The NEW Birmingham Students Medical Leadership Society

Ironically, it seems the health products with the least evidence are coming with the greatest assurances. A few years ago, a package holiday company advertised guaranteed sunny holidays in Queensland (Australia). The deal went something like this: if it rained on a certain percentage of your holiday days, you received a trip refund. An attractive drawcard indeed, but what the company failed to grasp was that the “Sunshine State” is very often anything but sunny. This is especially so where I live, on the somewhat ironically named Sunshine Coast. We had 200 rainy days last year and well over 2 metres of rain, and that was before big floods in January. Unsurprisingly, the guaranteed sunny holiday offer was short-lived. There are some things that really shouldn’t come with guarantees. The weather is one, health is another. Or so I thought… “Those capsules you started me on last month for my nerve pain didn’t work. I tried them for a couple of weeks, but they didn’t do nothin'.” “Perhaps you’d do better on a higher dose.” “Nah, they made me feel kinda dizzy. I’d prefer to get my money back on these ones an’ try somethin’ different.” “I can try you on something else, but there are no refunds available on the ones you’ve already used, I’m afraid.” “But they cost me over 80 dollars!” “Yes, I explained at the time that they are not subsidised by the government.” “But they didn’t work! If I bought a toaster that didn’t work, I’d take it back and get me money back, no problem.” “Medications are not appliances. They don’t work every time, but that doesn’t mean they’re faulty.” “But what about natural products? I order herbs for me prostate and me heart every month and they come with a 100% satisfaction guarantee. You doctors say those things don’t really work so how come the sellers are willing to put their money where their mouths are?” He decided to try a “natural” treatment next, confident of its likely effectiveness thanks to the satisfaction guarantee offered. Last week I had a 38-year-old female requesting a medical certificate stating that her back pain was no better. The reason? She planned to take it to her physiotherapist and request a refund because the treatment hadn’t helped. Like the afflicted patient above, she didn’t accept that health-related products and services weren’t “cure guaranteed”. “My thigh sculptor machine promised visible results in 60 days or my money back. Why aren’t physios held accountable too?” Upon a quick Google search, I found that many “natural health” companies offer money-back guarantees, as do companies peddling skin products and gimmicky home exercise equipment. I even found a site offering guaranteed homeopathic immunisation. Hmmm… In an information-rich, high-tech world, we are becoming less and less tolerant of uncertainty. Society wants perfect, predictable results — now! For all its advances, modern medicine cannot provide this and we don’t pretend otherwise. Ironically, it seems the health products with the least evidence are coming with the greatest assurances. A clever marketing ploy that patients seem to be buying into — literally and figuratively. I think we all need to be reminded of Benjamin Franklin’s famous words: “In this world, nothing can be said to be certain except death and taxes.” We can’t really put guarantees on whether it will rain down on our holidays or on our health, and should retain a healthy scepticism towards those who attempt to do so. This blog post has been adapted from a column first published in Australian Doctor http://www.australiandoctor.com.au/articles/11/0c070a11.asp Dr Genevieve Yates is an Australian GP, medical educator, medico-legal presenter and writer. You can read more of her work at http://genevieveyates.com/  

It was a Saturday, about tea-time in the quaint village of Athelstaneford, East Lothian. Mrs Alexandria Agutter sat in her cottage, enjoying the delights of the late-summer evening with a glass of gin and tonic. She listlessly sipped from the rather generous pick-me up, no doubt chewing over the happenings of the day. Blast! The taste was much too bitter to her liking. She stood up. And promptly crumpled to the floor in a dizzied heap. It had not been five minutes when a fiery pain gripped her parched throat and in her frenzied turn she watched the bleary room become draped in a gossamery silk. How Dame Agatha would approve. But this is no crime novel, on that fateful day, 24th August 1994, poor Mrs Agutter immortalised herself in the history books of forensic medicine; she was the victim of a revered toxin and a vintage one it was too. She had unwittingly imbibed a G&T laced with a classic poison of antiquity. A clue from the 21st century: do you recall the first Hunger Games film adaption? Those inviting purple-black berries or as Suzanne Collins coined them ‘Nightlock’; a portmanteau of hemlock and Deadly Nightshade. True to the laters’ real life appearance those onscreen fictional fruits played a recurring cameo role. Deadly Nightshade is a perennial shrub of the family Solanaceae and a relative of the humble potato (a member of the Solanus genus). It is a resident of our native woodland and may be found as far afield as Europe, Africa and Western Asia. The 18th century taxonomist, Carl Linnaeus gave the plant an intriguing name in his great Species Plantarum. The genus Atropa is aptly named after one of the three Greek Fates, Atropos. She is portrayed shearing the thread of a mortal’s life so determining the time and manner of its inevitable end. The Italian species name belladona (beautiful woman) refers to the striking mydriatic effect of the plant on the eye. The name pays homage to Pietro Andre Mattioli, a 16th century physician from Sienna, who was allegedly the first to describe the plant’s use among the Venetian glitterati - ladies of fashion favoured the seductive, doe-eyed look. Belladona is poisonous in its entirety. It was from the plant’s roots in 1831, the German apothecary Heinrich F. G. Mein isolated a white, odourless, crystalline powder: it was (surprise, surprise) atropine. Atropine is a chiral molecule. From its natural plant source it exists as a single stereoisomer L-atropine, which also happens to display a chiral potency 50-100 times that of its D-enantiomer. As with many other anaesthetic agents it is administered as a racemic mixture. How strange that atropine now sits among the anaesthetist’s armamentarium, its action as a competitive antimuscarinic to counter vagal stimulation belies its dark history. It was a favourite of Roman housewives seeking retribution against their less than faithful husbands and a staple of the witch’s potion cupboard. Little wonder how belladona became known as the Devil’s plant. Curiouser still it’s also the antidote for other poisons, most notably the organophosphates or nerve gases. On account of its non-selective antagonism, atropine produces a constellation of effects: the inhibition of salivary, lacrimal and sweat glands occurs at low doses; dry mouth and skin are early markers. Pyrexia is a central effect exacerbated by the inability to sweat. Flushing of the face due to skin vessel vasodilatation. Low parasympathetic tone causes a moderate sinus tachycardia. Vision is blurred as the eye becomes dilated, unresponsive to light and accommodation is impaired. Mental disorientation, agitation and ataxia give the impression of drunkedness or a delirium tremens like syndrome. Visual hallucinations, often of butterflies or silk blowing in the wind, are a late feature. It was then that Mr Agutter, seemingly untroubled by the sight of his wife’s problematic situation, proceeded to leave a message with the local practitioner. How fortunate they were to have the vigilant locum check the answering machine and come round to the Agutter’s lodge accompanied by an ambulance crew. The attending paramedic had the presence of mind to pour the remainder of Mrs Agutter’s beverage into a nearby jam jar, while Mr Agutter handed over what he suspected to be the offending ingredient: the bottle of Indian tonic water. As it soon transpired there were seven other casualties in the surrounding countryside of East Lothian – all involving an encounter with tonic water. In fact by some ironic twist of fate, two of the victims were the wife and son of Dr Geoffry Sharwood-Smith, a consultant aneasthetist. Obviously very familiar with the typical toxidrome of anticholinergic agents, he was quick to suspect atropine poisoning. Although for a man of his position with daily access to a sweetshop of drugs, it was not something to draw attention to. Through no small amount of cunning had the poisoner(s) devised the plan. It was elegant; atropine is very bitter. So much so that it can be detected at concentrations of 100 parts per million (0.001%). Those foolish enough to try the berries of belladonna during walks in the woods are often saved by the berry’s sour taste. They are soon spat out. But the quinine in the tonic water was a worthy disguise. The lethal dose for an adult is approximately 90-130mg, however atropine sensitivity is highy variable. In its salt form, atropine sulfate, it is many times more soluble: >100g can be dissolved in 100ml of water. So 1ml may contain roughly tenfold the lethal dose. There ensued a nationwide scare; 50 000 bottles of Safeway branded Indian tonic water were sacrificed. Only six bottles had been contaminated. They had all been purchased, tops unsealed, from the local Safeway in Hunter’s Tryst. Superficially this looked like the handiwork of a psychopath with a certain distaste for the supermarket brand, and amidst the media furore, it did have some verisimilitude: one of the local papers received a letter from 25 year old, Wayne Smith admitting himself as the sole perpetrator. The forensic scientist, Dr Howard Oakley analysed the contents of the bottles. They all contained a non-lethal dose, 11-74mg/litre of atropine except for the Agutter’s, it contained 103mg/litre. The jam jar holding Mrs Agutter’s drink bore even more sinister results, the atropine concentration was 292mg/L. It would appear Mrs Agutter had in some way outstayed her welcome. But she lived. A miscalculation on the part of the person who had added an extra seasoning of atropine to her drink. According to the numbers she would have had to swallow a can’s worth (330ml) to reach the lethal dose. Thankfully she had taken no more than 50mg. The spotlight suddenly fell on Dr Paul Agutter. He was a lecturer of biochemistry at the nearby University of Napier, which housed a research syndicate specialising in toxicology. CCTV footage had revealed his presence at the Safeway in Hunter’s Tryst and there was eye witness evidence of him having placed bottles onto the shelves. Atropine was also detected by the forensic investigators on a cassete case in his car. Within a matter of two weeks he would be arrested for the attempted murder of his wife. Despite the calculated scheme to delay emergency services and to pass the blame onto a non-existent mass poisoner, he had not accomplished the perfect murder. Was there a motive? Allegedly his best laid plans were for the sake of a mistress, a mature student from Napier. He served seven years of a twelve year sentence. Astonishingly, upon his release from Glenochil prison in 2002, he contacted his then former wife proclaiming his innocence and desire to rejoin her in their Scottish home. A proposition she was not very keen on. Dr Agutter was employed by Manchester University as a lecturer of philosophy and medical ethics. He is currently an associate editor of the online journal Theoretical Biology and Medical Modelling. We will never know the true modus operandi as Dr Agutter never confessed to the crime. Perhaps all this story can afford is weak recompense for the brave followers of the Dry January Campaign. Oddly these sort of incidents never appear in their motivational testimonials. Acknowledgements Emsley J. Molecules of Murder. 2008, Cambridge, RSC Publishing, p.46-67. Lee MR. Solanaceae IV: Atropa belladona, deadly nightshade. J R Coll Physicians Edinb. March 2007; 37: 77-84. Illustrator Edward Wong This blog post is a reproduction of an article published in the The Medical Student Newspaper January issue, 2014 http://www.themedicalstudent.co.uk/  

This month’s case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e, with 15% off using the discount code: MEDUCATION. The case below is followed by a quiz question, allowing you a choice of diagnoses. Select the one letter section that best describes the patient’s condition. The Case A 28-year old woman has an unremarkable pregnancy through her first 28 weeks of gestation, with normal weight gain and no serious complications. She has no previous history of diabetes, hypertension of other systemic disease before or during her current pregnancy. During her 30-week checkup, her blood pressure measures 128/85, and she complains about feeling slightly more “bloated” than usual with swelling in her legs that seems to get more uncomfortable as the day goes on. Her obsterician recommends that she get more bed rest, stay off her feet as much as possible and return for evaluation in one week. At the one-week follow-up, the patient presents with noticable”puffiness” in her face, and a blood pressure of 145/95. She complains she has been developing headaches, sporadic blurred vision, right-sided discomfort and some shortness of breath. She has gained more than 10 lb (4.5kg) in the past week. A urinalysis on the patient revelas no glucose but a 3+ reading for protein. Her obstetrician decides to admit her immediately to a local tertiary care hospital for further evaluation. Over the next 24 hours, the patient’s urine output is recorded as 500mL and contains 6.8 grams of protein. Her plasma albumin level is 3.1 g/dl, hemacrit 48%, indirect bilirubin 1.5mg/dl and blood platelets=77000/uL, respectively. Her blood pressure is now 190/100. It is decided to try to deliver the foetus. The expelled placenta is small and shows signs of widespread ischmic damage. Within a week of delivery, the mother’s blood pressure returns to normal, and her oedema subsides. One month later, the mother shows no ill effects of thos later-term syndrome. Question What is the clinical diagnosis of this patient’s condition and its underlying pathophysiology? A. Gestational Hypertension B. Preeclampsia C. Gestational Diabetes D. Compression of the Inferior Vena Cava Answer The correct answer is "B. Preeclampsia". The patient’s symptoms and laboratory findings are consistent with a diagnosis of Preeclampsia, which is a condition occurring in some pregnancies that causes life-threatening organ and whole body regulatory malfunctions. The patient’s negative urine glucose is inconsistent with gestational diabetes. Gestational hypertension or vena caval compression cannot explain all of the patient findings. The patient has three major abnormal findings- generalised oedema, hypertension and proteinuria which are all common in preeclampsia. Although sequalae of a normal pregnancy can include water and salt retention, bloating, modest hypertension and leg swelling (secondary to capillary fluid loss from increased lower limb capillary hydrostatic pressure due to compression of the inferior vena cava by the growing foetus/uterus), oedema in the head and upper extremities, a rapid 10 pound weight gain and shortness of breath suggests a generalized and serious oedematous state. The patient did not have hypertension before or within 20 weeks gestation (primary hypertension) and did not develop hypertension after the 20th week of pregnancy with no other abnormal findings (gestational hypertension). Hypertension with proteinuria occurring beyond the 20th week of pregnancy however is a hallmark of preeclampsia. In addition, the patient has hemolysis (elevated bilirubin and LDH levels), elevated liver enzyme levels and thrombocytopenia. This is called the HELLP syndrome (HELLP = Hemolysis, Elevated Liver enzymes and Low Platelets.), and is considered evidence of serious patient deterioration in preeclampsia. A urine output of 500 ml in 24 hours is 1/2 to 1/4 of normal output in a hydrated female and indicates renal insufficiency. Protein should never be found in the urine and indicates loss of capillaries integrity in glomeruli which normally are not permeable to proteins. The patient has substantial 24 urine protein loss and hypoalbuminemia. However, generally plasma albumin levels must drop below 2.5 gm/dl to decrease plasma oncotic pressure enough to cause general oedema. The patient’s total urinary protein loss was insufficient in this regard. Capillary hyperpermeability occurs with preeclampsia and, along with hypertension, could facilitate capillary water efflux and generalized oedema. However myogenic constriction of pre-capillary arterioles could reduce the effect of high blood pressure on capillary water efflux. An early increase in hematocrit in this patient suggests hemoconcentration which could be caused by capillary fluid loss but the patient’s value of 48 is unremarkable and of little diagnostic value because increased hematocrit occurs in both preeclampsia and normal pregnancy. PGI2, PGE2 and NO, produced during normal pregnancy, cause vasorelaxation and luminal expansion of uterine arteries, which supports placental blood flow and development. Current theory suggests that over production of endothelin, thromboxane and oxygen radicals in preeclampsia antagonize vasorelaxation while stimulating platelet aggregation, microthrombi formation and endothelial destruction. These could cause oedema, hypertension, renal/hepatic deterioration and placental ischemia with release of vasotoxic factors. The patient’s right-sided pain is consistent with liver pathology (secondary to hepatic DIC or oedematous distention). Severe hypertension in preeclampsia can lead to maternal end organ damage, stroke, and death. Oedematous distension of the liver can cause hepatic rupture and internal hemorrhagic shock. Having this patient carry the baby to term markedly risks the life of the mother and is not considered current acceptable clinical practice. Delivery of the foetus and termination of the pregnancy is the only certain way to end preeclampsia. Read more This case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at (lww.co.uk)[http://lww.co.uk] when you use the code MEDUCATION when you check out! About LWW/ Wolters Kluwer Health Lippincott Williams and Wilkins (LWW) is a leading publisher of high-quality content for students and practitioners in medical and related fields. Their text and review products, eBooks, mobile apps and online solutions support students, educators, and instiutions throughout the professional’s career. LWW are proud to partner with Meducation.  

When I first started thinking about Medical Leadership and Management (MLM) it was because I like to see things work. When anything doesn't work, or something is inefficient or I think a system could be designed to make life easier - I get pretty annoyed. So, being irritated in things is what got me interested in MLM, but now it seems that I spend quite a lot of time thinking about MLM just because it is so ubiquitous. Almost any day you spend in hospital will involve you witnessing MLM on an almost minute by minute basis - even if you don't notice it! Recently, I have being working on a number of projects in my spare time (mostly out of interest but partly to secure those elusive foundation program points), which involved reading quite a few journal articles on a number of subjects ranging from the "trauma care" to "gastric banding". What surprised me was the prevalence of phrases like "....teams need greater training in medical leadership to improve patient outcomes..." or "...medical education needs to include greater emphasis of soft skills such as communication, team work and team leadership.." The profession's views on MLM have obviously been developing for a while, within the literature and now some organisations are really taking this ethos to heart, but it is still not a universal phenomenon. So, I thought it would be interesting to post this blog and start documenting random places where MLM is mentioned. If anyone reading this finds any surprising mentions then please do paste the link to the article in the comments section.