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Management of Intermittent Claudication Case

Discussion in 'General Issues and Discussion Forum' started by Donna, Sep 1, 2008.

  1. Donna

    Donna Active Member


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    Hi everyone,

    I was hoping I could get an opinion on a patient seen at the clinic here with intermittent claudication of approximately 2.5 years duration. :eek:

    The patient is a 54 year old male, who presented 2/52 ago with cramping in the calves during exercise, which he cannot push through. The pain is relieved immediately on rest. The right leg is 3 times worse than the left leg, with regard to cramp/pain levels. The onset of the episodes of claudication began when the patient changed occupation - from standing at a newsagency to sitting at a desk job as a mortgage broker... The pain has progressively worsened over the past 2.5 years, and the patient was a previous smoker.

    On examination (from pt's file):
    "Stance:
    - very pronated midfoot - planus
    - miserable malignment syndrome
    - heel rise - left is fine - right difficult
    - splayed forefoot (4 to 6E width), narrower heels
    Circulation:
    Pulses:
    DP: L +++, R +++
    PT: L + to ++, R absent
    Popliteal: unable to palpate, non conclusive
    - No colour difference between feet
    - Right foot skin slightly more scaly
    - No muscle wasting
    Tarsal tunnel fluid ++ bilat - no pain on palpation"


    An ultrasound of the right calf and foot was performed (as advised by a colleague - musculoskeletal practitioner) and showed "The posterior tibial artery is patent with mural calcification and shows irregular thinning" and concluded "diseased but patent posterior tibial artery. Further assessment with CT angiography may be appropriate if the patient's renal function is preserved. Alternatively, a formal arterial Doppler of the right lower limb could be arranged".

    We haven't seen too many patients with intermittent claudication, and therefore are unsure what "Further assessment with CT angiography may be appropriate if the patient's renal function is preserved" means...

    We feel that biomechanical issues are contributing partially to the patient's chief complaint, and we can address that here, but where would it be appropriate to refer for further investigation of the claudication? Is a vascular surgeon the way to go? Or should we refer to a Podiatrist colleague (who we often refer to for second opinions and is more experienced in this field of vascular disease)?

    Any advice would be muchly appreciated.

    Regards

    Donna ;)
     
  2. LuckyLisfranc

    LuckyLisfranc Well-Known Member

    Donna

    CT angiography is probably overkill, and may provoke renal events following contrast administration. Hand held Doppler, Duplex and ABI and other non-invasive tests should easily confirm the diagnosis of PAD.

    In such cases the following can be considered, depending on the severity and nature of the occlusion;

    1. Graded exercise program to improve collateral flow
    2. Platelet modifiers
    3. Angioplasty
    4. Bypass

    If you feel don't feel confident, refer to a colleague with expertise in vascular disease or a vascular surgeon.

    LL
     
  3. David Wedemeyer

    David Wedemeyer Well-Known Member

    Hello Donna,

    What you describe sounds very much like neurogenic intermittent claudication of a spinal etiology, especially in light of the fact that ultrasound reveals a diseased but patent PT artery in this patient. I am no expert in arterial issues and I could be way off, but would like to offer another differential. Does he have a history of low back pain?

    Where vaso-occlusive claudication is generally relieved by rest, it is not positional. Neorogenic claudication can be relieved by sitting, bending forward and squatting, any position which increases the lumbar lordosis. It is almost always an acquired etiology ie. Spondylolisthesis causing spinal stenosis, space occupying lesion, disc herniation, but can be aggravated by congenital factors such as short pedicles, thickened ligamentum flava, scoliosis, increased lumbar lordosis or congenitally narrow spinal spinal canal dimensions (<12mm).

    In these patients the history and symptoms is all telling and although the seated position usually improves the pain of neurogenic claudication it can exacerbate the complaint in cases where there is a lumbar disc or space occupying lesion.. Where each type exhibits a complaint of cramping and weakness on exertion, neurogenic claudication will almost always include a burning sensation and include the thighs. There are also often skin and trophic changes in the vascular patient as well as impotence not found in the neurogenic patient.

    Any erect or extended position of the spine such as walking, laying prone or slouched seated positions will cause narrowing of the vertebral canal and this is where it gets confusing because walking affects each type of claudication but for different reasons. Neurogenic patients typically assume a stooped posture and this is very telling in my experience. A vascular claudication patient will experience a reduction in symptoms by resting the legs while standing where a neurogenic patient will not; in fact standing exacerbates the neurogenic patient.

    I think we need more history here.

    One simple test to differentiate the two is to have the patient walk or pedal a stationary bicycle until the cramping begins and then have the patient lie flat on their back with their legs elevated. If the pain is relieved immediately then you can assume that their complaint is of a vascular origin because while leg exertion increases vascular claudication and elevating the legs improves circulation, lying flat on the floor without support causes mild extension of the lumbar spine and does not relieve neurogenic symptoms.

    If this test is negative have the patient repeat the above exertion and when the symptoms resume have him assume a seated position while resting the elbows on the thighs. The change in position and release of tension on the lumbar spine will usually relieve the pain of neurogenic claudication rapidly.

    You could whittle down the differential in this way and thus make a sound clinical decision on which provider to refer out to for further evaluation. I see this complaint fairly often in practice and the majority is of a spinal etiology. Unless there are absent pulses, signs of trophic changes and impotence they are always referred to a neurologist and/or orthopedic spinal specialist initially.

    I agree with Lucky Lisfranc that CT is probably overkill at this point. If there is a low back history or findings that suggest a spinal etiology an MRI of the lumbar spine is indicated. Neurogenic claudication can affect deep tendon reflexes and evoke vascular changes over time so this is not an easy case and requires more investigation.

    I hope this helps and keep us posted as to this patient’s diagnosis.

    Regards,
     
    Last edited: Sep 1, 2008
  4. Admin2

    Admin2 Administrator Staff Member

  5. Donna

    Donna Active Member

    Thanks LL & David, we're seeing the patient again next week for review, so will take your advice on board. :drinks

    David, your comments about neurogenic vs vascular origin of claudication are fascinating, and the test that you described to differentiate between the two will be very useful to arrive at a more specific diagnosis...

    I'll keep you posted with how we go next week... ;)

    Regards

    Donna
     
  6. Adrian Misseri

    Adrian Misseri Active Member

    G'day Donna,

    Would be interesting to see the ABI/TBI results for this patient. With advanced atheroscosis you may still be able to palpate the pedal arteries as they are 1. held open, and 2. adequate for normal activity, however when more is asked of the muscles in the legs, symptoms occur. How much excercise is the patient able to do befoe symptoms? I find that my patients with intermittent claudication generally don't get too far before the cramping stops them, literally about 100 meters or so of walking, so if your patient is getting to an active excercising point, it may be a compartment syndorme developong in the posterior compartments. That being said, if it is early stage IC, the pain would definately be ischaemia. I'd be sending the patient back to the GP for a referal to a vascular surgeon, as well as encouraging the patient to continue excercise, as more excercise will help to improve the health and flow through the vessles less affected with the atherosclerosis. Look for other cardiovascular signs as well, most patinet I've found with IC generally have stable ischaemic heart disease, or at the very least hypertension.

    Hopefully that helps
    Cheers!
     
  7. Donna

    Donna Active Member

    Hi Adrian,

    Good point there... the patient reported that onset of symptoms was after 10 minutes of walking, and is worst with faster walking, therefore we were considering vascular, biomechanical, or a combination of both to be causes for the claudication-like pain. So compartment syndrome could definitely be a differential diagnosis to add to the list... ;)

    We've got a few more things to look for when we see the patient next week, so shall keep you all posted... Thanks heaps everyone for your advice, it's very much appreciated! :D

    Regards

    Donna
     
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