Diagnosis and management of patient with aneurysmal SAH pdfs/SAH Dr S… · Diagnosis and...

Diagnosis and management of a patient with aneurysmal SAH

Doctor, will my patient live?

• Incidence: 2-4/100,000/yr.

• seasonal and diurnal variation. G

• Greater frequency in winter and in early morning

• 30-day fatality rate: 30-40%

• 10-15% die before reaching a medical facility.

• Prevalence of cerebral aneurysms between 3-6% with 0.7% annual risk of

rupture.

Where has the bleeding occurred?

• AcommA: 36%

• MCA: 26%

• PCommA: 18%

• ICA: 10%

• Posterior circulation aneurysms: 9%

• multiple aneurysms: 20%

Is it only headache or SAH?

• Worst headache of life

• Sentinal headache (30-40%)

• Neck stiffness, back pain

• Seizures (20-25%) MCA,ICA, A1

Are there some symptoms peculiar to location of aneurysms?

• AComA: bitemporal hemianopia/b/l LL weakness. DI, Hypothalamic dysfunction

• PCommA: III N palsy.

• Caroticoophthalmic An: Unilateral visual loss:

• Cavernous carotid An: Facial/orbital pain, epistaxis, progressive vision loss or opthalmoplegia.

• Posterior circulation An: Symptoms of brain stem dysfunction

HuntandHessClassificationScale

GradeI Asymptomatic,mildheadache,slightnuchalrigidity

GradeII

Moderatetosevereheadache,nuchalrigidity,noneurologicaldeficitotherthancranialnervepalsy

GradeIII Drowsiness,confusion,mildfocalneurologicaldeficit

GradeIV Stupor,moderatetoseverehemiparesis

GradeV Coma,decerebrateposturing

*Addonegradeforthepresenceofaserioussystemicdisease(hypertension,diabetesmellitus,chronicobstructivepulmonarydisease,severeatherosclerosisorseverevasospasmonangiography).

How do I objectively assess Pt’s status?

Themodifiedclassificationhasthefollowingadditions:

Grade

Description

0 Unrupturedaneurysm

1a Noacutemeningeal/brainreaction,butwithfixedneurologicaldeficits

WorldFederationofNeurological

SurgeonsSubarachnoid

HemorrhageGradingScale

GlasgowComaScaleScore

MotorDeficit

I

15

Absent

II

14-13

Absent

III

14-13

Present

IV

12-7

Presentorabsent

V

6-3

Presentorabsent

FisherGradingScale

0

Unruptured

I

Nosubarachnoidblooddetected

II

Diffuseorverticallayer<1mmthick

III

Localizedandverticallayers>1mmthick

IV

Intracerebralorintraventricularclotwithdiffuseorno

subarachnoidblood

Hydrocephalus Sulcal blood Cistrens IVH Infarct: >6hrs shifts

How do I investigate?

ModifiedFishergrading

Grade Description

0 NoSAHorIVH

1 FocalordiffusethinlayerofSAH,noIVH

2 FocalordiffusethinlayerofSAH,IVHpresent

3 FocalordiffusethicklayerofSAH,noIVH

4 FocalordiffusethicklayerofSAH,IVHpresent

*IVH-intraventricularhemorrhage

Grade0and1patientshasalowriskofvasospasm,grade2patienthaveamoderate

risk,grade3patientshaveahighriskofvasospasmandgrade4patientshavethe

maximumriskofvasospasm.

CTA: sensitivity of 77% to 97% and specificity of 87% to 100% for detecting aneurysm > 3mm in size. In aneurysms of size < 3 mm, the sensitivity reduces to 40% - 91%.

When is DSA required?

• complex aneurysms with difficult anatomy • those planned for endovascular treatment • posterior circulation aneurysms • those with an additional vascular lesion like an AVM • negative CTA Negative DSA: Repeat after 6 wks

MRA Intraparenchymal bleed Non-nephrotoxic Fluid attenuated inversion recovery (FLAIR) and proton density sequences: acute blood Gradient echo T2 sequences: subacute blood

What do I do first of all? Airway, breathing, circulation H&H I and II: EVD for hydrocephalus, evacuation of IP hematoma H&H III-V: GCS<8: consider intubation, ICP monitoring Resuscitation; CPP: 55 to 77 mm Hg; MAP: 70 -90 mm Hg SBP: <140 mm Hg

bed rest, elevation of head-end of bed to 30 degrees, restriction on number of visitors, avoidance of unnecessary stimulation, graduated compression stocking or pneumatic compression devices Foley’s catheterization, nasogastric tube feeding, stool softeners, laxatives and analgesics, intravenous fluids, anticonvulsants

Are there some Electrolyte and fluid management issues?

Fluid depletion predisposes to vasospasm Hyponatremia with dehydration: Cerebral salt wasting with euvolemia/hypervolemia: SIADH

In the past, early intervention was advocated for patients with a good grade SAH while conservative management was advised for poor grade patients until they achieved a good grade. Recent studies have shown that with an early exclusion of aneurysm using coiling or surgery, patients are more likely to be discharged with a good outcome.

Clipping versus coiling: which is better?

The International Subarachnoid Aneurysm Trial (ISAT), a prospective, multicentric, randomised control trial compared endovascular treatment versus surgical coiling in good grade SAH patients. Primary outcome (death or dependency at 1 year): Better in the coiling group (23.5%) as compared with surgical clipping group (30.9%). Rate of rebleeding, however, was more frequent in the coiling group (2.6%) in comparison to surgical clipping (1%) at a 1-year follow up. 5-year follow up of results from ISAT trial re-affirm a reduced mortality rate in the coiling group in comparison to the clipping group.

Coiling Posterior circulation aneurysm CO, paraclinoid cavernous aneurysms Factors that may limits endovascular coiling Dome / neck ratio < 2 Neck width > 4mm Inadequate endovascular access Unstable intraluminal thrombus Aneurysm diameter less 3 mm Clipping Young patients with MCA, ICA aneurysms Hematoma Giant aneurysms with mass effect

What are the causes of delayed deterioration after SAH? Rebleeding Increase edema surrounding the hematoma, contusion and infarct. Infection Hydrocephalus Electrolyte imbalance Vasospasm

How does one manage vasospasm?

4-14 days 66% radiological 30% clinical

Angiography, transcranial Doppler, CT perfusion, MRA angiography and diffusion/perfusion weighted sequences TCD: maximum sensitivity for middle cerebral artery vasospasm. A velocity >120 cm/sec suggests mild vasospasm and a flow velocity >200 cm/sec is consistant with severe vasospasm. The ratio of flow velocity in intracranial and extracranial vessels is known as the Lindegaard ratio (Vmca/Vica). A Lindegaard ratio >3 is consistent with vasospasm

Nimodipine may be given by the intravenous or the oral route. Orally: 60 mg 4 hourly Intravenously 0.2 mg/ml at 10 ml /hr. Usually admininstered for 3 weeks. Statins act by multiple mechanisms of actions and have anti-inflammatory, antiplatelet, antioxidant and vasomotor effects.

Calcium channel blockers

What is the treatment of vasospasm?

What are the targets of Triple H therapy?

Hypertension + hypervolemia and hemodilution (improved rheology increase CBF) Noradr/Dopa Targets: CVP: 8–12 cm H2O, Venous hematocrit: 30–35%, and MAP:20 mm Hg >preoperative values

PerioperativegoalsformanagingahighgradeSAHParameter Pre-securing Post-securing Symptomaticvasospasm

SBP 100-140mmHg 100–180mmHg 140–200mmHg

MAP 70–90mmHg 70-100mmHg 100-130mmHg

Fluidstatus Euvolemic Euvolemic Euvolemic

CVP

5-8mmHg

5–8mmHg

5–8mmHg

What is the role of Endovascular therapy?

1. Coiling 2. Treating other pathology like AVMs 3. Balloon angioplasty and intrarterial nimodipine for vasospasm 4. Suction decompression of giant aneurysm

Post DSA status

Intra-arterial nimodipine injection

Outcome of aneurysmal SAH 1. Hunt and Hess grade at presentation 2. Age 3. Co-morbid conditions 4. Extent of bleed on CT 5. Intracerebral or intraventricular extension,

location 6. Size of the aneurysm 7. Presence of vasospasm.