Jambalaya

It was the evening of Christmas Day a few years back. The big feast was over, we had cleared up and were settling down for whichever blockbuster movie was on offer that year. The phone rang: it was our our younger daughter who had gone to her boyfriend’s home only to find him suffering a raging fever, sore throat with rigors, vomiting, the works. She asked if we had any penicillin in the house. I had, but was not prepared for her to simply come and collect it: I had to see the patient. Half an hour later I had confirmed a rather unhappy, unwell-looking suitor suffering a temperature of 39degC and markedly enlarged, inflamed tonsils with purulent exudate.

A suitable case for penicillin, I thought, and handed over the pills: not really the time or place for microbiological confirmation. I wrote a note for him to take to his general practitioner in a day or so, explaining my unofficial intervention. A few days later when next I saw him he was bright and bouncy and had seen his GP who, as it turned out, was the wife of a colleague and an aquaintance of many many years. She had apparently dismissed my pharmacological offering as lacking in evidence and basically out of date (or was the phrase she used ‘unfashionable’)?

This reminiscence was sparked by Robert Centor’s recent post about a patient with sinusitis who, whilst recognizing that antibiotics probably aren’t the answer, modern medicine wanted for decent alternatives. Sometimes, I think, we can use a little help from our friends.

A BBC News post today reports that scientists in Manchester have discovered that certain aromatherapy oils kill the ‘superbug’ MRSA (methicillin-resistant Staphylococcus aureus). This apparently serendipitous finding arose because the scientists were asked to test the oils to ensure that they would not harm immune suppressed patients.

Odd that the report does not mention which oils.

Assays of the d-dimer fibrin degradation product in the circulation have become ‘indispensible’ in the evaluation of patients with suspected venous thromboembolism (VTE: deep venous thrombosis and/or pulmonary embolism). But how useful are they, and are they used wisely?

Like many diagnostic aids, the utility of d-dimer assays is influenced by the clinical setting (to be more precise, the a priori or ‘pre-test’ probability that the disease being tested for is present). Unfortunately, this is a test with a very low specificity, albeit a high sensitivity [1], and a significant problem for the diagnostician using this test is that d-dimers behave like ‘acute phase’ reactants and can be elevated in a wide range of situations associated with an acute phase response, such as inflammation, infection and malignancy. The trouble is that many of these feature in the differential diagnosis of presentations suggesting venous thromboembolism (e,g. pleuritic chest pain:pleurisy, shortness of breath/hypoxia:pneumonia, painful swollen leg:cellulitis). And, to cap it all, patients with malignant disease are at high risk of VTE, but may have elevated d-dimers for other reasons [2].

In practice, the d-dimer test is only useful if the result is not elevated and the clinical probability of VTE is low, when it adds confidence to a conclusion that VTE is not present and that further investigation with scanning is unnecessary. Diagnostic dilemmas arise commonly, however, when the clinical probability of VTE is low but the d-dimer result is elevated. An elevated CRP in this situation indicates an acute phase response and renders the d-dimer result virtually worthless. An elevated d-dimer with a normal CRP may be more significant, but I don’t think the utility of the d-dimer assay in that situation has yet been adequately studied. In general, it is best not to order a d-dimer test if there is a high clinical probability that it will be elevated anyway.

Similarly, if the clinical suspicion of VTE is anything but very low then don’t bother with a d-dimer assay, just get on and do the appropriate scans.