SAH & TCD
-Dr.Nikhil
Cerebral arterial anatomy
SUBARACHNOID HAEMORRHAGE
• not into the brain parenchyma
• incidence of SAH is around
6/100,000
• F/M 1.24 : 1. Age 40-60yrs
• mortality is 50%, of which 15%
die before reaching hospital,
with up to 30% of survivors
having residual deficit-producing
dependency.
PATHOLOGY
• saccular (berry) aneurysms (85%),
• non-aneurysmal perimesencephalic haemorrhage (10%)
• arterial dissection,
cerebral or dural AVMs,
mycotic aneurysm,
pituitary apoplexy,
vascular lesions at the top of the spinal cord and
cocaine abuse
• bifurcations in the circle of Willis
• congenital weakness in the tunica media,
• Sudden hypertension plays a role in causing rupture,
RARE
CLINICAL PRESENTATION
• ‘thunderclap’ headache developing in seconds f/b
• period of depressed consciousness for less than 1 hour in 50% of
patients, with focal neurology in about 30% of patients
• Meningism – neck stiffness, photophobia, vomiting and a positive
Kernig’s sign,brudzinki sign – is common in those patients with higher
GCS
• Atypical features – Seizures, acute encephalopathy
Focal physical findings in SAH
CT IMAGING
first diagnostic tool
Blood-hyperdense
excluding other pathologies
Sensitivity -98.7% <6hrs
-85.7%@24hrs
-50%@7days
Pattern of hemorrhage
• false-positive - severe generalised oedema resulting in
venous congestion in the subarachnoid space.
• false-negative 2%. Small amounts of blood may not be
detected,
Lumbar puncture
TIMING – ATLEAST 12 HOURS
AFTER RUPTURE
suspicion of SAH is high despite a negative CT
LOOK FOR 1) RBC2) xanthochromia
presence of RBCs>2,000 × 106 in the fourth tube
Oxyhemoglobin- bilirubin – xanthochromia
Spectrophotometry-Oxyhemoglobin of traumatic tap Vs bilirubin of SAH
exclude infection
CT ANGIOGRAPHY
Alternative to LP after a negative non-contrast CT
When Lumbar puncture C/I
post-test probability of disease of < 1%( below which
no further investigation is required)
sensitivity of CTA is 92.3% for aneurysms < 4mm
MR ANGIO
95% sensitive aneurysms > 3 mm
atypical cases
long delay
DSAngiography
DSA is the diagnostic tool of choice in cases where CTA is still inconclusive
ED Management
• ABC and EVD (High grade acute SAH)
• Intubation - low GCS/protect the airway
• stabilization of hemodynamics/risk for
neurocardiogenic stunning
• next priorities -reduce SBP and reverse
anticoagulation to mitigate the risk of aneurysm
rerupture
• BP control : SBP< 160 / MAP < 110 mm Hg
Labetalol /Nicardipine/hydralazine
• Pain control/Antiepileptics – poor Neurological
exam or high SAH
• Disease Severity Scoring
• Admission/transfer to high volume centre
Nicardipine 5mg/h IVmay increase by 2.5 mg/h q5–
15 minutes (min); Max: 15 mg/h),
labetalol (start 20 mg IV ,40–80 mg iv q 10 min; Max
300 mg/total dose;
clevidipine (start 1–2 mg/h IV double rate q 90 sec;
max:32 mg/h)
hydralazine -setting of bradycardia
Nitroprusside and nitroglycerin should be
avoided(vasodilatory and inc ICP)
phenytoin (load 10–20mg/kg IV max: 50mg/min),
fosphenytoin (10–20 (PE)/kg IV; over 30 min;
max: 150mg PE/min) and
levetiracetam (15–20mg/kg over 30 min).
Fentanyl/paracetemal
1967 HESS & hunt scale
Higher grades - associated with increased surgical risk for the repair of ruptured intracranial
aneurysms
1975 Glasgow Coma Scale (GCS)
1988 - World Federation of Neurosurgical Societies (WFNS)
1980 – fisher CT GRADING scale
Modified fisher scale
Over the last 30 years, it has become clear that the greater the
amount of blood within the basal cisterns, the greater the risk of
vasospasm.
Ogilvy & carter grading – OUTCOME PREDICTION age>50/ HHS 4,5/ fs 3,4 /size>10mm
COMPLICATIONS
REBLEEDING - 9%–17% first few hours/
AHA- “For patients with an unavoidable delay in obliteration of aneurysm, a significant risk
of rebleeding, and no compelling medical contraindications, short term (< 72 hours)
therapy with tranexamic acid or aminocaproic acid is reasonable to reduce the risk of early
aneurysm rebleeding” (Class IIa recommendation;level of evidence B)
• ε-aminocaproic acid: 4 g IV loading followed by 1 g/h continuous IV infusion. Stop the
infusion prior to obliteration of the aneurysm
ACUTE HYDROCEPHALUS -15-20% first 24 hours/ characterised by a drop in the
GCS /sunset eyes /ventricular drain .
• Syndrome of the Trephined (Sinking Skin Flap Syndrome) paradoxical herniation after CSF diversion
DELAYED CEREBRAL ISCHAEMIA 30% onset of focal neurological deficit,
 a drop in GCS by 2 or more points,
 cerebral infarction that occurs typically 4–12 days post SAH unrelated to aneurysm treatment or
other causes hydrocephalus, cerebral oedema or metabolic disorder
PARENCHYMAL HAEMATOMA 30% worse prognosis
 mass effect - evacuation and simultaneous clipping
Definitive treatment
• Multidisciplinary
Neurosurgeon/Interventionali
st/Neurointensivist
• Coiling vs Clipping – Patient
age, aneurysm morphology
and location, comorbidities
ISAT trial
lower rate of dependence,mortality and
seizures in coiling group. However, non
complete obliteration and rebleed higher.
Overall,
coiling preferred to clipping when feasible.
ICU Management : Neurologic complications
?(A-comm) - coiling - ICU - ICP of 50 to 55 mm Hg / MAP of 100 mm Hg
Antishivering
first battle -against elevated ICP – stepwise approach
methods
negative impact on the CPP
Skin counterwarming
IV magnesium
EVD/Surgical Decompression
Buspirone,
IV dexmedetomidine
Step 1: Sedation with Short-Acting Agents
IV meperidine
IV propofol: 1 to 2 mg/kg initial bolus, maintenance 5 to 50 μg/kg/min
IV propofol
IV clonidine
IV midazolam: Load 0.01 to 0.05 mg/kg ,maintenance 0.02 to 0.2 μg/kg/h
IV fentanyl: IV bolus 25 to 100 μg, followed by maintenance 1 to 3 μg/kg/h
Step 2: Hyperventilation and Order Osmotic Agents
Hyperventilation-refractory ICP crisis and brain herniation/Target end-tidal PCO2, 30 mm Hg
Mannitol: 1 to 1.5 g/kg,q6h
Hypertonic saline (HTS): Avoid serum Na > 155 mEq/L.
Step 3: Barbiturate Coma
Pentobarbital: Load 10 mg/kg IV infusion over 1 hour, maintenance 1 to 3 mg/kg/h
Step 4: Therapeutic Hypothermia 32-34°C
CPP Optimization
• ICP, 40 mm Hg; MAP, 90 mm Hg; a CPP, 50 mm Hg,
?icp/start vasopressor
• systemic hypotension + high ICP + low CPP
?icp/start vasopressor
• Systemic hypotension and uncontrolled ICP
Worst combination
MAP- 100 ICP-15= CPP > 85 Pbto2 < 15 mm Hg, and the LPR is > 50?
Improve brain oxygenation reduce brain metabolic stress
Delayed cerebral ischemia
• Defined as any neurological deterioration ( focal
or global ) presumed secondary to cerebral
ischemia that persists for more than an hour
and cannot be explained by any local/systemic
complication.
• Diagnosis of exclusion –
Hydrocephalus/Seizures/Sedation/Metabolic
• ~ 30% of patients
• Pathophysiology
• Risk for vasospasm increases with thickness,
density, location and persistence of
subarachnoid blood
• Poor clinical grade, h/o LOC, smoking, cocaine,
hyperglycemia, SIRS, hydrocephalus increase
risk of delayed cerebral ischemia.
DCI - Management
• Prophylaxis : Nimodipine 60 mg q 4 hrly.
Euvolemia
• Monitoring : Clinical checks q 2hrly
: CT @ 24 hrs after securing aneurysm, 3-5 and 7-10 days
: TCD – Mean Cerebral blood flow velocity
< 120 cm/s – No vasospasm
> 200 cm/s – Vasospasm
Rise > 50 cm/s in 24-48 hrs – High risk
LindeGaard Ratio > 3 –Vasospasm
: CTA/DSA
: EEG/Brain tissue O2 monitoring
• Vasospasm Watch Period-typically bleed days 4 to 14, but can occur as late
as day 21
patient does not have any signs (clinical, TCD, CTA/P, or cEEG findings) of vasospasm
Euvolemic
Maintain normal BP
Normal CO and index
WHAT IF SIGNS +
Hypervolemic
Hypertensive
 Hyperdynamic cardiac perf.
Avoid anemia Hgb < 7.
• Avoid low PAWP < 10.
• Avoid low GEDVI < 680 mL/m2.
• Avoid high SVV and PPV > 13%.
• Avoid low SVI < 40 mL/m2.
• Avoid low UO< 0.5 mL/kg/h.
MAP, 60 to 90 mm Hg
CO, 5 to 8 L/min
• CI, 3 to 5 L/min/m2
Invasive therapeutic options for symptomatic vasospasm
Intraarterial (IA) therapy-papaverine, nicardipine, verapamil,
milrinone and nitroglycerin :positive effect may not last long
Balloon angioplasty :SAFETY
Intrathecal Infusion and Basal Cistern Implants of Calcium Channel
Blockers:nicardipine
Intra-aortic Balloon Counterpulsation Therapy : neurogenic stunned
myocardium /allow continuation of triple-H therapy
• NeuroFlo Device:acute phase of ischemic brain injury. SENTIS
? Mg, ? Statins , ? Endothelin antagonists
Systemic complications and management
• Cardiopulmonary
• Fever
• Thromboembolism : SCD ,
UFH after securing aneurysm.
• Glucose abnormalities : Target
80-180 mg/dL
• Hemoglobin : 8-10 g/Dl
• Hyponatremia : SIADH vs Salt
wasting .
Neurogenic Stunned Myocardium
• takotsubo cardiomyopathy/broken-heart syndrome/contraction band
necrosis syndrome/ Gebrochenes-Herz syndrome
• stress is mediated by the brain -acute SAH with intense ICP elevation,
inflammation, and sympathetic surge
• not to be induced by coronary artery atherosclerosis or plaque
rupture as in typical acute coronary syndrome (ACS).
• Normal base, abnormal apex
• triple-H therapy - >HARMFUL
systemic hypotension
forward/systolic failure with severely depressed EF
new-onset heart failure
nonspecific T-wave “cerebral T”or ST- abnormalities
Point-of-care transcranial Doppler
• 1982, Aaslid et al. introduced
• Principle: Doppler shift (ΔF).
Technique
• 2 MHz ultrasound probe /4 MHz or more for
extracranial vessels
• Acoustic windows - transtemporal, transorbital,
suboccipital and submandibular windows
• Depth to the distance of the third ventricle
• color Doppler box over the top half of the screen
(near field) where the MCA is located, just lateral to
the cerebral penducles
• Insonate ACAs (anterior angulation, depth 6–7 cm),
• Terminal ICAs (caudal angulation, 6–7 cm), and
• PCAs (posterior angulation, 5.5–7.5 cm),
In order to identify the intracranial arteries
1. Acoustic window through which the vessel is
insonated
2. Depth of sample volume
3. Transducer orientation during insonation
4. Direction of blood flow with respect to the
transducer
5. Relationship of the vessel to the junction of
MCA,ACA,ICA
6. Response to dynamic manoeuvres (e.g.,
compression of the common carotid artery
resulting in a temporary decrease in ipsilateral
MCA velocity).
GOSLINGS PI = PSV-EDV/MFV
0.5-1.19
PSV
EDV
MDV
TAPV/MFV
PI
HR
Duplex sonography refers to the use of TCD machine for
study of flow velocities along with tissue imaging.
power-motion mode Doppler (PMD)
provide information about the complete length of an artery.
SIMULATION
Vasospasm
• inverse relationship between cerebral blood vessel diameter and TCD
mean velocities, we are able to quantify and subcategorize vasospasm
Progressive increase of mean velocities during
the early stages of SAH to predictive of vasospasm
change in baseline mean velocity of
21 cm/s per 24 h in the first 3 days
to
be diagnostic of vasospasm
Lindegaard Ratio helps differentiate between hyperemia versus the onset of true
vasospasm
Vasospasm: limitations
• trans-orbital and trans-foraminal windows are less reliably insonated
compared to the trans-temporal window
• ACA and PCA are less sensitive and specific for vasospasm compared
to the MCA.
• basilar artery and vertebral artery with lower sensitivity and
specificity
• blood flow may be influenced by many factors (PaO2, PaCO2,blood
viscosity, collateral flow)
• operator experience is required
Midline shift
• Any amount of midline shift is considered abnormal, but
poor neurological outcome can be associated witha
clinically significant midline shift of as little as 0.5 cm
If positive, MLS is away from the ipsilateral sid
presence of hydrocephalus of the third ventricle does
not have much bearing on the MLS measurement
Intra-cranial pressure
• rough estimate for ICP, to help rule-in high ICP, GOSLINGS PI
• systolic velocity increases- diastolic flow becomes decreased/blunted
• Recommendations ICP and CPP trends THAN ICP absolute values
LIMITATIONS: PI affected by Paco2 and MAP
NON PULSATILE FLOWS
Cerebral circulatory arrest
• step-wise changes in cerebral blood flow
• decreasing or blunted diastolic flow, oscillating flow (diastolic flow
reversal),sharp systolic peak flows, then finally, zero FLOW
Cerebral circulatory arrest criteria by TCD
Certain situations (i.e., presence of spinal
reflexes, drug ingestions, and profound hypothermia/
shock) may lead to confounding with brain death
determination if relying on clinical testing alone.
If TCD rules in arrest by non-reassuring MCA flows,
ancillary testing (4-vessel cerebral angiography,
nuclear medicine radionuclide brain perfusion scan, CT
or MR cerebral blood flow angiography) could be sought
to formally confirm the diagnosis
TCD evaluates cerebral circulatory arrest, not brainstem function.
medical jurisdictions will not accept a TCD as its own ancillary test to confirm brain death
save premature,unnecessary serial ancillary tests, until the diagnosis can be first confirmed on TCD
MILRINONE LACTATE INJECTION
• inotropic/vasodilator, improves diastolic function,
not a beta-adrenergic agonist, no increased effect on
myocardial oxygen consumption
• Phosphodiesterase III inhibitor
• LOADING DOSE 50 mcg/kg
maintainence :0.2 mcg/kg/min to 0.7 mcg/kg/min
• elimination half-life of 2.4 hours
• excretion is via urine
• contraindicated in patients who are hypersensitive
Tachy arrythmias
Hypotension
Headaches
NIMODEPINE
• calcium channel blocker
• oral dose is 60 mg (two 30 mg capsules) every 4
hours for 21 consecutive days , within 96 hours
of SAH
• orally or via a naso-gastric tube
• hepatic cirrhosis - 30 mg capsules every 4 hours
( CLEARANCE )
ADVERSE EFFECTS
Take home points
SAH –more common in F>M 40-60ys age ,mortality >50%
HTN,smoking ,alchol,cocaine are only modifiable risk factors
saccular (berry) aneurysms (85%)
Thunderclap headache + meningism +unconsciousness favour SAH
CT IMAGING – FIRST DIAGNOSTIC TOOL 98.7% <6hrs
Lumbar puncture TIMING – ATLEAST 12 HOURS AFTER RUPTURE
DSA is the diagnostic tool of choice where CTA is still inconclusive
HHS - increased surgical risk for the repair
GCS & WFNS - long term outcome
MFS – vasospasm
REBLEEDING - 9%–17% first few hours/ tranexamic acid or
aminocaproic acid
ACUTE HYDROCEPHALUS -<24hRS – EVD
ISAT trial - coiling preferred to clipping when feasible
OPTIMIZE –icp/cpp/MAP/pbo2/LPR
Vasospasm Watch Period-typically bleed days 4 to 14, but can occur
as late as day 21
No prophylactic HHH therapy
Hyponatremia : SIADH vs Salt wasting
takotsubo cardiomyopathy - systemic hypotension + forward/systolic
failure with severely depressed EF <40%
• TCD -Principle: Doppler shift (ΔF).
• TAPV/MFV –lindegard ratio –vasospasm vs hyperemia
• Sensitivity and specificity more for MCA for detecting vasospasm
• GOSLINGS PI = PSV-EDV/MFV –----- ICP
• Lindegaard Ratio helps differentiate between hyperemia
versus the onset of true vasospasm
• Tcd – icp/mls/cerebral circulatory arrest
• Nimodepine and milrinone shown promising results others
need further trials for safety