Case

Case

Case

Subarachnoid hemorrhage (SAH)

Most common cause is rupture of saccular aneurysm. Others: bleeding from vascular formation and extension from a primary intracerebral bleeding. Most unruptured intracranial aneurysms are asymptomatic. Symptoms are usually due to rupture and resultant SAH.

Subarachnoid hemorrhage (SAH)

At rupture, ICP rises.
Sudden transient loss of consciousness Excruciating headache, worst headache of my life , generalized, change in usual headache pattern, most important is the sudden onset of headache Neck stiffness Vomiting

Subarachnoid hemorrhage (SAH)

Prodromal symptoms suggest location of enlarging aneurysm.
3rd cranial nerve palsy- junction of PCA and ICA 6th nerve palsy- cavernous sinus Occipital and cervical pain- PICA or AICA aneurysm Pain in or behind the eye and in the low templeMCA aneurysm

Vasospasm

Vasospasm
Pathological constriction of cerebral arteries which can cause ischemia or stroke from 4 to 21 days after SAH

Fisher Grading
Classifies SAH according to how they appear on CT scan To check for vasospasms most dreaded complication of SAH

Fisher Grading
Grade 1- No hemorrhage evident Grade 2- Subarachnoid hemorrhage less than 1mm thick Grade 3- Subarachnoid hemorrhage more than 1mm thick Grade 4- Subarachnoid hemorrahge of any thickness with intra-ventricular hemorrhage (IVH) or parenchymal extension

Management
Maintenance of optimal perfusion with hypertension & mild hypovolemia Administration of Nimodipine, a CCB that may decrease the incidence % degree of spasm Neurointerventional options for treating symptomatic vasospasm include intra-arterial papaverine or nicardipine, and ballon angioplasty for larger caliber vessels

Etiology & Presentation Treatment option & Timing of surgery Outcome & Prognosis

Etiology & Presentation

Aneursym is the focal dilatation of the vessel wall and is most often a balloon-like outpouching, but may also be fusiform It usually occur at branch points (e.g. ICA), or at the origin of small vessels (e.g. PCA or Ophthalmic artery) and are usually thin walled and at risk for rupture Rupture of major cerebral vessels in SAS results in SAH The tear my be small and seal quickly or may not Because of the meningeal linings of the brain are sensitive, SAH usually results in a sudden, severe thunderclap headache A patient will classically describe the the worst headache of my life Presenting neurologic symptoms may range from mild headache to coma to sudden death

Hunt-Hess clinical gra ing syste

f rS H

0- Assy pt atic; unrupture aneursy 1- Awake; assy pt atic r ild headache, ild nuchal rigidity derate t severe headache, cranial 2- Awake, never palsy (e.g. CN3 r 4), nuchal rigidity 3- Lethargic; ild f cal neur logic deficit (e.g. pronator drift) 4- Stupurous; significant neurologic deficit (e.g. he iplegia) 5- Comatose; posturing

Treatment option & Timing of surgery

Diagnosis Lumbar puncture CT scan MRI scan 4-vessel cerebral angiography

 Patients suspected with SAH should have CT immediately. If CT is (-), lumbar puncture (LP) should be performed. An LP with xantochromia and high RBC counts (usually 100,000/mL), which do not decrease between tubes 1 and 4, is consistent with SAH (-) CT and LP essentially rules out SAH Patients diagnosed with SAH require 4 vessel cerebral angiography within 24 hours to assess for aneurysm or other vascular malformation Catheter angiography is the gold standard for assessing the patient s cerebral vasculature, relevant anomalies and presence, location, and morphology of the cerebral aneurysms SAH patients should be admitted to the neurologic ICU Hunt-Hess grade 4 or 5 require intubation and hemodynamic monitoring and stabilization. The current standard of care for ruptured aneursyms requires early aneurismal occlusion

 There are 2 options for occlusion: Craniotomy & Coiling The patient may undergo craniotomy with microsurgical dissection and placement of a titanium clip across the aneurysm neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel The 2nd option is to coil the aneurysm via an endovascular approach. The patient is taken to the interventional neuroradiology suite for placement of looped titanium coils inside the aneurysm dome

 The coils support thrombosis & prevent blood flow into the aneurysm Factors favoring craniotomy & clipping: Young age Good medical condition Broad aneurysm necks Factors favoring coiling: Age Medical comorbidities Narrow aneurysm necks Due to coil migration or compaction overtime, surgical clipping is believed to result in a more definitive cure Long term outcomes may be better in younger patient with clipped aneurysms

Outcome
Mortality rate of 50% in the 1st month Approximately 1/3 of survivors return to pre SAH function, and the remaining 2/3 s have mild to severe disability Most require rehabilitation after hospitalization Long term outcomes may be better in younger patient with clipped aneurysms

References
Schwartz s Principle of Surgery. 9th ed Harrison s Principle of Internal Medicine. 17th ed

Classification Etiology Clinical Presentation Treatment Outcome

Classification
Congenital
Arterio-venous Malformation Venous Malformation Capillary Telangiectasias

cquired
Cavernous angioma (cavernous Malformation) Dural Arteriovenous Fistula (Dural Venous Fistula)

Harrison s Internal Medicine 17th ed

Vascular Malformations
Hemorrhage to subarachnoid space- picture almost identical to ruptured saccular aneurysm (SA)- less severe Most AVM s in cerebral tissue- intracerebral bleeding more than likely 1/10 as common as SA Avm and SA associated with 5% of cases
Association increases with size of AVM and age of patient

Arterio-Venous Malformation
Tangle of dilated vessels forming an abnormal communication bet arterial and venous systems across the cortical surface or within the brain substance. Vary in size and blood vessels usually thin and do not have normal structures. Occur in all parts of Cerebral hemispheres brainstem, and Spinal cord.
Largest at posterior half of hemispheres- wedge shaped lesion extending from cortex to ventricle

Clinical Features
Bleeding & seizures Present at birth; Onset 10-30 y/o First clinical manifestation

50%- cerebral subarachnoid hemorrhage 30%- seizure 20%- headache 10%- progressive hemiparesis and FND

Chronic recurrent headache migraine-like headaches- parieto-occipital

 Huge AVM- progressive FND due to compression of neighboring structures

Enlarging mass of vessels & shunting of blood to dilated vessels (intracerebral steel)

Hydrocephalus- enlarged vein of Galendrainage of adjacent AVM Pulsating carotid arteries on neck, mastoid process or eyeballs- pathognomonic of AVM Fundoscopy- retinal vascular malfomation

DIAGNOSIS
CT- contrast infusion- 90% MRI- shows previous bleeding AVM Arteriography/Conventional Xrayangiography- gold standard Autopsy- dissecting microscope

Treatment
Surgical Excision
20-40% block dissection

Endovascular Embolization Ligation of feeding arteries

Radiosurgery
Single dose of subnecrotizing stereotactically directed proton radiation.
Photon radiation, linear accelerator, gamma knife

Slow scelerosis of arterial channels for 2-3 years Complication: delayed radiation necrosis & venous congestion

Venous Malformation
Consist purely of distended veins deep in the white matter and results in an abnormal cerebral, cerebellar, or brainstem drainage. Functional venous channels Vs AVM Mostly seizures and headache Little significance- ignored Surgical resection- venous infarction and hemorrhage

Capillary telangiectasia
True capillary malformation that forms extensive vascular networks on normal brain structure. Common: Pons, deep cerebral white matter Osler-Rendu-Webber- Hereditary Hemorrhagic telangiectasia Rarely produces mass effect/ significant symptoms No treatment options

Classification
Congenital
Arterio-venous Malformation Venous Malformation Capillary Telangiectasias

cquired
Cavernous angioma (cavernous Malformation) Dural Arteriovenous Fistula (Dural Venous Fistula)

Harrison s Internal Medicine 17th ed

Dural AV Fistula
May be Cranial and Spinal Cranial- nidus of abnormal atrteries and veins with AV shunting contained entirely within the leaflets of dura Origin of lesion not settled- not developmental Arise adjacent to venous sinus thrombosis or in association with vascular atresia
Transverse sigmoid sinus/ adjacent cavernous sinus

Dural AV Fistula
Acquired connection of dural sinus to dural artery Manifestations
Pulse-synchronous cephalic bruit (pulsatile tinnitus) Headache Cortical ischemia, venous hypertension- > subarachnoid hemorrhage

Dural AV Fistula
After forceful injury- remote to site of contact Klippel-trenaunay or osler-weber rendu syndromes Subdural hemorrhage is infrequent dramatic mode of presentation Large fatal clot

Cerebral-subarachnoid hemorrhage- ant cranial fossa, tentorial incisura. Seizures uncommon

Dural AV Fistula
Pseudomotor cerebri- headache, vomitting, papilledema ( highflow) High-flow shunt0- cause CHF DX- CT & MRI- thickening or enhancement of region of dura generally close to a large dural venous sinus
Injection of Gadolinium

TX: Surgery- small lesions ;Endovascular Embolization-larger and inaccessible lesions

Cavernous Malformation
Small hemorrhages- clinically silent Small hamartomatous lesions of multiple juxtaposed endothelium- lined cavites without interposed neural tissues

Cavernous Malformation
Diagnosis hypodense ferritin on T1 weighted imagesproduct of previous small episodes of bleeding Mostly in brainstem, pons, cerebral hemispheres and adjacent venous anomalies Treatment:
Surgical resection of cavernous angioma Low-dose proton-radiation Clinical MRI- cluster if vessels surrounded by zone of

Prognosis
With an overall risk of intracerebral hemorrhage of 2-4% per year, angiographic assessment is recommended to further define prognosis for patients with AVM. Those with superficial, moderate-sized AVMs have a good longterm prognosis and may not have any additional benefit with interventional treatment. Lifetime risk of hemorrhage may be substantial for young patients with AVM. Prognosis after AVM hemorrhage is generally better than that after intracerebral hemorrhage from other causes. Better prognosis may be due to the relatively younger age of patients and a greater potential for reorganization of brain function. More accurate prognosis awaits the results of currently active, long-term, population-based outcome studies.

Management of SAH
Early aneurysm repair prevents rupture and allows the safe application of techniques to improve blood flow (e.g. induced hypertension & hypervolemia) should symptomatic vasospasm develop An aneurysm can be clipped by a neurosurgeon or coiled by an endovascular surgeon Medical management of SAH focuses on protecting the airway, managing the BP before and after the aneurysm treatment, prevent rebleeding prior to treatment, mnageing vasopasm, treating hydrocephalus, treating hyponatremia & preventing pulmonary embolus