38 e-Letters

published between 2017 and 2020

  • 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.

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

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  • Breathe in, Hold on and breathe out, effective exercise for COPD

    Letter response to the article “Effects of breathing exercises using home-based positive pressure in the expiratory phase in patients with COPD

    Following the publication of the manuscript “Effects of breathing exercises using home-based positive pressure in the expiratory phase in patients with COPD” in Postgraduate Medical Journal written by Lin Q. et al., we describe the rationale and origin of the respiratory technique derived from yoga practice and adapted as breathing exercise for a pulmonary rehabilitation programme strategy for COPD patients. The discussed technique consist of breathing with an expiratory resistive load, is a modified Pranayama yogic breathing practices tailored with focus on the specific need of patient with COPD, that allow the patient to breathe simultaneously through both the nostrils and with exhalation to be completed against a resistance to the free flow of exhaled gases. The described method has also been proven very useful in reopening non-ventilating lung areas for both chronic and acute patients.
    I have read with great interest the manuscript “Effects of breathing exercises using home-based positive pressure in the expiratory phase in patients with COPD” published in Postgraduate Medical Journal written by Lin Q. and collaborators 1. As reported by the authors in the acknowledgment of the paper, I was instrumental to inspire the study while working with the Respiratory and Critical Care Medicine and RICU in the...

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  • Re: [How good are doctors at introducing themselves? #hellomynameis]

    Dear Editor,

    It was a pleasure reading the explorative study by Gillen et al, which focused on the effects of introductions and handshakes on patient satisfaction by the end of a consultation. The study concludes that the majority of patients expected such gestures; which was received positively. The results reinforced how powerful the #hellomynameis campaign was; given it was a lucrative collective effort which ultimately made patients feel comfortable. The paper demonstrates how these simple, yet overlooked, consultation techniques are pivotal in building a positive rapport with patients, translating into a successful patient-doctor experience.

    On reflection of our own experiences as medical students, introducing oneself is one of the first communication skills we are trained to do. Nailing your introduction is taught to be the basis of forming a courteous and lasting first impression. As students, we spend excessive amounts of time trying to formulate a focused history, sifting through our medical knowledge in search for the next question to ask in order to rule in and out conditions. It’s fair to say that the first few attempts at history taking are longer than an average consultation with a senior clinician. Therefore, we agree with Gillen et al that clinicians and by extension, medical students- should introduce themselves by their full name and state their objectives so that the patient feels at ease knowing who they are speaking to. Furthermore, impl...

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  • Lost in translation

    Fortuitously, the re-evaluation of the medical consultation(1) has coincided with the advent of intrusion of the computer into the doctor-patient interaction, typified by the comment "Clinicians [now] find themselves interacting more with their computers than with their patients...."(2). What that intrusion has meant is that the component of symptomatology emanating from body language is now being actively deleted from both the narrative and the normative versions of the patient's medical history. Discerning patients are probably aware of this shift in the dynamics of the consultation, the predictable consequence that "If patients do not have the impression we are listening and watching attentively, they may not tell us what we need to know, or ..............follow our advice" (1).
    In the Ying and Yang of the medical consultation a medically qualified patient might or might not be at an advantage, depending on what version of the patient's own story one might wish to read. The author of his personal experience of post-traumatic benign paroxysmal positional vertigo was in the fortunate position of submitting, to his own doctor, a narrative which coincided with the normative version of that disorder. The consequence was a well thought out therapeutic strategy, culminating in complete cure(3). However, notwithstanding the fact that benign paroxysmal positional vertigo(BPPV) is by far the most common type of vertigo, with a r...

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  • Neuropathy by overachieved rapid glycemic oral control

    Letter response to the article "Under-recognised paradox of neuropathy from rapid glycaemic control."

    I am a data point of what the author says is elusive example of neuropathy (albeit in initial stages) by rapid glycemic control using only oral medication.
    My A1c reduced by about 1 point ( 7.7 to 6.8) in 3 months and further down to 6.1 in 3 more subsequent months.

    From the initial 7.7 A1c date, I was started on a higher oral dosage, as well as serious diet modification.

    Two months later, I had a rapid onset of feet burning symptoms. The symptoms came on and off. With subsequent tighter diet control that included episodes of low glucose levels, feet burning was still present and became more frequent. After reading up on this subject and its counter intuitive conclusions, I loosened diet control and also had my doctor reverse the last medication increase to previous levels. This seems to have helped and my left foot has been free of burning for a few days now, and the right foot also improving. Continuing monitoring and hoping for the best. Thanks to your and similar articles for highlighting this controversial and elusive phenomenon.

    Conflict of Interest
    None declared