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PMC3159000

Thrombotic thrombocytopenic purpura (TTP) is a disorder with characteristic von Willebrand factor (VWF)-rich microthrombi affecting the arterioles and capillaries of multiple organs. The disorder frequently leads to early death unless the patients are treated with plasma exchange or infusion. Studies in the last decade have provided ample evidence to support that TTP is caused by deficiency of a plasma metalloprotease, ADAMTS13. When exposed to high shear stress in the microcirculation, VWF and platelets are prone to form aggregates. This propensity of VWF and platelet to form microvascular thrombosis is mitigated by ADAMTS13, which cleaves VWF before it is activated by shear stress to cause platelet aggregation in the circulation. Deficiency of ADAMTS13, due to autoimmune inhibitors in patients with acquired TTP and mutations of the ADAMTS13 gene in hereditary cases, leads to VWF–platelet aggregation and microvascular thrombosis of TTP. In this review, we discuss the current knowledge on the pathogenesis, diagnosis and management of TTP, address the ongoing controversies, and indicate the directions of future investigations.  
ncbi.nlm.nih.gov
over 5 years ago
Preview
1
66

Untitled Document

The specialized nodal and conducting cells of the heart are responsible for heartbeat. These specialized nodal and conducting cells tend to contract weakly because they contain very few contractile cells (myofibrils). What makes these cells unique is that they can easily generate an action potential (electrical impulse that causes the heart to beat) without the assistance of neurotransmitters or any nervous system input like any regular neurons. Along with these special properties of self-excitability, these cells can also rapidly conduct impulses to atrial and ventricular muscles. This explains why after death, the heart continues pumping because of the nodal and conducting cells; this is because the nodal and conducting cells are not hooked up with any neurotransmitters. Therefore, these specialized cells provide a self-excitatory system for the heart to generate impulses and a transmission system for rapid conduction of impulses in the heart.  
odec.ca
over 5 years ago
Preview
1
30

Meningitis W: 'My son's death was unbelievably quick' - BBC News

BBC Breakfast spoke to Tracey and Emily Saunders, whose son and brother Edward died after contracting Meningitis W.  
BBC News
over 5 years ago
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1
46

Millie Thompson's mother: 'My daughter might not have died' - BBC News

Joanne Thompson, whose daughter choked to death at nursery school, talks about her charity, Millie's Trust, that has successfully campaigned for staff to have first aid training.  
BBC News
over 5 years ago
Www.bmj
1
7

People with diabetes have one third higher mortality risk than general population, audit shows | The BMJ

The risk of death is one third higher among people with diabetes in England and Wales than in those without diabetes, the National Diabetes Audit has said, adding that this is due to complications resulting from poor diabetes control. - currently located behind a paywall. Your institution may have access through Athens/Elservier or similar.  
bmj.com
over 5 years ago
Www.bmj
1
33

Leading campaigner for legalising assisted suicide dies from starvation

Debbie Purdy, the leading campaigner and activist for the legalisation of assisted suicide in the United Kingdom, has died at the age of 51 after starving herself to death.  
bmj.com
over 5 years ago
Www.bmj
1
20

Inspectors to investigate baby’s death in Sicily after neonatal bed could not be found

Concern over the state of Italy’s healthcare system has been raised after the death of a newborn baby who was transported across Sicily in search of an intensive care cot.  
bmj.com
over 5 years ago
Www.bmj
1
32

Resuscitating drowned children

The World Health Organization published its global report on drowning in November 2014, reporting a staggering 372 000 deaths a year from all types of water immersion. Worldwide, drowning is in the top 10 causes of death in children and young people, particularly in males and those aged under 5. An estimated 21 children and young adults are drowned every hour.1 Other public health matters have had disproportionately greater attention, despite the numbers of deaths from drowning being equivalent to two thirds of global deaths from malnutrition and over one half of deaths from malaria.  
bmj.com
over 5 years ago
Www.bmj
1
17

Trajectories of risk after hospitalization for heart failure, acute myocardial infarction, or pneumonia: retrospective cohort study

Objective To characterize the absolute risks for older patients of readmission to hospital and death in the year after hospitalization for heart failure, acute myocardial infarction, or pneumonia.  
bmj.com
over 5 years ago
Preview
1
18

What do doctors say to 'alternative therapists' when a patient dies? Nothing. We never talk | Ranjana Srivastava

Jessica Ainscough’s tragic death is all too familiar for oncologists. We’ve all lost patients to the ‘secret powers’ of alternative therapy  
the Guardian
over 5 years ago
11
0
3

How is it best to cope with situations in medical training that bring back bad memories?

I have a a friend who has had painful experiences with illness and death in her family. Obviously there are times where she struggles with sad memories as she is learning various parts of medicine. How is it best to deal with this sort of situation?  
Jeremy Walker
about 8 years ago
13
0
14

What is the future of organ transplants?

Give the death this week of Dr Joseph Murray, who won the Nobel Prize for performing the first-ever successful organ transplant (a renal transplant), I was wander what the future of this area is? Does anyone know what likely advances are going to be made to stop the risk of rejection while minimising the risk of anti-rejection drugs to the patient?  
Jon Michael
almost 8 years ago
Foo20151013 2023 t4jn?1444773937
9
362

Death by Powerpoint.

Introduction Computerised presentations are a part of every medical student's / junior doctor's life. Sometimes we give them, often we sleep through them and occasionally we even listen to them. They are the backbone of medical education besides traditional bed-side teaching, having rapidly replaced the now extinct OHR (Over Head Projector) acetate-sheet presentations of years gone-by. The problem is that Doctors and medical students often struggle with creating and presenting coherent slides. This is most probably due to the general apathy most have for actually talking in front of an audience, or because those asked to present are often taken unawares, and therefore have little time to prepare. In these times of avolition or last-minute hurriedness, people often reach out for the industry standard of presentation production: PowerPoint. PowerPoint is the most commonly used tool for making presentations because it is simple to use and comes with a whole load of free templates. Unfortunately, most of these templates look disgusting. If a template doesn't look disgusting, then it is most certainly overused and you run the risk of having a presentation that looks identical to the student before you at the weekly seminar teaching - a scenario that can be easily likened to turning up to a lecture wearing exactly the same clothes as another person in the room, which would just be awkward. Another problem with PowerPoint is the phenomenon of 'Death By Powerpoint,' which refers to the general boredom and apathy experienced by those who have received way too much information in way too short a space of time via a series of over-cramped, poorly stylised slides. But why on earth do you care? People should care about 'Death By Powerpoint' because if your presentations cause people to zone out, then you are not getting your message across. And if you aren't getting your message across then you. are. not. presenting. at. all. (take a moment to reflect on that particularly Zen statement). Let me explain using a metaphor, if I am a sales person and I present my talk with well-designed slides, in an enthusiastic and well-rehersed manner to an appropriate audience I will make more sales than if I present using poorly designed slides at the last minute. Similarly, in Medicine if I present well designed, aesthetic slides I am more likely to convey accurate information to my colleagues that may very well be retained and enjoyed by all involved. Of course, this blog assumes a degree of presentation-related Altruism. The recommendations I am about to make require you to 'step out of the mould' and say 'no' to poor presentations. They require you to forgive others for the presentations they have inflicted on you in the past. You will 'lead by example'. Unfortunately I am not capable (or qualified) to make you an excellent designer, nor can I give you the motivation to feel as passionately about design aesthetics as i do when all you've got to do is slam some slides together for your monthly journal club. But what I can do is present to you a series of resources that might tempt you away from the horrific PowerPoint templates that currently infest medical student seminars and young doctors presentations. If you really couldn't care less, then I suggest using Prezi, a website where you can make quite eccentric looking presentations rapidly and for free. The only problem is that Prezi became cliched even before its debut and you risk inflicting travel sickness on your poor audience, what with all the funky zooming in and out of slides that occurs during a typical Prezi presentation (you will know what I mean if you've ever seen one). So, without further ado, here are my top 5 tips for making your presentations look smoother and more polished... Irrespective of whether the contents of your talk are any good. Step One: Typography Get yourself a good font. Typography is really important, when you speak to someone you use a variety of tones and gestures to convey the meaning of the words you are using. Fonts are effectively the printed version of your tone and gestures. Good font choice can help give 'umph' to a particular point in your presentation and help give character to what you are saying. Of course, it's important to remain professional so 'Wingbats' might not be your first choice, but anything that you could envisage on a nice business card is probably a good shout. Fonts are usually something you have to pay for if you want anything beyond the set given to you when you download Microsoft Word (for example). However, there are whole hosts of free fonts available from sites like [dafont])(http://www.dafont.com). The key is to be willing to trawl through these sites to find fonts that are actually useful! Beware those fancy fonts unless you know your audience can take it! If you are stuck on choosing a font, which is a common complaint, then maybe this flow diagram will help! Oh yeah, and never ever use Comic Sans. Ever. Step Two: Colour A good font isn't going to get you very far on its own. You need a solid colour scheme to bring your presentation alive. It seems blunt to say, but some people are not very good at picking colours that go well with one another. This is well evidenced in PowerPoint presentations where the yellow-text-on-blue-background is far too common. I mean yeah, in theory blue and yellow 'compliment' each other, but thats where the relationship between blue and yellow should stay... in theory. Luckily there are some useful colour palette websites available out there, which will match colours for you... Step Three: Structure After you've picked a sensible font and a suitable colour scheme, it's time to think about the structure or layout of your slides. It's absolutely crucial that you avoid putting too much information on your slides even if you are giving an academic presentation. An overloaded slide is about as useful as a dead cat. At this point, some of you may be tempted to resort to those dodgy PowerPoint default templates but there is another way! There are sites out there that have some pretty fresh templates you can use and they are completely free! They are sure to add a bit of spice to your slide's aesthetic. There will probably be a separate tutorial on this in the future, but basic principles apply. As a general rule stick to Left Alignment *and avoid *Central Alignment like the plague. Step Four: Imagery Images help to spice up a presentation, but try and keep them related to the topic. Google Images is a great resource but remember that most images will be a low resolution and will be poorly suited to being shown blown up full-size on a presentation screen. Low resolution images are a presentation killer and should be avoided at all costs. For high-quality images try sites like Flikr or ShutterStock. Step Five: Consider Software The interface of Powerpoint does not lend itself well to having images dropped in and played with to make nice looking layouts. I would recommend Adobe Photoshop for this kind of work, but not everyone will have access to such expensive software. Cheap alternatives include Photoshop Elements amongst others. Once you have created slides in Photoshop it is quick and easy to save them as JPEG files and drag and drop them into PowePoint. Perhaps that can be a tutorial for another time... Step 5: Additional Stuff Presentations typically lack significance, structure, simplicity and rehearsal. Always check over your presentation and ask 'is this significant to my audience?' Always structure your presentation in a logical manner and (it is recommended you) include a contents slide and summary slide to tie things together. Keep your verbal commentary simple and keep the slides themselves even more simple than that. Simplicity is crucial. Once you have produced your beautiful slides with wonderful content you will want to practice them. Practice, Practice, Practice. Rehearsing even just once can make a good presentation even better. Conclusion: This blog entry has covered some basic points on how to improve your medical presentations and has given a series of useful online resources. Putting effort into designing a presentation takes time and motivation, for those without these vital ingredients we recommend Prezi (whilst it is still relatively new and fresh). Perhaps the rest of you will only use these tips for the occasional important presentation. However, I hope that soon after you start approaching presentations with a little more respect for their importance and potential, you too will find a desire to produce high-quality, aesthetically pleasing talks. LARF - Mood: damn tired and feeling guilty that I just wrote this blog instead of revising haematology notes. Follow me on Twitter. Follow the Occipital Designs original blog. Check out my Arterial Schematic.  
Dr. Luke Farmery
over 7 years ago
Foo20151013 2023 1ilnrlb?1444774017
6
178

Itraconazole Toxicity and Cardiac Health Problems

Itraconazole is an antifungal drug used widely to treat fungal infections and is active against Aspergillus, Candida and Cryptococcus. It is effective and now much cheaper as it has passed out of the period of time granted to its inventor to exclusively sell it - there are now several competing manufacturers. It seems to be an increasingly useful and used drug now it has become more accessible which is a good thing in the main but this makes it increasingly important that this drug is properly understood and its very severe potential side effects appreciated and guarded against. These are the warnings published by the World Health Organisation Risk of congestive heart failure The agency says that while the available evidence suggests that the risk of heart failure with short courses of itraconazole is low in healthy, young patients, prescribers should exercise caution when prescribing the drug to at-risk patients. Amendments to the product information of all itraconazole formulations have been made to reflect this information. Risk to pregnant women By April 2000 the UMC had received 43 case reports from 5 countries regarding the use of itraconazole by pregnant women. 25 of these pregnancies ended in embryonic or foetal death. The remaining 19 reports described a variety of congenital malformation or neonatal disorders. In the 38 reports in which the route of administration was specified the drug was taken orally. The data suggested that: inspite of the approved recommendations and warnings itraconazole is being taken by pregnant women for minor indications, reported human experience seems to lend support to the experimental evidence that itraconazole is teratogenic, there is a predominance of abortion, and more firm warnings may be needed in the product information.Although not apparent from the UMC reports, a further question of interest was if itraconazole might decrease the reliability of oral contraceptives and so lead to unintended exposure in pregnancy. Care thus needs to be taken about which patients are prescribed itraconazole, adequate monitoring needs to be put in place if needed and sufficient advice given with the drug to ensure the patient is aware of the risks involved and the signs & symptoms to look out for.  
Graham Atherton
over 7 years ago
Foo20151013 2023 2njk5o?1444774020
4
1336

LWW: Case Of The Month - April 2013

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.  
Lippincott Williams & Wilkins
over 7 years ago
Foo20151013 2023 4ktnps?1444774050
4
191

Poo transplants

When is it medically advisable to eat some one else's poo? When you need a poo transplant. Poo transplants could be the solution to one of the biggest problems facing the NHS today- the bacterial infection Clostridium difficile. C.diff, as it's known to its friends, infects about 18,000 people in England and Wales every year and is involved in the deaths of about 2000 people. C.diff typically arises due to imbalances in the normal gut bacteria. The gut is like a city, a city with about 100 trillion bacterial residents happily munching away on a banquet of bowel contents. The average person has about 1000 different types of bacteria in their gut, and about 3% of healthy adults have C.diff in that mix. The C.diff doesn't cause them any problems because its numbers are kept in check by the other gut bacteria. However treatment with broad spectrum antibiotics such as clindamycin, cephalosporins, ciprofloxacin and co-amoxiclav, can disrupt this happy community- killing off vast swathes of bacteria but crucially not the C.diff. Given free rein the C.diff multiplies rapidly and produces toxins which damage the gut. In some people this causes mild diarrhoea and abdominal pain, in others it can lead to torrential diarrhoea, perforation of the colon and death. Traditional treatment includes stopping any broad spectrum antibiotics and possibly prescribing antibiotics which target the C.diff such as metronidazole or vancomycin. However with antibiotic use comes the risk of resistance. Moreover our current approach isn't entirely effective and about 22% of patients treated suffer a recurrence. This can result in a cycle of illness and hospital admission which is costly to the patient and the hospital. So it's time to start thinking outside of the box. Cue the poo transplant. The thinking goes like this- if the cause of the problem is disruption to the normal community of gut bacteria, why not just pop those bacteria back in to crowd out the C.diff? Simples. Practically, the first step is to identify a donor, usually a close relative of the patient, and screen them for a range of infectious diseases and parasites. It's also advisable to make sure they haven't recently consumed anything the intended recipient is allergic to, before asking them to make their "donation". You then pop it in a household blender and blitz it down, adding saline or milk to achieve a slurry consistency. Next you need to strain your concoction to remove large materials- one medic in the UK uses coffee filters. Top tip. Then you're ready to administer it- about 25ml from above (e.g. via nasogastric tube), or 250ml from below. Now, its important to note that poo transplants are still an experimental treatment. To date only small case studies have been carried out, but with 200 total reported cases, an average cure rate of 96% and no serious adverse events reported to date, it's worth carrying out a large trial to assess it thoroughly. Poo transplants- arguably the ideal treatment for a cash strapped NHS. It's cheap, plentiful and it seems to work. Now to convince people to consume someone else's poo... Bottoms up! FYI: This was first posted on my own blog. Image Courtesy of Marcus007 at de.wikipedia [Public domain], from Wikimedia Commons  
Dr Catherine Carver
over 7 years ago
Foo20151013 2023 s45v8o?1444774247
2
74

Money-back guarantees

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/  
Dr Genevieve Yates
over 6 years ago
%3fr=0
2
132

A Modest Man

The registrar's face was taking on a testy look. So enduring was the silence our furtive glances had developed a nystagmic quality. “Galactosaemia” came her peremptory reply. Right on queue the disjointed chorus of ahs and head nods did little to hide our mental whiteboard of differentials being wiped clean. At the time conjugated bilirubinaemia in children only meant one thing: biliary atresia. A fair assumption; we were sitting in one of three specialist centres in the country equipped to treat these patients. Ironically the condition has become the unwieldy yardstick I now measure the incidence of paediatric disease. Biliary atresia is the most common surgical cause of neonatal jaundice with a reported incidence of 1 in 14-16ooo live births in the West. It is described as a progressive inflammatory obliteration of the extrahapatic bile duct. And Dr Charles West, the founder of Great Ormond Street Hospital, offers an eloquent description of the presenting triad of prolonged jaundice, pale acholic stools and dark yellow urine: ‘Case 18...It was born at full term, though small, apparently healthy. At 3 days however, it began to get yellow and at the end of 3 weeks was very yellow. Her motions at no time after the second day appeared natural on examination, but were white, like cream, and her urine was very high coloured.’ 1855 was the year of Dr West's hospital note. An almost universally fatal diagnosis and it would remain so for the next 100 years. The time's primordial classification of biliary atresia afforded children with the 'noncorrectable' type, a complete absence of patent extrahepatic bile duct, an unfortunate label; they were beyond saving. Having discovered the extent of disease at laparatomy, the surgeons would normally close the wound. The venerable Harvardian surgeon, Robert E. Gross saved an enigmatic observation: “In most instances death followed a downhill course…” K-A-S-A-I read the ward’s board. It was scrawled under half the children's names. I dismissed it as just another devilishly hard acronym to forget. The thought of an eponymous procedure had escaped me and in biliary atresia circles, it's the name everyone should know: Dr Morio Kasai. Originating from Aomori prefecture, Honshu, Japan, Dr Kasai graduated from the National Tohoku University School of Medicine in 1947. His ascension was rapid, having joined the 2nd department of Surgery as a general surgeon, he would assume the role of Assistant Professor in 1953. The department, under the tenure of Professor Shigetsugu Katsura, shared a healthy interest in research. 1955 was the landmark year. Katsura and Kasai operated on their first case: a 72 day old infant. Due to bleeding at the incised porta hepatis, Katsura is said to have 'placed' the duodenum over the site in order to staunch the flow. She made a spectacular postoperative recovery, the jaundice had faded and there was bile pigment in her stool. During the second case, Katsura elected to join the unopened duodenum to the porta hepatis. Sadly the patient's jaundice did not recover, but the post-mortem conducted by Kasai confirmed the development of a spontaneous internal biliary fistula connecting the internal hepatic ducts to the duodenum. Histological inspection of removed extrahepatic duct showed the existence of microscopic biliary channels, hundreds of microns in diameter. Kasai made a pivotal assertion: the transection of the fibrous cord of the obliterated duct must contain these channels before anastomosis with the jejunal limb Roux-en-Y loop. This would ensure communication between the porta hepatis and the intrahepatic biliary system. The operation, entitled hepatic portoenterostomy, was first performed as a planned procedure for the third case at Tohoku. Bile flow was restored and Kasai published the details of the new technique in the Japanese journal Shujutsu in 1959. However, news of this development did not dawn on the West until 1968 in the Journal of Pediatric Surgery. The success of the operation and its refined iterations were eventually recognized and adopted in the 1970s. The operation was and is not without its dangers. Cholangitis, portal hypertension, malnutrition and hepatopulmonary syndrome are the cardinal complications. While diagnosing and operating early (<8 weeks) are essential to the outcome, antibiotic prophylaxis and nutritional support are invaluable prognostic factors. Post operatively, the early clearance of jaundice (within 3 months) and absence of liver cirrhosis on biopsy, are promising signs. At UK centres the survival after a successful procedure is 80%. The concurrent development of liver transplantation boosts this percentage to 90%. Among children, biliary atresia is the commonest indication for transplantation; by five years post-Kasai, 45% will have undergone the procedure. On the 6th December 2008, Dr Kasai passed away. He was 86 years old and had been battling the complications of a stroke he suffered in 1999. His contemporaries and disciples paint a humble and colourful character. A keen skier and mountaineer, Dr Kasai lead the Tohoku University mountain-climbing team to the top of the Nyainquntanglha Mountains, the highest peaks of the Tibetan highlands. It was the first successful expedition of its kind in the world. He carried through this pioneering spirit into his professional life. Paediatric surgery was not a recognized specialty in Japan. By founding and chairing multiple associations including the Japanese Society of Pediatric Surgeons, Dr Kasai gave his specialty and biliary atresia, the attention it deserved. Despite numerous accolades of international acclaim for his contributions to paediatric surgery, Dr Kasai insisted his department refer to his operation as the hepatic portoenterostomy; the rest of the world paid its originator the respect of calling it the ‘Kasia’. Upon completion of their training, he would give each of his surgeons a hand-written form of the word ‘Soshin’ [simple mind], as he believed a modest surgeon was a good one. At 5 foot 2, Kasai cut a more diminutive figure one might expect for an Emeritus Professor and Hospital Director of a university hospital. During the course of his lifetime he had developed the procedure and lived to see its fruition. The Kasia remains the gold standard treatment for biliary atresia; it has been the shinning light for what Willis J. Potts called the darkest chapter in paediatric surgery. It earned Dr Kasai an affectionate but apt name among his peers, the small giant. References Miyano T. Morio Kasai, MD, 1922–2008. Pediatr Surg Int. 2009;25(4):307–308. Garcia A V, Cowles RA, Kato T, Hardy MA. Morio Kasai: a remarkable impact beyond the Kasai procedure. J Pediatr Surg. 2012;47(5):1023–1027. Mowat AP. Biliary atresia into the 21st century: A historical perspective. Hepatology. 1996;23(6):1693–1695. Ohi R. A history of the Kasai operation: Hepatic portoenterostomy for biliary atresia. World J Surg. 1988;12(6):871–874. Ohi R. Morio Kasai, MD 1922-2008. J Pediatr Surg. 2009;44(3):481–482. Lewis N, Millar A. Biliary atresia. Surg. 2007;25(7):291–294. This blog post is a reproduction of an article published in the Medical Student Newspaper, April 2014 issue.  
James Wong
over 6 years ago
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Dying to do an expedition

As a hospital doctor, surgeon or GP we encounter death frequently. We quickly learn to cope. It helps when we know that we have done everything within our power to prevent death. When death is close we have the ability, medication and specialists services to make the process as 'comfortable' as possible. In the final moments it is rare that the patient is alone; whether in the company of family, friends or health care professionals. When an individual dies on expedition it may have been avoidable, you have very little kit to prevent it, they may be alone and they probably were your friend. No one prepares you for the potential of a client dying. But it happens. First of all, I am not trying to put you off doing an expedition. I love expedition medicine and have dedicated the last five years of my life to it. But I was not prepared for my first near death experience and I want to make sure you are. AVOIDABLE DEATHS During an expedition injuries, near misses and deaths are sometimes avoidable. There may have been a faulty bit of kit, medication which wasn't packed or route marker that fell down ... Hindsight is a wonderful thing. You, the team and the organisers work within what is feasible and normal health and safety don't and can't apply. I am NOT saying it is ok to be negligent, but a degree of pragmatism is need. What you need to remember is the competitors/ clients are aware of the dangers and, as medics, we should be too. LIMITED KIT Many medics are shocked by the lack of kit taken on expedition. But you need to think about the environment you are in and then think rationally. If your nearest decompression chamber is 3 days away by boat, is there much point taking oxygen on a diving expedition? If you are on expedition in the middle of the jungle is there any point taking a defib if any client in need of a defib is unlikely to survive extrication. You have to work within the limits of your environment and with the kit you have. As the medic you need to be aware of the nearest hospital and their facilities, the nearest large hospital with surgical and ITU facilities and the casevac plan. THE CLIENTS During expeditions the clients often become good friends. You will experience their highs and lows and share incredible experiences. This makes it especially hard when unfortunate events occur. At this point our role as medic often broadens to counsellor and bereavement officer. The other clients, organisers and medics need support during this time. Try to start this process whilst you are out there. Even with near misses, the psychological effect on people can be huge. Signs and symptoms are generally easy to spot, but screen for them at clinics. Be aware during race events that grief may manifest though clients pulling out, loss of performance and increased injuries due to lack of sleep, low mood or poor concentration. No matter what happens when you are on expedition my advice is; you can only work within your skill set and with the equipment you have. As a foundation doctor, if you’re faced with an unresponsive client - you are not expected to perform RSI and intubate. Work through your ABCDE and work within your limitations. If you would like to suggest any other blog topics or have any questions please post below.  
Dr Rachel Saunders
over 6 years ago