16.2 Transcranial Doppler (02.D)

Transcranial Doppler (TCD) is pulsed-wave ultrasound of the large intracranial arteries through relatively thin bone windows. On the exam it appears as a surveillance tool after aneurysmal subarachnoid hemorrhage, a way to separate vasospasm from hyperemia, a detector of microemboli, and—carefully—an ancillary pattern in death by neurologic criteria. Independent OpenExamPrep teaching covers TCD as listed under diagnostic studies (02.D). It does not replace catheter angiography, the clinical diagnosis of delayed cerebral ischemia, or the full brain-death chapter.

What the probe actually measures

TCD reports peak systolic, end-diastolic, and mean flow velocity (MFV), usually in centimeters per second, plus derived indices. Mean velocity in the middle cerebral artery (MCA) is the workhorse number after subarachnoid hemorrhage because the MCA is the easiest large vessel to insonate and because MCA spasm is common.

The Gosling pulsatility index (PI) is (peak systolic − end-diastolic) / mean velocity. A rising PI can accompany high distal resistance, including high ICP or distal vasospasm, but PI is not a substitute for an ICP catheter. Direction of flow (toward or away from the probe) and depth of insonation tell you which vessel you think you are in; guessing the vessel from velocity alone is a common error.

Windows and technical failure

Four windows matter:

1. Transtemporal — MCA, ACA, PCA, terminal ICA. This is the daily SAH study.
2. Transorbital — ophthalmic artery and carotid siphon; reduce power because of the eye.
3. Suboccipital / transforaminal — vertebrals and basilar.
4. Submandibular — extracranial ICA for the Lindegaard ratio.

Technical failure is not rare. About 10–20% of adults, disproportionately older patients and people with thicker temporal bone (hyperostosis), have inadequate temporal windows. Absent Doppler signal then means you could not insonate, not that the MCA is occluded. Confirm with another window, a different operator, or a different modality (CT angiography, catheter angiography, or perfusion imaging) before you treat absent TCD as absent flow. Poor angle of insonation, restless movement, and surgical dressings also degrade studies. TCD is operator-dependent; a single high number on one shift should be compared with the patient's baseline velocities from earlier days, not with a textbook in isolation.

Vasospasm surveillance after subarachnoid hemorrhage

Angiographic vasospasm and delayed cerebral ischemia (DCI) are related but not identical. TCD detects velocity changes that often accompany large-vessel narrowing. DCI remains a clinical diagnosis (a new focal deficit or a drop in consciousness not explained by hemorrhage, hydrocephalus, seizure, or infection). Do not start intra-arterial therapy from a velocity alone in a well patient, and do not dismiss DCI because yesterday's TCD was reassuring.

Commonly taught MCA MFV bands (always interpret with the Lindegaard ratio and the examination):

Daily studies from roughly day 4 through day 14 after aneurysm rupture catch the usual spasm window. A rising trend is more informative than one isolated value. Anterior cerebral and basilar spasm are harder to catch; the Sviri ratio (basilar MFV / extracranial vertebral MFV) is sometimes used for the posterior circulation, but MCA plus Lindegaard is the exam's core pair.

Lindegaard ratio: spasm versus hyperemia

High velocity is not automatically spasm. Fever, anemia, hypercarbia, induced hypertension, and global hyperemia all raise flow. The Lindegaard ratio is:

Lindegaard ratio = MCA MFV / extracranial ICA MFV

(the extracranial ICA sampled in the submandibular window)

Common teaching:

Worked example: MCA MFV 210 cm/s and extracranial ICA MFV 30 cm/s give a ratio of 7, which is severe-spasm teaching territory. MCA MFV 180 cm/s and extracranial ICA MFV 90 cm/s give a ratio of 2, which is hyperemia despite the impressive MCA number. Treating the second patient with balloon angioplasty as if the artery were string-like is the classic error.

TCD sensitivity versus digital subtraction angiography is only moderate and is best for the MCA; specificity is higher at extreme velocities. A normal TCD does not exclude distal or small-vessel spasm. Catheter angiography remains the anatomic reference when endovascular treatment is on the table.

Emboli detection

High-intensity transient signals (HITS) or microembolic signals are brief, unidirectional intensity spikes in the Doppler spectrum. They appear in carotid stenosis, after carotid or cardiac procedures, with mechanical valves, and in some dissection or vasculitis cases. Counting emboli is a specialized monitoring mode (often with a headset for a set time), not a 30-second bedside sweep. A few signals do not by themselves prove an indication for anticoagulation; they add a mechanism when the clinical question is artery-to-artery embolization versus hemodynamic failure.

Ancillary patterns in death by neurologic criteria

When the clinical examination and apnea test cannot be completed, some jurisdictions accept ancillary tests of cerebral blood flow. TCD patterns that support circulatory arrest include:

• Oscillating / to-and-fro flow (anterograde systole, retrograde diastole)
• Short systolic spikes without diastolic flow
• Eventually, no demonstrable flow if windows are adequate

These patterns are ancillary. They do not replace prerequisites, a complete brainstem examination, or apnea testing as taught in the brain-death chapter. Inadequate windows make TCD unusable as an ancillary test. Do not pronounce death by neurologic criteria from a single TCD screenshot, and do not confuse a high-resistance waveform in a living patient with intracranial hypertension for a death study.

What to do with a concerning study

If velocities and the Lindegaard ratio climb and the patient is worse, look for a treatable cause of DCI: hypovolemia, hypotension, anemia, hypoxia, fever, hyponatremia, hydrocephalus, and seizure. Nimodipine 60 mg orally every 4 hours for 21 days remains standard for aneurysmal SAH as a DCI-outcome drug; it is not a TCD-triggered rescue. Induced hypertension (not classic triple-H therapy) is the usual hemodynamic step for symptomatic DCI after the aneurysm is secured. Endovascular angioplasty or intra-arterial vasodilators are reserved for selected patients with clinical and imaging evidence of large-vessel spasm, not for hyperemia.

TCD is a trend tool. Pair it with the examination, ICP/CPP when a monitor is in place, and vessel or perfusion imaging when the story does not fit.