Issue 20 / 1 June 2015

WE all understand that clinical suspicion has a low sensitivity and poor specificity for venous thromboembolism.

This does not reduce our distress when a patient dies from pulmonary embolism (PE) after some days or weeks of intermittent or progressing symptoms that, in retrospect, were precursor events.

In days when autopsies were done more often, fatal PE was notoriously unsuspected or misdiagnosed before death. How could we have better recognised these warnings, requested imaging, started therapy and perhaps avoided the fatal outcome?

Coroners are required to make recommendations that “might prevent, or reduce the likelihood of, a recurrence of an event similar to the event that was the subject of the inquest”.

Two cases of fatal pulmonary embolism in South Australia have aroused the interest of the State Coroner.

In two separate incidents during 2012, a 52-year-old man and 63-year-old woman had both attended their community general practice during the weeks before they died, suddenly and unexpectedly.

They were both previously well but had noted calf discomfort attributed to “muscle strain”.

In the man, the diagnosis of deep vein thrombosis (DVT) was considered but thought to be unlikely (a Wells DVT likelihood score of zero or less was quoted in evidence), imaging was not requested, and persisting calf discomfort was managed with physiotherapy for 2 weeks before death.

At autopsy, he had extensive acute and subacute deep leg vein thrombosis plus a massive acute PE.

In the woman, shortness of breath with palpitations and cough was attributed first to stress and then to bronchospasm. DVT was not suspected as a possible cause of calf discomfort.

This autopsy discovered embolism that had recurred during several weeks or months. Leg veins were not examined but DVT was considered the likely source. A month before presenting, the patient had returned by aeroplane from Europe but did not mention travel during consultations. It was also thought she was taking hormone replacement therapy.

The coroner found that early venous imaging for calf pain could have prevented both deaths, as this would have revealed DVT and led to anticoagulant therapy.

The coroner recommended, inter alia, that GPs should, when evaluating calf pain, explore “risk factors including recent long haul air travel” and “symptoms … attributable to pulmonary embolism”, should “not exclude a diagnosis of DVT on clinical grounds alone” or “place undue reliance on the DVT Probability: Wells Score System in attempting to diagnose or exclude DVT or pulmonary embolism” and should have “a low threshold for diagnostic imaging and/or D-Dimer blood testing”.

These recommendations are excellent but do invite commentary.

The prime requirement for diagnosing DVT or PE is clinical suspicion. The common predispositions for venous thromboembolism (VTE) are well known.

We are more likely to suspect DVT or PE during or soon after hospital admission, injury, cancer or long distance travel, or while taking an oestrogen-containing medication. This is natural. But in up to one-third of people with VTE there is no apparent cause, so it follows that we should not rely on predisposition alone to suspect DVT or PE.

The Wells DVT score is an aid for the clinical assessment of patients who attend an accident and emergency, outpatient or community clinic with a first episode of what could be acute DVT (it does not work for hospital inpatients).

Both the score and its clinical use have evolved since it was first published almost 20 years ago. In its most useful form, the score predicts that ultrasound imaging is “unlikely” (≤ 1 points) or “likely” (≥ 2 points) to show DVT; the published prevalences are 5.5% and 28%.

This means the Wells score alone cannot exclude DVT. To do this in outpatients with an “unlikely” Wells score, we must add a D-Dimer test. If the D-Dimer level is normal with an “unlikely” Wells score (the finding in about one in three outpatients with suspected DVT), then we do not need an ultrasound examination, because the risk of a symptomatic VTE during the next 3 months of untreated follow-up is below 1%.

D-Dimer testing is unhelpful when the score is “likely”, and these patients should proceed to imaging, as should those with an “unlikely” score and elevated D-Dimer level.

This diagnostic pathway is supported by evidence-based guidelines and gives us the clinical confidence to minimise low-yield requests for imaging in clinically suspected DVT.
 

Professor Alex Gallus is professor of haematology at Flinders University School of Medicine and a consultant haematologist at Flinders Medical Centre and the Repatriation General Hospital, Adelaide.

4 thoughts on “Alex Gallus: DVT suspicions

  1. Dr. Christoph Ahrens says:

    The old clinical guide: “If you start thinking about it, then better take it seroius…”   would have prevented at least the death of the male patient. Unfortunately our clinical judgement is more and more pressed into procedure guidelines which leads to the attitude of kissing common sense and use of our intuition good bye.

  2. Dr Paul Griffiths says:

    These Deaths are tragic firstly,

    There however has to be a discusssion about the concept of test threshold.  A fantastic discussion on this is done by the chaps at SMARTEM in the united states in their podcast http://www.smartem.org/podcasts/pulmonary-embolism-diagnosis-and-treatment.

    For the short of it they have trawled the evidence and come up with the concept that we need to get the probability of the patient having a VTE (combination DVT PE) less than 2%, if they have a pretest probability below that then you do not even do a d-dimer as they are below the test threshold.  The reason for this is that below this rate we are more likely to cause harm from testing and treating than they face from the VTE disease that they have and yes some of that population will have a fatal PE which is a bitter pill to swallow for most.  We need to remember that anticoagulation does not stop the big PE from the DVT it just reduces the chance of further propagation and the formation of the next clot.  Anticoagulation is a danger in itself, we are meant to have blood that clots, it stops us from bleeding to death.  If we test and treat too many we will be causing morbidity and mortality from bleeding issues, possibly contrast anaphylaxis/nephropathy and in a much smaller proportion radiation harm, that is not to mention health expenditure.  

    But the coroner wont ask questions about that will they?

  3. Dr Christoph Ahrens says:

    Dear Paul,

    Ultrasound testing is cheap as chips and doesn’t cause any harm. If you decide to treat, then there must be a positive diagnosis and you weigh up the pros and cons. My comment was about the situation where someone thinks about his patient having a DVT, but then deceides to do nothing about it, not even US.

    regards

    Christoph

  4. Belinda Cochrane says:

    I have a very close professional AND personal relationship to the disease PTE. Treating suspected and proven PTE is part of my core business. Perhaps ironically, some years before I qualified, my 62 yer old father succumbed suddenly and unexpectedly to a pulmonary embolism (as per the coronial report).

    In my experience, many patients with PTE fail to have leg symptoms and many do not have demonstrable clot in the deep veins of the legs, even if you do search for it. Hence, I would challange the coroner’s finding;  “The coroner found that early venous imaging for calf pain could have prevented both deaths, as this would have revealed DVT and led to anticoagulant therapy”.  The female patient may not have had a DVT. The coroner’s finding is made on the premise that pulmonary embolism arises from clots in the deep veins of the legs, a fact which all medical students were taught when I was studying in Medical School. However, this “fact” has not been substantiated in my practice nor can I find it substantiated by others’ evidence-based research.

    It’s true that PTE is a diagnosis that we sometimes struggle to make correctly in advance of a life-threatening event. We are unlikely to perform better until we challenge the unproven dogma and seek to better understand the pathophysiology. Pulmonary embolism could equally well originate as clot within the right atrium/heart or deep veins of the pelvis (NB PTE in pregnancy) or it could even develop in situ within the pulmonary arteries. Until then, I agree with others, the trick is to remain vigilant to the diagnosis, when presenting symptoms are consistent and not otherwise explained and to use the existing diagnostic algorithms with due consideration.

     

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