast – which is an advantage in some patients with kidney problems or contrast allergy
5- Catheter conventional angiography: is the gold standard test for diagnosis, understanding and treatment planning of AVM
ttt of AVM
1- Conservative expectant treatment in cases of asymptomatic unruptured AVM is supported by some clinical trials
2- Microsurgical excision of AVM
3- Endovascular embolization of AVM using some liquid embolizing material
4- radiosurgery techniques Gamma knife or cyber knife techniques
5- combination of all above techniques
