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This is really an oddity.  Elaine, I must ask this; when you say no intervention since December, is that statement limited to PERIPHERAL interventions?  If the patient had a coronary intervention (LMA stenting or perhaps even dual LAD or OM stents), cardiac output could have increased dramatically and be the cause of such a change. Just curious.
David Williams
David M. Williams, MS, RDCS, RVT
Technical Director, Vascular Ultrasound Lab
MUSC Health - Cardiovascular Surgery and Pulmonology
Florence Medical Pavilion
Suite B300, 805 Pamplico Highway, Florence, SC 29505
843-676-2760 (o) | 843-601-6629 (m)
[42D20F15]



From: UVM Flownet <[log in to unmask]> On Behalf Of Patricia Poe
Sent: Friday, May 10, 2019 9:13 AM
To: [log in to unmask]
Subject: [EXTERNAL] Re: Hyperemia flow


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This is an interesting scenario.  Can you describe the systolic acceleration / upstroke to the peak, or post an image of the waveforms?



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________________________________
From: UVM Flownet <[log in to unmask]<mailto:[log in to unmask]>> on behalf of Elaine Erickson <[log in to unmask]<mailto:[log in to unmask]>>
Sent: Thursday, May 9, 2019 10:30:03 PM
To: [log in to unmask]<mailto:[log in to unmask]>
Subject: Hyperemia flow

Hi, I  am looking for any published literature that could explain the following. In Dec 2018 patient presented with severe foot infection/would for arterial duplex. Waveforms were consistent monophasic from CFA through pop with flow through diastole, no focal stenosis. Contralateral normal waveforms. Read as possible inflow. Patient refused angiography and opted for follow up ultrasound that was performed today.

Today the patient stated that her wound has significantly improved and that she had no intervention since Decemer 2018. Today's waveforms were multiphasic throughout. The pop area was heavily calcified but there were high velocity and waveform abnormalities detected presumably from the pop but again heavily calcified. I don't  recall the pressures. What happened to the monophasic waveforms from 5 months ago?

I suspect hyperemia from more critical phase of the wound in December could have contributed to monophasic flow due to low resistance in inflamed foot.  I am hoping to find a paper on low resistant lower extremity waveforms for reasons other than proximal obstruction.. I am especially interested in proximal LE waveforms in the presence of distal infection/inflammation. Can anyone please lead me to a source. Thank you.

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