What is transcranial Doppler (TCD) monitoring?

Transcranial Doppler (TCD) monitoring is a non-invasive technique that uses ultrasound to assess blood flow velocity in the intracranial arteries. It provides real-time information on cerebral hemodynamics.

What arteries are typically monitored with TCD for vasospasm?

The middle cerebral artery (MCA), anterior cerebral artery (ACA), and posterior cerebral artery (PCA) are commonly monitored with TCD for vasospasm. These arteries are prone to vasospasm after SAH.

NEUROIMAGING / NEUROSONOLOGY

TCD/TCCD vasospasm monitoring

David Goldemund M.D.
Updated on 19/06/2024, published on 31/03/2021

vasospasm is a contraction of the muscular wall of an artery, resulting in its stenosis and reduced flow
the prevalence of vasospasms (VSP) following SAH is 50-70%
vasospasms in SAH patients occur around days 3 to 5 and last up to 3-4 weeks
approx. 30% of patients with aneurysmal SAH develop delayed ischemic deficit (DID) (Yamaki, 2019)
- DID is the leading preventable cause of poor outcome
increased risk of VSP is associated with:
- higher Hunt-Hess and Fisher scores
- baseline blood pressure
- fluid depletion
- low ejection fraction (EF)
the risk of complications increases with the number of affected arteries and hemodynamically significant spasms

Methods for Vasospasms Detection and Monitoring

transcranial Doppler ultrasound (TCCD/TCD)
- optimal bedside, cost-effective, and non-invasive method
CT angiography
- CT perfusion imaging (CTP) may help predict DID
MR angiography
- low sensitivity for detection of distal vasospasms
- MR perfusion may help predict DID
digital subtraction angiography (DSA)
- reserved for local endovascular treatment

TCCD criteria

it is recommended to start the examination on days 2-3 to obtain baseline velocities and then repeat every 24 hours to assess the dynamics
examine:
- PSV, EDV, V_mean
- PI and RI → more here
- to exclude the effect of hyperemia, determine the ACM/ACI ratio (Lindegaard Ratio – LR)
  - a value of LR >3 indicates spasm
a significant increase in velocity indicates vasospasm [Vora, 1999] [Lindegaard,1988]
- V_mean ≥ 120 cm/s ( ACM, ACA) + LR >3
- V_mean ≥ 80 cm/s (AV)
- V_mean ≥ 85-95 cm/s (AB) + LR > 2.5-3
critical value is ↑ Vmean > 50 cm/s/24 h or > 25%/24 h

Vmean = 1/3 (PSV-EDV)+ EDV

there is no correlation between the severity of vasospasm detected by ultrasound and the clinical course; the development of DID cannot be reliably predicted
a sudden increase in peripheral resistance (PI > 1.5) indicates either distal VSP or decompensated intracranial hypertension (if detected in multiple vessels)

Vessel	V_mean	Sensitivity/specificity
MCA, ACA	≥ 120 cm/s ≥ 200 cm/s (severe spasm)	88% / 78% 27% / 98%
ICA	≥ 90 cm/s	25 % / 93%
VA BA	≥ 60-80 cm/s ≥ 85-95 cm/s	44% / 79% (60cm/s) 77% / 79% (60 cm/s)
the positive predictive value of angiographic vasospasm in MCA is 87% with Vmean > 200 cm/s the negative predictive value of angiographic vasospasm in MCA is 94% with Vmean < 120 cm/s [Vora, 1999]

Lindegaard Ratio	vasospasm on DSA
< 3	no VSP
3-4.5	mild VSP
4.5-6	moderate VSP
> 6	sever VSP

[Lindegaard, 1988]