Clinical History
A 60-year-old male patient admitted for the evaluation of a syncopal episode. The patient had been in his usual state of health until the morning of admission when, while climbing a flight of stairs,
he had turned his head to the right and had abruptly passed out. The patient denied any history of chest pain, palpitations, visual changes or aura, bowel or bladder incontinence, tongue biting, or
postictal state.
Imaging Findings
A 60-year-old male patient was admitted for the evaluation of a syncopal episode. The patient had been in his usual state of health until the morning of admission when, while climbing a flight of
stairs, he had turned his head to the right and had abruptly passed out. The patient denied any history of chest pain, palpitations, visual changes or aura, bowel or bladder incontinence, tongue
biting, or postictal state. He had had no previous episodes of presyncope or syncope. His medical history included longstanding hypertension, hypercholesterolaemia, and tobacco usage. On physical
examination, his body temperature was found to be 36.5 ÂșC, the blood pressure was 150/89 mm Hg (right arm), heart rate 86/min and respiratory rate 21/min. No carotid bruits were heard. The lungs
were clear bilaterally. The cardiac examination showed a regular rate and rhythm, normal S1 and S2, and no murmurs, rubs, or gallops. The findings of abdominal and neurological examinations were
normal. The peripheral pulses were positive throughout, with the notable exception of the left radial and brachial pulses. On discovering the nonpalpable left radial and brachial pulses, the blood
pressure was measured in the left arm and found to be markedly low, at 80/40 mm Hg. The admission complete blood count, chemistry panel (including cardiac enzymes and troponin), electrocardiogram,
and chest radiograph were all found to be unremarkable. The result of noncontrast computed tomography of the head was negative for haemorrhage, infarct, or mass effect. The clinical findings were
highly suggestive of a subclavian steal. The carotid duplex ultrasonography showed antegrade flow in early systole, retrograde in mid and late systole, and antegrade in diastole, and the presence of
an abnormal, stenotic left subclavian artery.
Discussion
The standard colour-duplex sonogram of the carotid circulation includes images of the vertebral artery. Despite an often limited image of this vessel in its intervertebral segment, significant
information can be inferred about the proximal brachiocephalic vessels. The blood flow pattern should resemble that of the internal carotid artery. The normal direction of blood flow is towards the
head. A completely reversed pattern of blood flow is seen when the subclavian artery on the same side of the neck is occluded or has a severe stenosis. An occlusion or near occlusion of the
subclavian or brachiocephalic artery proximal to the vertebral origin will result in retrograde flow in the ipsilateral vertebral artery as it fills via the contra-lateral vertebral artery through
the basilar artery. On the left side, the subclavian steal can be caused only by occlusion or near occlusion of the left subclavian artery. On the right side, the subclavian steal can be caused by
occlusive disease of the right subclavian artery or the brachiocephalic artery. These two right-sided lesions can be differentiated by the appearance of the right common carotid artery waveform. If
the lesion involves the subclavian artery, the common carotid artery waveform will be unaffected. When the lesion is in the brachiocephalic artery, retrograde flow in the vertebral artery will supply
not only the distal subclavian but also the right common carotid artery. As the right common carotid artery flow is via collaterals, the waveform is parvus-tardus with a slower-than-normal upstroke
and diminished peak systolic velocity. Clinically, the subclavian steal syndrome can produce symptoms of vertebrobasilar insufficiency, especially when the arm is exercised. The other findings
include an arterial insufficiency of the arm and a diminished brachial blood pressure. Subclavian steno-occlusive disease produces neurological symptoms when compensatory flow to the subclavian
artery from the vertebral artery diverts too much flow toward the arm and away from intracranial structures. The quality of collateral blood supply and the capacity to increase collateral flow to the
intracranial circulation (the brainstem in particular) may be the principle determinant according to which the patient develops neurological symptomatology. Significant stenosis of the subclavian
artery can produce a partial steal. The flow in the ipsilateral vertebral artery is antegrade in early systole, retrograde in mid and late systole, and antegrade in diastole. It is only during
systole as the velocity rises, that the pressure gradient across the stenosis is great enough to be haemodynamically significant. The pressure in the arm distal to the stenosis becomes lower than the
pressure in the vertebral system, and the flow proceeds retrograde, down the vertebral and into the distal subclavian artery. In diastole, the gradient across the stenosis is low and the pressure in
the distal subclavian artery reverts to its normal relationship with its branches, and antegrade vertebral artery flow occurs. The goals of treatment are to restore antegrade vertebral artery flow,
to alleviate cerebral hypoperfusion and its associated symptoms, and to improve arterial perfusion to the upper extremity. The treatment options are the percutaneous revascularization and the
surgical revascularization procedures.
Differential Diagnosis List
Partial subclavian steal syndrome.
Final Diagnosis
Partial subclavian steal syndrome.