eLetters

32 e-Letters

published between 2017 and 2020

  • FMTVDM – Evidence-based outcomes are defined quantitatively.

    Malhotra, et al [1] correctly defines a concern regarding the treatment of patients and the selection of appropriate interventions. However, to provide this “right care and high-value” cardiac care requires the shedding of incorrect beliefs and opinions – including diagnostic, etiologic and treatment - and the quantification of CAD itself.
    Quantification [2] makes it possible to diagnostically define the true extent and severity of CAD present in an individual and to accurately measure CAD treatment outcomes. Only by using true quantification can we remove the errors (sensitivity and specificity) in imaging [2] and treatment studies [3] and provide patients with “right care and high-value cardiology” free of physician bias and misperceptions. To provide this type of care we must focus our full attention on evidence-based medicine; avoiding the errors of the past.
    The very foundation of evidence-based medicine is the ability to accurately, consistently and reproducibley measure quantifiable outcomes [2] as shown in Figure 1, and to avoid the use of qualitative or semi-quantitative methods, which misdiagnose the presence (sensitivity) or absence (specificity) of disease [2]. This is now possible using “The Fleming Method for Tissue and Vascular Differentiation and Metabolism (FMTVDM) Using Same State Single or Sequential Quantification Comparisons” [2].
    FMTVDM is able to accurately, consistently and reproducibly define the extent and severity of CAD by fir...

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  • The truth is more complicated

    The medical myths, using anti-MMR as an example, follow a formula of being easy to understand and not difficult to retell. Similar to urban myths, the knowledge of a medical myth is not reduced by distance from the case. For example, as told to me in my paediatric emergency department, a patient's cousin's friend whose child became autistic following vaccination is viewed as an absolute truth.

    Compare this with medical rebuttal. Frequently the caveats of more research is needed or the results from a small study litter the conclusion sections. Typically the writing is dense and heavy on jargon. It's also common for there not to be an absolute answer.

    Perhaps we should sharpen our writing and be more definitive. ‘Tweetorials’ are useful but they need to be short and snappy.
    Conflict of Interest
    None declared

  • The differential diagnosis should include dissecting aneurysm of the aorta

    The differential diagnosis of pneumothorax with haemodynamic compromise(1) ought to include the two subtypes of tension pneumothorax associated with dissecting aneurysm of the aorta(DAA), namely, tension pneumothorax with concurrent haemothorax(2), and tension pneumothorax without concurrent haemothorax(3)(4).
    In the report of DAA-related haemopneumothorax(2), antemortem chest radiography clearly documented the presence of tension pneumothorax without concurrent fluid collection in the pleural space. The patient collapsed and died soon after insertion of a chest drain intended to relieve the pneumothorax. Autopsy revealed an adhesion between the visceral lung pleura and the aortic aneurysm through which the dissection had penetrated the lung parenchyma. The parenchymal haematoma had subsequently “spouted out” from a 20 mm tear on the pleura, giving rise to haemothorax(2). The sequence of events might have been similar, in some respects, to the sequence of events in a 79 year old man who experienced a haemopneumothorax which was, however, much less striking in its severity(5). In the latter case there was no haemodynamic compromise. The patient had initially complained of “spitting” blood, without concurrent chest pain, back pain or breathlessness. Chest radiography revealed an abnormal air-fluid level in middle lung field on the right side. Subsequent contrast-enhanced tomography revealed Type B aortic dissection, a pneumothorax adjacent to the dissection(pre...

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  • coexistence of tuberculosis and sarcoidosis needs to be ruled out

    Given the fact that tuberculosis and sarcoidosis have many stigmata in common (including the occurrence of noncaseating granulomas), a diagnosis of multiorgan sarcoidosis (1) can only be established beyond doubt if care has been taken to rule out the coexistence of sarcoidosis and tuberculosis using the strictest criteria for ruling in or for ruling out tuberculosis. Evaluating tissue samples for M tuberculosis through the use of the polymerase chain reaction (PCR) is one such strategy, given the fact that sensitivity for M tuberculosis infection is significantly higher for PCR than for BACTEC radiometric culture (74.4% vs 55.8%), although the two modalities have comparable specificity, namely, 97.2% vs 100% (no significant difference) (2). Accordingly, when the authors state "All biopsy specimens and bronchial washings were negative for TB (1), we need to know whether those samples were subjected either to mycobacterial culture or to evaluation by PCR.
    The coexistence of sarcoidosis and tuberculosis was documented unequivocally in a 35 year old woman who initially presented with histologically and bacteriologically confirmed tuberculous lymphadenitis. She subsequently developed bilateral lung infiltrates. Histological specimens obtained via transbronchial biopsy and open lung biopsy showed features consistent with sarcoidosis. In addition, however, the presence of mycobacterial DNA in those tissue specimens was documented by PCR (3).
    In another report, a...

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  • Alternatives to the short synacthen test

    Even when one takes into account the possibility that measurement of plasma cortisol after 60 min administration of synthetic ACTH might be a sufficient screening test for adrenal insufficiency(AI)(1), it is important to recognise that there are risk-free alternatives to the short synacthen test(SST) for validating the diagnosis of AI(2)(3)(4).
    According to a retrospective study which evaluated, not only the 30 min and the 60 min cortisol levels, but also the pre-synacthen cortisol levels, a pre-synacthen serum cortisol level of 100 nmol/L or less(obtained during the median time period 08.20 h) is associated with a positive predictive value of 93.2% for the diagnosis of AI, when the gold standard for the latter is a failed SST. In that study of 330 subjects with suspected AI tested with the 250 mcg dose of tetracoscatrin , the subgroup with an eventual diagnosis of AI were tested at the median time of 08.20h(interquatrile range 07.55-09.26). The subjects who passed their SST were tested during the median time of 08.33(interquatrile range 08.01h-09.55h). Conversely. a pre-synacthen serum cortisol of 450 nmol/L or more generated a 98.7% negative predictive value to rule out AI(2). These observations were largely corroborated by a retrospective study of 231 subjects with suspected AI in whom AI was validated by an SST which incorporated 30 min as well as 60 min serum cortisol levels. In that study some patients(unspecified number) were tested at 08.00h...

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  • The issue of non-anaemic iron deficiency

    The heading which reads "Heart failure with Reduced Ejection Fraction(LVEF < 40%) & Iron Deficiency Anaemia"(fig 1)(1) fails. by implication, to recognise that heart failure-related iron deficiency has an outcome which is detrimental irrespective of whether or not the patient is anaemic(2). In the latter study, among heart failure patients who had a marker of iron deficiency(ID), namely, mean corpuscular haemoglobin concentration(MCHC) equal to or less than 330 g/L, there was a significant association with increased mortality(Hazard Ratio 1.7, 95% Confidence Interval 1.4 to 2.0) which persisted even after adjusting for anaemia(HR 1.5, 95% CI 1.3 to 1.8)(2). The use of the cut-off MCHC value of 330 g/L or less as a marker of ID (1) is supported by studies where mean values for MCHC amounted to 319 g/L and 327.9 g/L, respectively, among subjects with ID(3)(4). In those two studies the iron-replete subjects were characterised by MCHC values amounting to 339 g/L and 340 g/L, respectively. The mean values for MCHC in ID subjects(namely, 319 g/L and 327.9 g/L, respectively) were significantly(p=0.001, p < 0.001) lower than the mean values for MCHC(339 g/L and 340 g L, respectively) in their iron-replete counterparts. In those two studies, as well, mean values for mean corpuscular volume(MCV) in ID subjects ranged from 85.5 fl to 90.2 fl in spite of proven ID(serum ferritin < 30 mcg/L) and MCHC < 330 g/L. Accordingly, to optimise the i...

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  • Other treatment opportunities in acute decompensated heart failure

    Among the recommendations for inpatient management of acute decompensated heart failure(1), special mention should be made of those patients who present with the association of congestive heart failure (CHF) of left ventricular origin, chronic obstructive pulmonary disease (COPD) and hypoxia (with or without hypercapnia). This diagnostic triad is easily overlooked because the obstructive ventilatory defect of COPD is simulated by the obstructive ventilatory defect of left ventricular failure (LVF) even in the absence of COPD(2). The obstructive ventilatory defect is more likely to be attributable to COPD when hypoxia is associated with hypercapnia, as was the case in a 70 year old woman who presented, not only with radiographically validated LVF, but also with the association of hypoxia and hypercapnia(3).
    The management of patients with combined left ventricular failure and suspected hypoxic COPD includes standard antifailure treatment (such as diuretics and angiotensin converting enzyme inhibitors) and adjunctive supplemental oxygen, the latter for a minimum of 15 hours a day(3)(4). Crucially, such patients should undergo formal assessment for long term oxygen therapy(LTOT) after a period of stability of at least 8 weeks from their lat exacerbation. This evaluation involves two arterial blood gas measurements at least 3 weeks apart(4). This might also be an opportunity to repeat the lung function tests so as to ascertain if the obstructive ventilatory defect has pe...

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  • acute heart failure in diabetic ketoacidosis

    The emergency management of acute decompensated heart failure(1) would be incomplete without mention of the unique problems posed by the simultaneous occurrence of acute heart failure and diabetic ketoacidosis (DKA). Myocardial infarction, a recognised precipitating factor for DKA(2)(3), is a potential cause of the association of DKA and acute heart failure. This association poses the challenge of simultaneous management of fluid overload, ketoacidosis, and potassium status.
    In the acutely breathless patient the priority is to relieve symptoms of fluid overload(4)(5), fundamentally by avoiding the imposition of an additional fluid burden, while simultaneously relieving the patient's symptoms. This approach flies in the face of the equivocal guideline advice that "fluid replacement may need to be modified"(6). Treatment choices for symptomatic relief include bolus intravenous frusemide(4)(without supplementary intravenous fluids) or simply initiating intravenous insulin infusion, again "without supplementary intravenous fluids"(5). The latter strategy works especially well in DKA-related patients in whom chronic renal failure has impaired the patient's ability to excrete the excessive amount of fluid that has accumulated in the extracellular fluid compartment as a result of osmotic shifts generated by DKA-related hyperglycaemia. Restoring the optimum osmotic balance by lowering the blood glucose concentration generates relief of the sympt...

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  • raising the index of suspicion for constrictive pericarditis and index of suspicion for iron deficiency

    The point is well made that monitoring of the response to congestive heart failure(CHF) treatment should include documentation of changes in jugular venous pressure (JVP) and changes in body weight. That should especially be the case in patients with markedly elevated JVP, especially in the presence of ascites. There should be a heightened index of suspicion for constrictive pericarditis when a patient with those characteristics experiences a significant fall in body weight without a concurrent fall in JVP(2).
    Coexistence of CHF and iron deficiency(ID) is the other issue that requires a heightened index of suspicion when certain parameters are operative. Notwithstanding the fact that the work-up of suspected ID recommended by Guyatt et al highlighted mean corpuscular volume(MCV) to the total exclusion of mean corpuscular haemoglobin concentration(MCHC)(3), there is now overwhelming evidence that MCHC outperforms MCV in predicting ID, both in non anaemic and in anaemic subjects(4)(5)(6). Among non anaemic female athletes aged 15-20, when a comparison was made between 33 ID subjects(characterised by serum ferritin < 30 mcg/L) vs 87 non-ID subjects, mean MCHC amounted to 327 g/L vs 340 g/L(p < 0.001), whereas MCV( 85.5 fl vs 87.2 fl) did not significantly differentiate between the two subgroups(4). In a smaller study comprising 41 CHF subjects(including 17 with ID validated by bone marrow studies) the Receiver Operating Curve for ID generated an area under the cur...

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  • Have guidelines lost their way?

    With all due respect to Dr Philip Welsby 1I think he has misunderstood my paper on the 5*3*5 rule for examining the upper limb. The 5*3*5 rule is not a guideline, it represents a paradigm shift in the way we should examine the upper limbs.

    In my experience guidelines are written by experts using what little evidence we have liberally laced with "expert opinion" to help guide clinicians to manage patients. I would agree with Dr Welsby that guidelines are often complex, impossible to memorise and difficult to use.

    The 5*3*5 rule does not require any knowledge of neuroanatomy nor does it need to be memorised. The idea is that the clinician has the pictures and the tables readily available in their clinic. All they have to do is examine the muscles, establish which muscles are weak and then consult the relevant table(s). A previous rule that I have published, the rule of four of the brainstem2 is used in this way. I have been informed by colleagues that they've seen this rule on computers in Accident and Emergency Departments.

    The 5*3*5 rule is not intended only for neurologists, it empowers non-neurologist's to accurately diagnose the cause of weakness in the upper limb. I have taught the rule to medical students in Australia, Rwanda and Fiji, to postgraduate physician trainees and osteopaths who have all found it useful.

    References
    1. Welsby PD. Have guidelines lost their way? Postgrad Med J 2019; 95(1127): 469.
    2....

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