Dr John Hinds Bike Crash Prehospital Care and Emergent Thoractomy

I have been looking for the best medical documentaries, and while searching the r/documentaries setion on reddit I found a great post linking the video below. While not entirely a documentary per se it is a super interesting lecture on the specifics of bike crash prehospital care. He is a fantastic lecturer with a great sense of humour, well worth a worth.



Dr Hind died while responding to an accident at the 2015, Skerries Road Races, in County Dublin, Ireland, RIP. 

Another lecture by Dr Hind, this time on Emergent Thoractomy and more cases from the races.

Twitter Conference: Charing Cross Vascular Symposium #cx2017 Day Two

Since my paper is being presented and I am unable to be there, I will be 'attending' the Charing Cross Vascular Symposium through the wonderful medium of twitter. Following the hashtag #CX2017  I hope to catch as much as possible here on my blog. This is what I caught from Day 2:

Again the organisers continued with there fantastic ask the audience sections

And the results were interesting...

thanks to the twitter warriors: @cookEVAR @claudicant @perealtes @ozvascdoc @veryanmed1 @torbjornlundh @cxsymposium @vascularMD

Twitter Conference: Charing Cross Vascular Symposium #cx2017 Day One

Since my paper is being presented and I am unable to be there, I will be 'attending' the Charing Cross Vascular Symposium through the wonderful medium of twitter. Following the hashtag #CX2017  I hope to catch as much as possible here on my blog.

#timelapse at the very busy #CX2017 @CXSymposium pic.twitter.com/Ob8w7NfqbN

— BIBA MedTech (@BIBAMedTech) April 25, 2017

The first day was all about peripheral artery disease and the audience were asked some interesting questions regarding the their views on PAD, here are the results:

Dr Hauton alongside Dr Mastracci with her wonderful video in my last post addressed concerns on radition exposure, pointing out that 1 DSA image is roughly equal to 500 fluoro images:

 Mr Weinberg posted the following, pointing out that PAD patients receive better outcomes when combining exercise with revascularisation (linkhere):

Lucky man Dittmar Bockler loves his DynaCT:

What about smoking cessation in vascular patients, try try again:

 Dr Anders Wanhainen on the need for a disease specific solution for type B dissection.

Currently watching closely the twitter-web today, following todays focus on Abdominal aortic aneurysms... watch this space. 

Thanks to @PereAltes @Angiologist @CXsymposium @CookEVAR @ozvascdoc 

Dose Awareness Matters

New video produced by the Vascular surgeons at the Royal Free Hospital in London. Right now it is the Charing Cross vascular symposium one of the biggest vascular surgery conferences in the world. Stay connected by following the hashtag #cx2017

DNACPR Top Tips on how to start conversations for healthcare providers

Michael Kiwanuka - Cold Little Heart

The Obesity Paradox in Type 2 Diabetes

Summary of a guest lecture given today by Dr P Costanzo an Interventional radiologist working in the UK. You can find him on pubmed here and on twitter here: 

Increasing BMI has been shown to increase all cause mortality in this NEJM study in 1.46 million white patients. Further extrapolation showed this was mainly due to cardiovascular death. 

Furthermore obesity levels are on the rise. So too are the levels of type 2 diabetes. However, the mortality levels for patients with type 2 diabetes has not shown the same rise infact it has been petty stable for many years. 

A large cohort of type 2 diabetic patients (T2DM) was taken by Costanzo et al. and divided into categories of weight and then following up over 10 years for mortality. The kaplan meier survival curve was interesting, displaying the so called obesity paradox. Patients who were underweight with a low BMI (less than 20 or 18.5) had the highest mortality. Increasing BMI showed a protective effect with the highest BMI values having the lowest mortality. A paradox indeed. 

Further extrapolation of the data by cause of death showed a protective effect of obesity in T2DM in sepsis and cancer (again paradoxical, considering cancers relationship with obesity). 

Dr Costanzo went on to explain possible mechanisms of this, citing the important relationship between low birth weight and increased lifetime risk of T2DM. And how this may be part of the so called evolutionary Thifty phenotype, a phenotype in which high blood sugar can be maintained in starvation providing a survival advantage. It is well known that subsaharan populations (and also indian populations) who move to say the UK  (or anywhere) and start a western diet are likely to develop diabetes. He mentions the lipgenic model of T2DM and how subcutaneous fat is neutral to us but visceral fat is the fat that as it accumulates increases cardiovascular mortality. There is a kind of tipping point where when lets say SC fat is full, visceral fat begins to accumulate (where is the level?). 

The last part of Dr Costanzos talk was incredibly interesting. HB1AC levels documented across all values of BMI is more or less the same in his cohort (unreleased data unfortunately, paper release in 2017), except for the underweight BMI values in which it generally higher. You can postulate that HB1AC is therefore not linked to mortality, and infact other studies confirm this. My notes run out at this point, I guess I was trying to concentrate, but the final part of this section he shows that good BP control in T2DM can reduce mortality in T2DM and perhaps glycemic control has little to do with cardiovascular mortality. 

In fact a nice point was that two new anti-diabetic drugs being studied at the moment; Liraglutide and Empagliflozin, are the only drugs that have been shown to reduce cardiovasuclar mortality in T2DM. These two drugs also have a blood pressure lowering effect. 

This is Hilarious

My 2017-2019 Foundation Programme (UK) Application Experience

Almost a year after starting the process, I finally got my foundation programme (FP) placement on Thursday. I am dead excited to start work as a junior doctor, seriously cannot wait! I thought I would do a quick breakdown here of how the process went, so maybe some future applicants can have a better idea.

Some Background:
-International undergraduate from Italy
-Fourth Decile class rank (This doesnt tell you anything about the level of clinical skill just how awesome your class is, :P)
-Previous degree
-A single publication (nothing groundbreaking, but many a late night spent writing and researching)

Eligibility (August 2016):
In order to start the whole process the FP office had to make sure I was eligible. This eligibility process required identity documentation and a deans statement from my university (basically a statement saying I have enough clinical experience from my degree for the programme). I also had to sit the IELTS english exam in June in order to be eligible for the programme. This was all done in the summer 2016 (before foundation programme allocation applications began).
My IELTS academic score average was 8.

October 2016:
In October the applications began properly and I submitted evidence of my degree and all my personal data. I also had to find two references, a clinical one (my mentor) and academic one (dean of the school who knew me well).
My final EPM score was 44 (not bad)

Within that application in October I had to rank the UoAs (the different regions of England). I ranked the UoAs in the following order:

December 2016: I then sat the SJT (situational judgement test) on the first sitting in December. I flew in from Italy and stayed in Brighton the night before. Unfortunately, I ate the dodgiest salad at the LEON restaurant in Brighton centre (sorry to call them out, but there was no doubt that that salad was dodgy). After explosive vomiting all night, and no sleeping a wink, I got the train to London the next morning for the exam, dehydrated and pale as milk. Sat the exam and staggered home.

My final SJT score 36.66 (awful score considering the studying I did, brilliant score considering the physical state I was in ha).
Finished the entire exam without leaving any questions, reviewed about half my answers before time was up.

Beginning of March 2017: Got into South Thames Foundation school!! Fantastic!

Due to the fact that South Thames foundation school is so large (over 800 placements in total), they decided to split the area into six STHAM groups. I had to do an additional ranking of the six STHAM groups. Due to the lack of crossover between the two cities I had the hard choice of choosing between London or Brighton. I really wanted to go to Kings College for the liver transplant unit and London for other reasons so I ranked the groups like this:

End of March 2017: Got into London Links 2 area, woohoo!

Then I had to rank my programme preferences. There were 152 in total to rank. In the end I ranked about 110 of them. I realised at this point I had probably made a big mistake, having got my second choice of STHAM group I would probably have a low decile compared to the other applicants for entering the programme I wanted. (In fact I checked the STFS website and the decile averages for each STHAM were released, I was in the last deciles, sad face).

Ranking all the programmes is difficult and you have to decide what you want to priotize, the location or the rotations (London or surgery, which is more important?). You also want a good variety in your programme without any lets say 'wasted'  or repeated rotations.
I spoke to a bunch of friends who had gone through the programme and this was their advice:

• Don't do emergency medicine in the first year, do it in the second year
• Avoid highly specialised rotations for example like opthalmology (sorry eye guys, no offense)
• GP rotations are nicer in the summer
• Get as much ward time as possible
• Rotations are more important than location but try and get at least one year in a big teaching hospital

Spending about two days on excel with the list of placements, I ordered everything based on the advice above and with two main priorities:

Had to contain Surgery

Had to have Emergency Medicine in F2

After finding all these rotations, I then ranked them in order of location, prioritising placements at Kings College or Guys hospitals (which I'm sure everyone did). 

(There were about 40/50 of these, the rest I literally ranked based on the awesomeness of rotations). 

The excel file I created kind of looked like this after colour coding and moving around everything a million times.

(looks like a mess right, but I had a system)

Last Thursday (April 2017): I found out my placement! F1 Maidstone F2 Croyden! Cannot wait! 

Pretty damn chuffed, the placementwas my 17th ranked placement. 

So from today there is still lots to do, mainly issues now regarding provisional licensing and transfer from Italy to England. I'll keep y'all posted. 

(Pretty sweet ey, look forward to many blog posts relating to these topics)

(Disclosures: All the information is regarding my own application and I do not believe I am revealing any information without consent). 

Pancreas Transplantation BMJ State-of-the-Art Review Summary

(Another medical student orientated summary of a recent review, this time Pancreas Transplantation.)
Successful pancreas transplantation can result in durable glycemic control and improved survival for patients with diabetes. There seems to be no other treatment in medicine that has the same improving success rates over time and is being applied less and less (the number of pancreas transplants performed in the US has decreased every year during the past decade). In other words, more patients could probably benefit from pancreas transplantation than currently undergo the procedure. 

Most people are diagnosed with type 2 diabetes, with type 1 diabetes accounting for 8-10% of all diabetes cases.
In the UK 3.5 million people are diagnosed with diabetes, with approximately 0.5 million still to be diagnosed. The incidence is increasing.

First successful pancreas transplant was in 1966, at the University of Minnesota.
The number of transplants increased steadily until 1996.
Survival at this point (1996) was 91% at one year and 84% at three years.
The introduction of ciclosporin in the 1980s dramatically increased survival, further efficacy of transplant was enhanced with introduction of tacrolimus and mycophenolate in the 1990s.

Between 2005 and 2014 pancreas transplantation number decreased by 20%. Reasons for this decline were probably; improved medical management of diabetes, decline in organ donor quality (more obese and old), lack of consistent referral of transplant candidates from endocrinologists.

Three main pancreas transplantation types:

• PAK = pancreas after kidney transplant (the main role of this type is avoid the morbidity and mortality asociated with dialysis therapy; patients with type 1 diabetes have at least a 33% mortality in teh first five years after starting dialysis). 
• PTA = pancreas transplantation alone (has higher rates of technical graft loss and acute cellular rejection, however a very small number of this type are performed, no no reports have rigorously studied the efficacy or quality of life benefits)
• SPK = simultaneous pancreas kidney transplant (most common type of pancreas transplant, typically both organs from the same donor)

Success rates of pancreas transplantation have improved with time likely due to increasing experience with these complex patients.

UK current survival rates SPK five year survival 88%, Pancreas only transplants five year survival 78%.

No real studies have directly compared the costs of pancreas transplant vs conventional medical therapy but there have been theoretical models that concluded that SPK is the most cost effective strategy after accounting for varying probabilities of patient and graft survival.

• To date there have been no randomised controlled trials comparing the different forms of pancreas transplantation against for example intensive insulin therapy, islet transplantation. 
• However many single centre studies and registry analyses suggest that pancreas transplantation provides a net benefit compared to kidney transplant alone for patients with both diabetes and chronic kidney disease. 
• More controversial is the impact of pancreas transplantation on patient survival in patients with diabetes and preserved renal function. One analysis of transplant registry data reported a survival disadvantage for PAK and PTA recipients. 

Because pancreas transplantation can also establish normoglycemia it is reasonable to infer that this intervention would also improve or stabilise end organ complications (eg. retinopathy, nephropathy).

Complications:
Diabetic nephropathy (a microvascalur complication of diabetes) is one of the most important complications of diabetes.
Single centre studies with small cohorts have suggested that pancreas transplantation has a beneficial effect on secondary complications of diabetes.
Data is limited on the long term complications, have been reports of increased infections and hematologic cancers after transplantation.

Quality of life:
QoL improved rapidly after transplantation (measured at four months), the effect did however flatten out later. A minority had decreased QoL emphasising the importance of pre-transplant education to establish realistic expectations for the patient.

Clinical trials:
No multicentre trial has been designed to truly evaluate the true efficacy of transplant compared to best medical therapy in type 1 diabetes.

Islet transplantation (ITA):
ITA is less invasive.
Has good short term results but five year insulin Independence rate are around 11%, despite this these patients achieved avoidance of hypoglycemia and near normal glucose control.
Comparison of ITA vs PTA; PTA has higher morbidity, authors of mentioned study concluded that ITA produces similar outcomes to PTA.

Artificial pancreas:
A closed loop system with a subcutaneous sensor that transmits glucose measurements to an external insulin pump that deliver insulin subcutaneously when needed.
Addition of glucagon in the future could prevent hypoglycemia.
The use of such devices requires the patient reaches a certain level of understanding.
Results from international diabetes closed-loop trial conducted on real patients will be out in 2019.

Future directions:

"Pancreas transplantation stands at a crossroads—without a systematic approach to the procedure and its outcomes, transplant volumes, especially those for PTA and PAK, may continue to decline and the procedure take second stage to therapies such as islet transplantation and closed loop insulin and glucagon delivery systems..... a more systematic approach to characterizing the successes and limitations of pancreas transplantation is needed."

Need to develop a uniform definition of graft failure. The most common definition of graft failure at the moment is the requirement of exogenous insulin therapy.
Need the development of biomarkers to diagnose rejection and monitor patient immune status.

UK guidelines:

In the UK, patients with the following conditions are considered for pancreas transplantation135: 

•  Pancreas transplantation alone or islet transplantation alone: patients with severe hypoglycemic unawareness but normal or near normal renal function

•  Simultaneous pancreas and kidney transplantation or simultaneous islet and kidney transplantation: patients with renal failure and insulin dependent diabetes 

•  Pancreas after kidney transplantation or islet after kidney transplantation: patients with functioning kidney transplants and diabetes. Most patients who are considered have type 1 diabetes but some patients with insulin dependent type 2 diabetes may also be suitable candidates.

This summary was for the following paper: http://www.bmj.com/content/357/bmj.j1321
(all the information and images were from the above paper).

NEJM Maternal Immunization Review 2017 Summary

(A medical student orientated summary of a recent NEJM review)
Most childhood vaccines do not start providing adequate protection until the infant is several months old. The immunity gap between birth and this time can be addressed by maternal immunization.

Sex hormones modify immune responses:

• Increase in estradiol is associated with increased Th2 responses and reduced Th1 immune responses.
• Increased progesterone levels is associated with reduced immune response in general
• Overall phagocytic responses, alpha-defensin expression, neutrophil, monocyte and dendritic cell numbers may be increased in 2nd and 3rd trimester in general during preganacy. 
• (may explain suboptimal responses to viral infections such as influenza in pregnancy)
• pregnancy is not a generalised state of immunosuppression.

Evidence regarding the immunogenicity of vaccines administrated  during pregnancy is mixed

Current recommendations are for pregnant women to have influenza and Tdap (tetanus-diphtheria-acellular pertussis) maternal immunisations

Influenza vaccine:

• Few low income countries regularly vaccinate pregnant women against influenza
• A substantial burden of illness among pregnant women is attributable to seasonal influenza
• The efficacy within infants after birth ranged from 30% to 63% (good for mom, ok for baby)
• There may be potential for protection against adverse birth outcomes, two studies detected a difference in low birth weight however the others did not. One study was sufficicnetly powered to detect a difference but the promising result was offset perhaps by the overall low baseline birth weight. So perhaps the vaccine is more useful as a protection against adverse outcomes. 
• influenza infection is associated with  an increased rate of subsequent bacterial infection particularly pneumococcal disease. (in fact a substantial proportion of deaths during the 1918 flu epidemic were probably due to strep.pneumoniae). 
• use of maternal vaccine and infant vaccine together showed better results than infant vaccine alone in prevention of respiratory illnesses with fever and medically attended acute respiratory illnesses. 

Pertussis vaccine:

• Young infants have a disproportionately high burden of severe pertussis in the population.
• studies on the pertussis vaccine have shown high effectiveness and a reassuring safety profile (there were no increaes in adverse birth or pregnancy outcomes). 
• There was a slightly higher rate of chorioamnionitis but the authors explained this as perhaps due to practice of labelling fevers as chorioamnionitis to protect from litigation in the USA where the study was conducted
• There is concern though that the vaccine may reduce the immungenicity of the infant DTP (diphtheria-tetanus-pertussis) vaccine. With studies suggesting this, however the clinical relevance is uncertain. 

Maternal vaccines in development include vaccines against RSV (respiratory syncytial virus) and GBS (group B streptococcus).

RSV vaccine:

• RSV is the leading cause of viral acute lower respiratory tract illness and the highest morbidity is among preterm infants. Most deaths due to RSV occur in infants
• 2-3% of all neonatal deaths are attributable to RSV.
• Vaccine is needed due to the high burden of RSV infection, particularly among young infants.
• Several RSV vaccines are in development, targeting the RSV F and G proteins mainly. 
• Given that preterm infants are a high risk group, recommendation for the gestational age of vaccination will have to take into account adequate antibody transfer for preterm infants. 
• In the 1960s a formalin inactivated form of the vaccine against RSV for children was researched. It led to an 'enhanced RSV disease', and increased rates and severity of RSV lower respiratory illness. Thought now to be due to a lack of protective antibodies being produced with an increase in CD4+ priming in the absence of CD8+ cells. This abherrent vaccine slowed further research into RSV vaccines.
• The benefit of a maternal vaccination is that it would bypass immunologic events that would lead to an enhanced RSV disease in infants. 

Group B strep vaccine:

• Early onset GBS infection occurs in neonates younger than 7 days and is characterised by sepsis without a focus, pneumonia or meningitis.
• Late onset GBS infection occurs in infants who are 7 to 89 days of age and is characterised with higher rates of meningitis.
• Invasive GBS infection in pregnant women is associated with stillbirth
• GBS is transmitted from colonised mothers during birth (hence why there is universal maternal screening with intrapartum antibiotic prophylaxis).
• One in five pregnant women have evidence of GBS rectal or vaginal colonisation at 23-26 weeks. 
• Screening with prophylaxis programmes mentioned above have resulted in reductions in early-onset GBS disease but NO reduction in late onset disease. 
• A maternal GBS vaccine could help reduce the burden of GBS disease, particularly late-onset disease in infants. 
• there is a trivalent vaccine in development that covers serotypes Ia, Ib and III. The global disease burden includes serotypes II and V, therefore a vaccine will need to be developed still to cover against also these subtypes

Incorporating maternal vaccines into antenatal care has been a challenge in many locations, with the maternal influenza vaccination rate in the US estimated to be around 50%.

Link to paper: http://www.nejm.org/doi/full/10.1056/NEJMra1509044

(all the points above and images were taken from the paper linked above)

Michael Debakey: The Janitor and I, Saving Lives Together

There are already milions of blog posts all over the internet about the many wonderful things Michael Debakey did and invented. I love reading stories about him, besides being the father of cardiothoracic and vascular surgery and prolific surgeon he was also a down to earth and wonderful man it seems. below is my favourite story of his;

In one particular encounter, DeBakey began chatting with an elderly janitor who was sweeping the floor. DeBakey asked the man about his wife and children. He told the older man, obviously not for the first time, that the hospital couldn’t function without the janitor because germs would spread, increasing the chances of infection in the hospital. Later in the day, our colleague tracked down the janitor and asked him, “What exactly do you do? Tell me about your job.” With pride, the janitor replied: “Dr. DeBakey and I? We save lives together.”

He’s right. After all, consider what would happen to our healthcare systems if the cleaning crews went on strike. DeBakey understood that showing the janitor exactly how he contributes to a larger, more heroic cause is crucial. This creates a powerful dynamic. Realizing that he is working toward a worthy goal, the janitor’s perceptions about his work changed. It had new meaning and his enthusiasm for the job was rejuvenated.

Source: http://www.freibergs.com/resources/articles/leadership/10-things-we-can-learn-from-the-worlds-greatest-surgeon/  (its a great post and worth a read, it certainly makes a young doctor feel inspired).