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...
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(morning cortisol subgroup), and the rest were tested at 09.00h-13.00h(basal cortisol subgroup). A basal cortisol level of < 85 nmol/L was associated with a specificity of 99.7% and a sensitivity of 24.7% for the diagnosis of AI when the gold standard for AI was a failed SST. for ruling out AI, a serum cortisol of 350 nmol/L or more was associated with a sensitivity of 98.9% and a specificity of 32.2%(3). In that study the receiver operating curve generated a significantly higher area under the curve for basal cortisol than for morning cortisol in predicting a failed SST.
In the specific context of hypoglycaemia, regardless of the time of day, a single measurement of serum cortisol can unequivocally establish the diagnosis of AI. The rationale is that hypoglycemia is a stressor that activates the entire hypothalamic-pituitary-adrenal axis , thereby exceeding the stressor potential of the SST. All that it needs is for clinicians to be alert to opportunities to utilise the stressor potential of hypoglycaemia. A missed opportunity to do so was exemplified by the cautionary tale of a 19 year old man with type 1 insulin-treated diabetes and autoimmune hypothyroidism, both being the components of the autoimmune polyglandular syndrome. When he was admitted to hospital with hypoglycaemic coma the opportunity was not taken to explore fully the underlying cause of that complication . After his discharge he experienced recurring episodes of hypoglycaemia despite reducing his insulin dose. Eventually, 5 months post discharge, a SST was performed and it showed that he had AI. That diagnosis could have been established with a single measurement of serum cortisol during the episode of hypoglycaemia necessitating his hospital admission.
The additional advantage of a single measurement of serum cortisol that validates AI is that it obviates the need for a subsequent SST , and its attendant risk(albeit rare) of potentially fatal allergic reaction to exogenous tetracosactrin(5).
Finally, robust prospective studies are still needed to validate the hypotheses enunciated in (1)(2)(3)
I have no funding and no conflict of interest
References
(1) Kumar R., Carr P., Moore K et al
Do we need 30 min cortisol measurement in the short synacthen test: a retrospective study
Postgrad Med J 2019;1doi.org/10.1136/postgradmedj 2019
(2)struja T., Briner L., Meier A et al
Daignostic accuracy of basal cortisol level to predict adrenal insufficiency in consyntropin testing results from an observational cohort study with 804 patients
Endocrine Pract 2017;23: 949-961
(3) Mansrol W., Phimphllal M., Khorana J., Atthakolol P
Diagnostic performance of basal cortisol level at 09.00-13.00h in adrenal insufficiency
PLOS ONE 2019;doi.org/10.1371/journal.pone.0225255 November 18, 2019
(4) McAulay V., Frier BM
Addisons's disease in type 1 diabetes presents with recurrent hypoglycaemia
Postgrad Med J 2000;76:230-232
(5) Anonymous
Today's drugs
Tetracosactrin
BMJ 10.1136/bmj.2.5545.160 on 15th April 1967
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...
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 identification of ID(irrespective of coexistence of anaemia), the screening test should be an MCHC of 330 g/L or lower(ideally < 330 g/L). To confirm the diagnosis of ID the next step should be evaluation of serum ferritin and transferrin saturation, respectively.
With regard to treatment, for the non-anaemic ID patient the optimum treatment should be either intravenous iron(1) or oral iron taken as a single dose on alternate days(5). The latter is an innovation which optimises iron absorption in nonanaemic ID subjects who do not have heart failure(5). It is reasonable to extrapolate the efficacy of that dosing regime to heart failure patients with non-anaemic ID if they cannot tolerate intravenous iron. Whether or not that regime optimises iron absorption in the anaemic phase of ID remains to be proven by future studies. I agree that anaemic subjects with ID should receive intravenous iron. In the presence of heart failure and intolerance of intravenous iron it is unproven whether or not the dosing regime of Stoffel et al(5) would be appropriate.
Finally, although the guideline appears to confine its recommendation for further investigation only to patients who are in the anaemic phase of ID(final paragraph of fig 1)(1), it seems logical to investigate the underlying cause of ID regardless of whether or not the patient is anaemic. After all, anaemia is a manifestation of ID which occurs relatively late in the natural history of the underlying cause of ID. Furthermore, the underlying cause of ID needs to be eliminated even in the absence of anaemia.
I have no funding and no conflict of interest
References
(1) Simon S., Ioannou A., Deora S et al
Audit of the prevalence and investigation of iron deficiency anaemia in patients with heart failure in hospital practice
Postgrad Med J 2019;doi:10.1136/postgradmedj-2019-136867
(2)Kleber M., Kozhuharov N., Sabti Z et al
Relative hypochromia and mortality in acute heart failure
Int J Cardiol 2019;286:104-110
(3) Urrechaga E., Borque L., Escanero JF
Clinical value of hypochromia markers in the detection of latent iron deficiency in non-anaemic premenopausal women
Journal of Clinical Laboratory Analysis 2016;30:623-726
(4) Malczewska -Leneczowska J., Orysiak J et al
Reticulocyte and erythrocyte hypochromia markers in detection of iron deficiency in adolescent female athletes
Biol Sport 2017;34:111-118
(5)Stoffel N., Cercamondi C., Brittenham G et al
Iron absorption from oral iron supplements given on consecutive days versus alternate days and as a single dose versus twice-daily dosing in iron depleted women, two open-label, randomised controlled trials
Lancet Haematol 2017;4:524-533
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...
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 persisted. A residual obstructive ventilatory defect that is associated with a higher than normal total lung capacity is diagnostic of COPD(5). A high index of suspicion for the association of systolic heart failure and COPD-related hypoxia generates opportunities to optimise the long term management of these patients, thereby improving their life expectancy.
I have no funding and no conflict of interest.
References
(1) Raj L., Maidman SD., Adhyari BB
Inpatient management of acute decompensated heart failure
Postgrad Med J 2019-136742
(2)Jolobe OMP
Unrecognised heart failure in elderly patients with stable chronic obstructive pulmonary disease
Eur Heart J 2006;17:372
(3) Jolobe OMP., BenHamida AA., Basu-Choudhuri B
Bleeding peptic ulcer
Gut 2003;52:315
(4) Hardinge M., Annandale J., Bourne S et al
British Thoracic Society guidelines for home oxygen use in adults
Thorax 2015;70:l1-l43
(5) Jolobe OMP
The yield of a diagnostic hospital dyspnoea clinic for the primary care section
Journal of Internal Medicine 2002;251:366-367
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...
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 symptoms of extracellular fluid overload(5). In the context of underlying chronic renal failure there is minimal risk of generating hypokalaemia through the use of intravenous insulin. In such patients it is not only water excretion that is impaired (hence the pulmonary oedema) but there is impairment of potassium excretion as well(5).
As an adjunct to intravenous insulin infusion consideration should also be given to the use of intravenous nitrate infusions to relieve symptoms of cardiogenic pulmonary oedema. This is a successful strategy outside the context of DKA(7). Its advantage over bolus intravenous frusemide is that it is less likely to precipitate hypokalaemia, the latter a potential risk in DKA heart failure patients with relatively intact renal function.
Guidelines are silent on the emergency relief of heart failure-related acute breathlessness in DKA. In that information vacuum there is an abundance of conflicting recommendations(4)(5)(6)(8).
I have no funding and no conflict of interest
References
(1) Raj L., Maidman SD., Adhyaru PB
Inpatient management of acute decompensated heart failure
Postgrad Med J 2019;136742
(2) Anupama B., Chandrasekhara P., Krishnamurthy MS., Aslam M
Clinical and laboratory profile of diabetic ketoacidosis in elderly with type 2 diabetes mellitus
BLDE Univ Health Sci 2018;3:79084
(3) Elmehdawi RR., Elmagerhei HM
Profile of diabetic ketoacidosis at a teaching hospital in Benghazi, Libyan Arab Jamahiriya
EHMJ 2020;16:292-299
(4) Jolobe OMP
Potassium should be evaluated also when diabetic ketoacidosis is complicated by heart failure
Am J Med Emerg 2016;29:955
(5) Varama R., Karim M
Lesson of the month 1:Diabetic ketoacidosis in established renal failure
Clin Med 2016;16:392-393
(6) Dhatariya K., Savage M
Joint British Diabetes Societies Inpatient Care Group
The management of diabetes ketoacidosis in adults. 2nd Edition. NHS Diabetes
September 2013
(7)Alzahri MS., Rohra A., Peacock WF
Nitrates as a treatment of acute heart failure
Cardiac Failure Review 2016;2:51-55
(8) Philip l., Poole R
Double trouble: managing diabetic emergencies in patients with heart failure https://onlinelibrary-wiley-com.rsm.idm.oclc.org doi.org/10.1002/pdf.2181
Conflict of Interest
None declared
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...
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 curve(AUC) amounting to 0.773 for MCHC(95% Confidence Interval 0.618 to 0.929) vs 0.645(95% CI 0.469 to 0.821) for MCV. For transferrin saturation(TSAT) AUC amounted to 0.932(9%% CI 0.861 to 1.000). A TSAT of 19.8% or lower showed the best performance for identifying ID.(5).
Among 1821 CHF subjects of mean age 66, mean MCHC amounting to 329 g/l was significantly lower in ID subjects(defined as being characterised by serum ferritin < 100 mcg/L or serum ferritin 100-299 mcg/L in association with TSAT < 20%) than mean MCHC amounting to 338 g/L(p < 0.001) in CHF subjects with no ID and no anaemia (6). Accordingly, MCHC amounting to 330 g/L or lower should raise the index of suspicion for ID(7), thereby prompting evaluation of serum ferritin and TSAT to confirm the diagnosis.
I have no conflict of interest
References
(1) Raj L., Maidman SD., Adhyari BB
In patient management of acute decompensated heart failure
Postgrad Med J 2019-136742
(2) Conti CR., Friesinger GC
Chronic constrictive pericarditis. Clinical and laboratory findings in 11 cases
John Hopkins Med J 1967;120;262-274
(3) Guyatt GH., Oxman AD., Ali M et al
Laboratory diagnosis of iron deficiency. An overview
J Gen Intern Med 1992;7:145-153
(4)Malczewska-Lenczowska J., Oryslak J., Szczepanska B et al
Reticulocyte and erythrocyte hypochromia markers in detection of iron deficiency in adolescent female athletes
Biol Sport 2017;34:111-118
(5) beverborg NG., Klip UT., Meijers WC et al
Definition of iron deficincy based on the gold standard of bone marrow iron staining in heart failure patients
Circ Heart failure 2018;11:e004519. DOI.10.11161/CIRCHEARTFAILURE.117.004519
(6) Tkaczyszyn M., Comin-Colet J., Voors AA et al
Iron deficiency and red cell indices in patients with heart failure
Eur J mHeart Failure 2018;20>114-122
(7) Kleber M., Kozhuharov N., Sabti Z et al
Relative hypochromia and mortality in heart failure
Int J Cardiol 2019;doi.org/10.1016/j.ijcard.2019.02.060
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....
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. Gates P. The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular syndromes for the non-neurologist. Intern Med J 2005; 35(4): 263-6.
Letter response to the article “Effects of breathing exercises using home-based positive pressure in the expiratory phase in patients with COPD
Abstract
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...
Letter response to the article “Effects of breathing exercises using home-based positive pressure in the expiratory phase in patients with COPD
Abstract
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 First Affiliated Hospital of Wenzhou Medical University, China.
I congratulate the authors, and in particular Dr. Chang Cai who planned and coordinated the study at my suggestion, the reviewers and the editorial staff who prepared and published this interesting article.
The main merit of the study consists in presenting significant evidence of a helpful method used empirically for a long time to perform breathing exercise in acute and chronic respiratory diseases.
In this study the method has been used as a rehabilitation exercise to improve ventilation and quality of life of COPD patients, although current available evidence in the literature are low to moderate 2-4.
The rationale and origin of this respiratory technique derived from Pranayama yoga practice.5 6.
This technique involves: 1. Inhale through the left nostril to a count of four; 2. Close both nostrils and hold breath to a count of sixteen; 3. Exhale through the right nostril to a count of eight; 4. Inhale through the right nostril to a count of four. 5. Close nostrils and hold breath to a count of sixteen. 6. Exhale through the left nostril to a count of eight.
This yogic technique has been tailored by us allowing the patient to inhale simultaneously through both nostrils and exhale only through the mouth against a resistance to the free flow of exhaled gases.
Specifically, the breathing technique involves: 1. Inhale through both nostrils to a count of four; 2. Hold breath to a count of six to ten (according to the patient’s resistance); 3. Exhale through the mouth towards an expiratory resistive valve to a count of eight. The exhalation occurs through a tube that attaches to a water valve (Positive End-Expiratory Pressure – PEEP).
The rationale of the method can be summarised in three phases, specifically:
1st Phase: The inspiration for about 4-5 seconds allows the introduction of a typical amount of air (tide volume) for each patient into the lungs. In this phase the inhaled air goes preferentially toward the lung areas with lower resistance and better compliance.
2nd Phase: At the end of inhalation, the start of the expiratory phase is delayed between 6- 10 sec (in Pranayama practice 16 seconds is suggested). The duration of this apnea must be adapted progressively according to the improvement and patient’s acceptance.
In this phase the gas present in the lungs is redistributed to the lung areas that need more time to be opened. This allows the recruitment of not ventilating lung areas to steady flow.
3rd Phase: The exhale is done through a plastic or PVC tube (about 2 cm in diameter and 80 cm in length) whose terminal part is immersed in water. Exhalation must be done progressively to a count of 8 seconds.
The level of tube immersion can be regulated from 5 to 15 cm H2O according to the lung pathology and the progressive adaptation of the patient to the method. It is generally suggested to increase the immersion level by 2-3 cm every 5-6 days in relation to the patient's tolerance.
The resistance offered to the free exhalation of the gas from the lungs, controlled by the level of tube immersion, allows small bronchi and terminal bronchioles to stay open longer improving the closure volume. Leaving the terminal bronchioles and the alveoli open longer, on one end promotes the elimination of the sputum, on the other, improves gas exchange.
It is recommended to perform the manoeuvre 2-4 times a day, no less than 2 times, for the duration of 10-15 min. The technique may present some initial difficulty of adaptation on the part of the patient, for which it requires particular attention on the part of those who teach the method, especially if the patient is not completely cooperative.
The beneficial and indispensable method of rehabilitation becomes evident and better accepted as soon as the patient begins to improve. Chronic patients usually notice the benefit after the first week of treatment as clearly demonstrated by the study to which I refer, and by themselves tend to increase the duration of respiratory exercise. Generally the acute patient perceives the benefit earlier.
Reference
1. Lin Q, Zhuo L, Wu Z, et al. Effects of breathing exercises using home-based positive pressure in the expiratory phase in patients with COPD. Postgrad Med J. 2019;95:476-481.
doi: 10.1136/postgradmedj-2019-136580. Epub 2019 Jul 22.
2. Holland AE, Hill CJ, Jones AY, et al. Breathing exercises for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2012;10:CD008250.
doi: 10.1002/14651858.CD008250.pub2
3. Garvey C, Bayles MP, Hamm LF, et al. Pulmonary Rehabilitation Exercise Prescription in Chronic Obstructive Pulmonary Disease: Review of Selected Guidelines: AN OFFICIAL STATEMENT FROM THE AMERICAN ASSOCIATION OF CARDIOVASCULAR AND PULMONARY REHABILITATION. J Cardiopulm Rehabil Prev. 2016;36:75-83.
doi: 10.1097/HCR.0000000000000171.
4. Ubolnuar N, Tantisuwat A, Thaveeratitham P, et al. Effects of Breathing Exercises in Patients With Chronic Obstructive Pulmonary Disease: Systematic Review and Meta-Analysis. Ann Rehabil Med. 2019;43:509-523.
doi: 10.5535/arm.2019.43.4.509. Epub 2019 Aug 31.
5. Liu XC, Pan L, Hu Q, et al. Effects of yoga training in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis. J Thorac Dis. 2014;6:795-802.
doi: 10.3978/j.issn.2072-1439.2014.06.05.
6. Beutler E, Beltrami FG, Boutellier U, et al. Effect of Regular Yoga Practice on Respiratory Regulation and Exercise Performance. PLoS One. 2016;11(4):e0153159.
doi: 10.1371/journal.pone.0153159.
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...
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, implementing non-verbal gestures such as handshakes upon introduction and having a compassionate demeanour will encourage the patient to give a more thorough and engaging history-increasing the likelihood of a positive patient-doctor experience amongst the sick and often irritable.1
Although the literature suggests the consensus is that it is encouraged to have thorough introductions, there still remains grey area regarding both clinicians and patients’ perspectives on what constitutes to be the most appropriate method of greeting (handshake, introductions, first name only, first and last names). An observational study by Makoul et al conveyed a consistent pattern for males and females, African or white patients and patients across educational levels, whereby shaking hands was positively received across these categories as an appropriate introduction.2 However, Marcinowicz et al reported that handshakes were of the less frequent non-verbal cues practiced, more often replaced by tone of voice, eye contact and facial expressions.3
It is difficult to offer reliable conclusions when it comes to the effects of ethnicity on the different subtypes of introductions, due to the scarce literature to benchmark with this study. However, focusing on Gillen et al alone, the ethnicity of the patient was not used to draw any correlations, arguably because of the lack of data on non-Caucasian participants. Furthermore, there is limited data on religious groups, which would have been interesting in analysis, considering religious influence is a potential confounding factor to the results of the study.
Gillen et al does not necessarily address or offer conclusive answers to the question of what caused the lack of introduction. For example, it is known that for some members of the Muslim community, shaking hands is not always common practice between people of opposite genders4. Therefore, as a melting pot of medical students with various ethnicities, faiths and worldly views - we want to use this letter to highlight the importance of being receptive to peoples’ body language and to be sensitive towards their way of life.
We offer a suggestion that the lack of “handshakes” in introductions may have been associated with religious or ethnic practices, and for the study to take into consideration a cohort of clinicians who are heavily influenced by these external factors. We also suggest that an introduction of a patient quota per ethnic background could be used in order to investigate the effects of ethnicity as a single variable on the types of introductions offered.
Finally, there was a heavy focus on the patients’ expectations when it comes to having an introduction made and which type is preferred. We suggest that an interesting angle would be to consider the clinicians needs too.
In summary, we agree that introducing yourself to patients is an excellent way of building satisfactory doctor-patient relationships. However, the sensitivities related to the type of introduction and religious or cultural backgrounds might have provided answers for the lack of introduction by some clinicians if it were to be explored in more detail. It is also equally as important to look at both the clinician and patients’ preferences when it comes to preferred gestures, so that consultations are tailored to meet both parties comfort thresholds.
References:
1) E Bedell S, B Graboys T. Hand to Hand. Pubmed [Internet]. 2002 [cited 23 September 2019];. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1495090/
2) Makoul G, Zick A, Green M. An Evidence-Based Perspective on Greetings in Medical Encounters. JAMA internal medicine [Internet]. 2007 [cited 23 September 2019];. Available from: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/412602
3) Marcinowicz L, Konstantynowicz J, Godlewski C. Patients' perceptions of GP non-verbal communication: a qualitative study. British journal of medical practice [Internet]. 2010 [cited 23 September 2019];. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2814260/
4) Attum B, Waheed A, Shamoon Z.
Cultural Competence in the Care of Muslim Patients and their families. [Updated 2019 Jun 15]
In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-.
Available from: https://www.ncbi.nlm.nih.gov/books/NBK499933/
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...
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 reported prevalence between 10.7 and 64.0 cases per 100,000 population(4), patients who do not have the skills to translate "narrative" to "normative" are often fobbed off with the diagnosis of "labyrynthitis", with the consequent risk of having to surrender their driving licence, given the fact that , under the heading "Dizziness or vertigo and driving", DVLA specifies that "You can be fined up to £1,000 if you don't tell DVLA about a medical condition that affects your driving"
I have no funding and no conflict of interest.
References
(1) Launer J
The Yin and Yang of medical consultation
Postgrad Med J 2019;95:575-576
(2) Gorroll AH
Emerging from the EHR purgotary - Moving from process to outcomes
N Eng J Med 2017;376:2004-2005
(3)Mumford CJ
Post-traumatic benign paroxysmal positional vertigo
Pract Neurol 2019;19:354-355
(4) Kim J-S., Zee DS
Benign paroxysmal positional vertigo
N Engl J Med 2014;370:1138-1147
(5) Gov.UK
Dizziness or vertigo and driving https://www.gov.uk/transport/driving-and-medical-condtions http://www.gov.uk/transport/driving-and-medical-conditions
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.
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).
Show MoreAccording 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...
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...
Show MoreAmong 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).
Show MoreThe 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...
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.
Show MoreIn 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...
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).
Show MoreCoexistence 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...
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
Show More1. Welsby PD. Have guidelines lost their way? Postgrad Med J 2019; 95(1127): 469.
2....
Letter response to the article “Effects of breathing exercises using home-based positive pressure in the expiratory phase in patients with COPD
Abstract
Show MoreFollowing 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...
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...
Show MoreFortuitously, 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).
Show MoreIn 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...
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
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