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