Lacerations in the ER Part 1: Before you stitch!

Here are my notes from the 'Advanced wound care' lecture, the last lecture before graduation. After just an hour with this prof I felt like I could handle any laceration that comes into the ER. Hopefully after this post you will feel a similar confidence:

History is important!
Before touching the wound, you should know exactly how it happened, when it happened and what instrument/surface cause the laceration. Its important because wounds heal differently and are devitalised in many different ways depending on these factors.

Location is relevant, the face heals better than the hands. Some areas are more mobile and better perfused.

Patient factors;
Patient factors will affect healing and can be important clues for risk of infection (diabetes), healing time etc.
Steroids slow healing, HIV doesnt affect wound healing, Keloids are common in afro-americans.

Find out the patient's Tetanus Status,  you have probably heard about tetanus prone wounds, this is a myth. You can get tetanus from a corneal abrasion. Make you sure you find out about the primary series of vaccinations! no good giving a booster if someone hasn't had their primary series! this is a common situation with immigrants in our ER. Many people forget to ask! CDC advice

The key to good wound practice is IRRIGATION. rememeber: "the solution to pollution is dilution" Water is the best irrigant, you can use plain old tap water, its the volume that matters, taking the patient over to the tap you can supply much more water than a simple syringe from a saline bag. You will never completely eliminate the bacteria, it just needs to have a lower enough concentration so that colonies don't form (sample principle as the lab). Consider the environment, kid falls and hits head on table legvs kid who falls and hits head on road kerb. You need volume and pressure

Sensation:
The gold standard to test sensation is a 2 point discrimination (5mm apart for the hands), make sure there eyes are closed of course. A plastic surgeon can repair most nerves proximal to the DIP joint of the fingers, you will need them to fix any nerve injuries. From a malpractice point of view you need to perform the gold standard.

You can investigate tendon injuries in a variety of ways, a good way to test is to ask the patient to assume the position of  function, you will spot any flexor injuries easily.
Position of function: arms raised to shoulder height, with hands pointing up and open chest position. imagine a policeman says "hands up!"
Flexor injuries you should call the surgeon. There is a small no mans land, the deep palmar lacerations. If the palm hurts when they move their hand then they have probably knicked the palmar sheath. With little pain you can probably leave this but a surgical referral is probably best.
Many extensor tendon injuries can be splinted and will heal well.

Remove foreign bodies. 90% of glass can be seen on X-ray

Use anaesthetic, local anaesthesia or nerve block. nerve blocks are very useful and with ultrasound very easy to perform (with practice). Use Lidocaine (short acting) or Bupivicaine (medium acting 8hours half life). Some areas are tender, for example the sole of the foot, do a nerve block!
Allergic reactions to lidocaine itself are impossible! (only to the preservatives used within, which are rare now). You can be almost 100% sure  there will be no allergic reaction if you use single use vials or cardiac lidocaine.
There has never ever been a documented case of allergci reaction to cardiac lidocaine.
Most lidocaine reactions are just a vasovagal reaction to the needle ha.
When dealing with the face or kids, topical agents are great eg. Tetracaine. You can wack it on in triage.

Explore all Wounds!

Anaesthesia, Betadine on the neighbouring skin surface (not inside the wound). you are ready to suture!

SUMMARY:

• History of injury
• Location considerations
• Pateint factors
• Tetanus status
• Good neurovascular and functional exam
• Irrigation
• Anaesthesia

Get ready to stitch this guy up

An Incredibly Trippy History of the World

I actually learnt so much from this video! Although unbearably trippy it is actually really entertaining and surprisingly accurate. hats off to Bill Wurtz for this creation.

Quality Improvement in Hospital

These notes are based on a wonderful lecture I had today titled 'quality improvement in health care pathways'. It was a short lecture full of simple but powerful ideas.

I am quite fortunate that my hospital is modern and has a lot of money. One of the ways the administration has decided to spend this money is on a 'quality care' unit whose job is simply to improve patient outcomes and increase the 'quality' of care. 

Quality is notoriously difficult in healthcare to measure. The main way that quality is measured in most institutions is by comparison to local and national mortality and infection rates. Yet these gives you no idea about the actual quality of care, it only tells you if more or less people are dying at your hospital compared to another hospital.
Quality is the actual clinical outcome, the treatment of the 'disease' and the patient well being, does the patient leave the hospital in a condition comparable to how he/she was before getting the 'disease'?
A great idea that came out was to use the percentage of patients that returned for follow up as a surrogate for quality, and they are investigating that now.

One way you can indirectly determine quality of care is by using patient forums (groups of patients meeting together), or using patient questionnaires. Many points that are raised by patient forums are simple and often overlooked. One group of patients who had urological operations, noted how they all had no idea what underwear to wear. It may sound stupid to the consultant who is focusing on defeating the cancer being treated (yes the true priority), but the underwear was important to the patient and the source of a great deal of stress.

"If you improve the little things the cancer becomes just a little less important"

The quality care programme at the hospital is a relatively new concept and has taken a very long time to be adopted. Apparently it took about 7 months to get a group of 20 people to talk together, 20 people all involved in different parts of the patients care pathway; nurses, doctors, physiotherapists, radiologists etc.
Communication is a big issue if you want to work on improving quality.
Unfortunately many doctors didn't appreciate advice from the nursing staff at the start, it took a long time for this communication loop to open up. Doctors interpreted the advice as nurses telling the doctors how to do their job, hostile thinking. Just because you’ve done something for 20 years doesn’t mean it is right or couldn’t be better.

Once the problem of communication is solved, drastic changes are seen. The benefits are seen not only among the hospital staff. Patient counselling groups offered to all the patients undergoing prostate cancer resection, were very popular. Patients spoke in a large group with all the staff involved in their care. Hearing about all the people going through the same problem was incredibly enlightening for the patients, even if it regarded embarrassing topics like sexual life after surgery. Understanding the process and what life is like around and after the surgery was helpful. Clinical outcomes were even seen to improve, for example continence after prostate resection was improved. Well prepared patients took their pelvic floor muscle training before surgery seriously, understanding the importance and hearing from other patients.

The quality care team started their approach with observation. They took doctors along and tried to be patients, from the start of the process to the very end. Starting from the parking lot straight away they realised why the little things are important, they couldn't even find the department, there were no signs! We need to take care of patients from the very beginning.

Their are little things you can do that can have a massive impact on patient outcomes and quality of care. Two small examples of changes at our hospital that improved quality of care:
- When a stroke victim is on the way to the hospital emergency department in the ambulance the neurologist is called before and is ready at the door when the patient arrives. as apposed to waiting ten minutes for the neurologist to arrive who has been called only on patient arrival. Time is brain after all. The Dr waits for the patient the patient doesn't have to wait.
- A case manager, who calls patients and organises their follow ups with them on the phone as apposed to the normal "see so and so after six months for ct scan" etc. speaking directly with the patient you can assure they book an appointment and also it fits around them.

Some of the hospitals ideas came from the famous Toyota LEAN method which you can find out about in this interesting BBC discovery podcast:

http://www.bbc.co.uk/programmes/p042k1bf

A Brief History of Stroke

Stroke is a leading global cause of death and disability-adjusted life years (DALYs, see below for definition), second only to ischemic heart disease. The incidence of stroke varies across different countries and increases exponentially with age. 

First defined as ‘apoplexy’ by the father of medicine Hippocrates himself in 2400BC, it was not until around the 1600’s that the link between the potentially devastating sudden symptoms and the brain was made (hence the name ‘apoplexy’, which meant in Greek ‘struck down by sudden violence’). This discovery was made by the documentation of intracranial haemorrhage in the brains of cadavers who died of stroke by Johannes Wepfer (Since 2005 the “Johann Jacob Wepfer Award” is given at the European Stroke Conference for outstanding work in cerebrovascular diseases). 

After extensive work in defining the anatomy of the cerebral vasculature by Thomas Willis in Oxford 1664, and the discovery of an anatomo-pathological association by the Paris Medical School in the late 1800s, apoplexy became better known as ‘cerebrovascular accident’.  The term ‘stroke’ was a lay term, originating from the belief the disease was a sort of ‘stroke of gods hand’ or ‘stroke of justice’, a punishment for wrongdoing or pleasure-seeking. It later became the definitive name for the disease in 1962 when the chest and heart association produced a booklet titled ‘Modern Views on ‘Stroke’ Illness’.

Even at this time, the mid twentieth century, it seemed doctors still approached stroke with slight nihilism or hopelessness. Up until 1935 bloodletting was the primary therapy for stroke. Vomits, purges and enemas were all treatments for stroke in the beginning of the nineteenth century, not so different from Hippocrates own ‘replacement of humours’ before the start of the millennium. Nothing seemed to improve the prognosis, patients miraculously recovered, died or faded away with permanent disability; modern medicine had a long way to go still!

Bloodletting, 'back in the day'

In the 1950s doctors began to experiment with angiography, anticoagulants and surgery for the treatment of stroke. A few years later, team approaches to stroke patients started in many hospitals with the collaboration of physiotherapists, nurses, dietitians, surgeons, internists, occupational therapists, speech therapists and general practitioners. Rehabilitation became one of the main contemporary treatment responses to stroke. By the end of the 20^th century and with birth of stroke associations around the world, there seemed to be some light in the tunnel, perhaps stroke is curable and preventable. 

Stroke treatment and management has come a long way in the last fifty years, advancements in angiography and the introduction of aspirin therapy and intravenous thrombolysis have improved survival massively. 

In 2008, stroke moved from being the 3^rd leading cause of death in the USA to the fourth, it then jumped a further rank to fifth in 2013, a reflection of accelerating science and improving prognosis!

DALY: The sum of years of potential life lost due to premature mortality and the years of productive life lost due to disability. One DALY can be thought of as one lost year of "healthy" life. The sum of these DALYs across the population, or the burden of disease, can be thought of as a measurement of the gap between current health status and an ideal health situation where the entire population lives to an advanced age, free of disease and disability.

References:

-http://vizhub.healthdata.org/gbd-compare/ Institute for health metrics and evaluation. Accessed 03/04/2017. Images.

-Catherine E. Storey, Hans Pols, Chapter 27 A history of cerebrovascular disease, In: Michael J. Aminoff, François Boller and Dick F. Swaab, Editor(s), Handbook of Clinical Neurology, Elsevier, 2009, Volume 95, Pages 401-415, ISSN 0072-9752, ISBN 9780444520098, http://dx.doi.org/10.1016/S0072-9752(08)02127-1.

 -Molnár Z. Thomas Willis (1621-1675), the founder of clinical neuroscience. Nat Rev Neurosci. 2004;5(4):329-35.

-Van der worp HB, Van gijn J. Clinical practice. Acute ischemic stroke. N Engl J Med. 2007;357(6):572-9.

-Pound P, Bury M, Ebrahim S. From apoplexy to stroke. Age Ageing. 1997;26(5):331-7.

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).

An important message for the coming year

Finally back blogging here after a month out for exams. I have recently been reading alot of scary posts about the way things are going with the new president in america, you-know-who (calling him that, as if hes not villian enough). Building walls and banning refugees, its amazing how wrong the optimistic 'oh-he'll-be-alright-ers' have been already. Anyway 'you-know-who' is the least of our worries.
There is a sneakier and worse problem at hand and it masks itself in ideologies and group thinking. Humans are social animals, some scientists say that our social abilities is what made our species survive sabretooth tiger attacks and ice ages. The forming of small communities and social groups is inherent to human behaviour but ideologies as Prof Jordan Peterson explains in the video below can be harmful. We have to remember a simple fact and this danish advert below illustrates it perfectly, We are all the same! yes we have own individuality and our ways of doing things, beliefs arnt harmful and a little bit of spirituality can go a long way (referencing religious ideology here), but we must make sure that anyone who isn't part of our group/ideology/religion doesnt become the enemy. Black/White/Indian/Christian/Gay/Straight/Rich/Poor/Old/Young/Fat/Trans/..... the list is endless, and its amazing the variation among people.
Watch the video its great!

4 things I am going to do to try and save the environment.

Climate change is upon us and after having recently watched 'Before the Flood', the Leonardo Di Caprio super documentary on it, I am starting to feel a little bit guilty about it all. We are all to blame, we can't point the finger at any one single cause, there are so many factors contributing to the accumulation of noxious gases in the atmosphere. HOWEVER we can do our little bit, and 2017 I think I am going to try and be more environmentally conscious. Here are the four things YOU can do to lesson your environmental impact:

1) Use less plastic, a product mostly derived from crude oil. I mean have you heard of the Great pacific garbage patch!!

Source

2) Stay away from 'Fast Fashion', invest in clothes that will last or are easily repairable, buy what is needed. Fast fashion is literally drowning the world, It has the biggest environmental impact after crude oil! check out the facts. 

3) Cycle to work more and use public transport whenever necessary. Simples 

4) Last but not least, eat vegan... well at least try. I'm not going to completely write off beef just yet and the whole vegan argument is complex (another post another day) but one can't deny the huge environmental impact the meat and dairy industry has.

Simple approach to PAIN

Pain is ubiquitous in medicine and often overlooked. Despite a thorough definition, 'an unpleasant, sensory and emotional experience associated with actual or potential tissue damage', it is impossible to really understand someones pain unless you have felt it yourself. It is a highly diffuse symptom with a massive impact on patient well being and quality of life (it may even be much more diffuse than believed). It is an all encompassing entity which if you take Dame Cicely Saunders concept of 'total pain' concerns not only physical aspects but also social, spiritual and emotional aspects. 

If you take cancer pain, it is the most frequent presenting symptom and present overall in the majority of cancer patients. Shockingly pain is reported in a minority of cancer medical records, it would seem that many oncologists dont assess pain, probably fixating on battling the cancer itself (one of the toughest battles in medicine to add). Pain should be considered a disease entity itself and if it is properly assessed, addressed and treated, it could go a long way to enhance patient quality of life.

Here is a simple approach to pain you should consider whenever a patient says they are in pain:

First ASSESSMENT:

ABCDE 

A is for Ask: Ask about the pain: use the OPQRST approach:

• Onset
• Provoking factors 
• Quality of pain
• Region and Radiation of pain
• Severity 
• Timing and history 

When assessing severity use the NRS or VAS technique; "on a scale of zero to ten, where ten is the worst pain imaginable and zero is no pain, how would you describe your pain severity" (this is NRS, VAS is the application of a mark on a 10cm line to indicate pain severity in the same way).

score of 1-3 is mild  (VAS would be 1-3cm)

score of 4-6 is moderate pain (4-6cm mark)

score of 7-10 is severe pain (7-10cm mark)

One really important thing to think about after you have taken a thorough history is "what is causing the pain?"

B is for Believe the patient, don't dismiss them.

C is for Control: choose and appropriate pain control method, best way to apparoch pain treatment is with the WHO pain treatment ladder, which can be applied to all pain and not just cancer pain. move up the steps if pain is not well managed or still present.

• 1st step: PARACETOMOL (to treat mild pain)
• 2nd step: WEAK OPIOIDS (for example tramadol or codiene, these are opioids with a ceiling effect where inceasing drug dosgae will not improve effect from a certain point)
• 3rd step: STRONG OPIOIDS (consider for mod-severe pain). (for all opioids "start low and go slow"
• at any point you can add adjuvants to the ladder: NSAIDS, corticosteriods, antidepressants, anticonvulsants, benzodiazepines.

D is for Deliver pain control in a timely manner

E is for Empower the patient in pain control, patient education is so important. 

Second MANAGEMENT:

The four A's:

• Optimize ANALGESIA
• Optimize ACTIVITIES of daily living
• Minimize ADVERSE EFFECTS due to treatment
• AVOID unnecessary  drug taking

Third REASSESSMENT:

Simply, reassess often!

Summary: ABCDE OPGRST AAAA Reassess!

Hollywood needs to be more unpredictable

Jennifer Lawrence and Chris Pratt , two of the most popular A-list hollywood stars around at the moment, some romance, great CGI, and chuck some 3D effects in there, you’ve got a box office money maker.  I guess that was what was going through the mind of the producers when they decided to produce ‘Passengers’.  With the absence of any real decent major Hollywood films in 2016, passengers was Hollywoods last gasp to make something of 2016. With harsh reviews from major newspapers and a measly 31% on Rotten Tomatoes, you could say they failed.

Chris Pratt puts in an awesome performance, managing to act convincingly as a type of castaway-esk stranded-in-space near suicidal space caveman in the first half of the film. Probably the most interesting and captivating part of the film was Jim’s (Chris Pratt) struggle wih loneliness and the choice whether to wake up Aurora (Jennifer Lawrence). When he finally does choose to wake her up (come on, not a spoiler, obvious isn’t it!), you find yourself involuntarily on the edge of your seat trying not to scream, don’t DO  IT! And its horrifying..

Unfortunately its from this point the film goes down hill. Not to reveal spoilers, basically despite the interesting relationship dynamic between Jim and Aurora, there is a very predictable sequence of impending doom with a very predictable they save the day type rhetoric. (see no spoilers)

I mean, who doesn’t love a film where the hero saves the day. You leave the cinema feeling or fuzzy and warm. But they win Every. Single. Time. In. Every. Single. Film.

Maybe its time the bad guys win?

AA Gill Faces Up To His Cancer

Yesterday the prolific writer and restaurant reviewer AA Gill died. 2016 has been a torture to many and just when you thought it couldn’t get worse, it took away another loved human being. The cycle of life and death is of course inevitable but even that resounding truth doesn’t make it any better. (someone please please put Sir David Attenborough in a bubble or something).

I actually first came across AA Gill when I was quite young and had just moved to the UK, my mom would read the Sunday times leave it lying on the dining room table after she finished. I would come in and pick through the various smaller newspapers and magazines in search for sports, motoring or kids sections and briefly read about the rugby scores or some fantastic gadget that will come out in the future (can you believe this iPhone gadget!). As I was flicking through the pages looking at the pictures of far off paradises in the travel section and the contrasting war torn battlegrounds in the Sunday Times magazine as I usually would, my mom came in once and pointed out I should actually READ the paper and not just look at the pictures. Of course I wasn’t interested in Tony Blair or The Foot and Mouth crisis but defiantly I decided to read something and one of the many articles I read that day was by the late great AA Gill.

Today I read his final piece in the Sunday Time magazine, a fantastically written and honest piece about his cancer and experiences with the NHS. I highly recommend reading it. 

The article: “More life with your kids, more life with yourfriends, more life spent on earth — but only if you pay” AA Gill.

He points out that the UK shockingly has some of the worse cancer survival rates in Europe, a third the percentage as Sweden in some instances. This is primarily due to the late diagnosis of cancer propagated by waiting times and turtle paced referral. The NHS, The jewel of the british isles, the pride the UK, might not be so brilliant after all, AA Gill writes:

“We say it’s the envy of the world. It isn’t. We say there’s nothing else like it. There is. We say it’s the best in the West. It’s not. We think it’s the cheapest. It isn’t. Either that or we think it’s the most expensive — it’s not that, either. You will live longer in France and Germany, get treated faster and more comfortably in Scandinavia, and everything costs more in America.”

RIP Mr Gill 

Picture: pic.twitter.com/A7WI9o8jWX @jenbalcombe 

St Emlyn's Emergency Medicine Blog

Shout out to this fantastic blog! Based out of the Manchester Royal Infirmary, St Emlyn's is an emergency medicine blog full of great insights into life as an EM doctor. There are lots of #FOAMed resources for those who are jumping on the social education bandwagon (a more modern version of medical education).
I particularly enjoyed this recent post about the risks of training in EM and why some Dr's quit and how to avoid those lows. @baombejp brings up the following points:

• Dont expect results too fast, take the SMART approach
• Dont fear failure, there are three ways you can react to a setback: you fly, you dive, you thrive
• With regards to the future find the right balance between competence and confidence when progressing and be careful of the unknown'unknowns (the things you dont know you dont know ha)
• Have a life! why have a job if you don't have a life
• There will be ups and downs, find someone to talk to about it

The blog is full of great posts, I enjoyed reading this morning about this consultant dealing with his junior knowing more than him and the following teaching tips. 

Acute Renal Failure and Acute Kidney Injury (ARF vs AKI)

If you look up the definition of acute renal failure (ARF) you will probably find this; "an abrupt and sustained decrease in renal function". Thats all very well but what do any of these words mean?! how abrupt? how long is sustained? renal function measured how? Whats more, over 35 different definitions of ARF are used in the literature with varying mortality and incidence rates. This post should hopefully clear everything up about ARF and AKI and give some tips about how to manage ARF and AKI.

First of all, scrap the term ARF, the term AKI is used now and reflects much better the fact that small decrements in organ function not resulting in organ failure are still clinically important! ARF is used for the last stage of AKI where the kidney actually fails and RRT (renal replacement therapy, for example hemodialysis) is needed. 

Diagnosis:

How do you know if a patient has AKI? look at serum creatinine and urine output!

There are two main ways for classifying AKI, the RIFLE criteria and the AKIN criteria, both perform equally well in studies, but I will use AKIN criteria because it is used by the KDIGO guidelines which most of this post is based on.

Picture above shows the AKIN criteria in the red box, as you can see you can divide AKI into three stages depending on the level of serum creatinine (sCr) or urine output (UO) (or directly place them into stage 3 if they are on RRT or anuric for greater than 12 hours). Stage 3 AKI is synonymous with ARF. 

So you have assessed your patients sCr and UO and find that he/she has an AKI. what do you do next?

AKI Management:

• monitor diuresis (bladder catheterise if not already catheterised)
• careful physical exam (pay attention to whether the patient is 'wet or dry', you should be careful giving fluids in a 'wet' pt, see later notes on pulmonary edema)
• monitor fluid balance
• arterial blood gases
• order labs: sCr, Na+, K+, Ca2+, Cl-, CBC, urine dipstick, BUN, 
• renal US (you are looking for the easy dx of obstruction, see etiology below)
• CXR (pulmonary edema?)
• avoid contrast agents if at all possible
• consider ICU if stage 2 and up
• avoid hyperglycemia
• careful drug review: 

1. discontinue nephrotoxic drugs (eg. vancomycin, gentamycin)
2. discontinue drugs that impair GFR autoregulation (NSAIDs, ACEi, ARBS(angiotension receptor blockers))
3. adjust dosage of drugs undergoing renal excretion (many antibiotics)
4. withhold exogenous potassium (look for K+ containing infusions (such as isolyte) that the patient may be on) and stop potassium sparing diuretics like spironolactone and eplerenone. 

AKI treatment:

Treatment is mainly directed at the underlying causes, for example if the cause is dehydration give fluids, if the cause is haemorrhage consider giving blood transfusion etc. immunosuppressants for vasculitis, discontinue drugs, relieve urinary tract obstructions....

note: No specific treatment for AKI actually exists but we have to manage all the complications well. 

AKI causes:

The causes of AKI are best divided into three main catergories

• pre-renal
• intrinsic (parenchymal)
• post-renal

Pre-renal AKI:

Basically anything that causes a drop in blood pressure low enough that the kidneys own auto-regulation is unable to preserve renal function. consider:

Volume loss: hemorrhage, dehydration, diarhhea, polyuria, burns

Sequestration of fluids (3rd spacing): pancreatitis, peritonitis, rhabdomyolysis

Blood pressure drop: any form of Shock, hypotensive medications 

(note that not all patients have the same capacity to autoregulate their renal filtration)

Intrinsic AKI:

diseases that affect the kidney directly, consider:

Arteries: thrombosis, embolic events

Pre-glomerular arterioles: Vasculitis, malignant hypertension, atheroembolism, DIC, eclampsia

Glomeruli: glomerulonephritis, thrombotic microangiopathy

Tubulo-interstitium: Acute tubular necrosis (ATN), crystalluria, cast nephropathy, contrast agents

(note that anything that can cause a sustained hypotension can damage the renal epithelium and cause ATN)

Post-renal AKI:

This is caused by an obstruction to the urinary tract, consider:

Bladder outlet obstruction: BPH, urethra stenosis, neurologic bladder

Ureter obstruction in pts with 1 kidney: stones, cancer, papillary necrosis

AKI Complications:

AKI patients can die of four main causes:

• Hyperkalemia
• Metabolic acidosis
• Fluid accumulation (pulmonary edema)
• Uremic syndrome

Hyperkalemia occurs when serum K+ is >5 mmol/l

Symptoms of hyperkalemia include: intestinal colic, diarhee, weakness/paralysis, arthymias

Hyperkalemia has a distinct ECG: flattened P waves, wide QRS, peaked T waves

(peaked T waves is the first feature to appear)

Metabolic acidosis is caused by the failure of tubular interstutium to excrete normal daily acid load. symptoms include: nausea and vomiting, abdominal pain, hyperventilation, hypotension

(note that acidosis may worsen hyperkalemia)

Fluid accumulation is quite often iatrogenic! careful with hydration. 

Uremic syndrome has many presentations and may cause: pericardial effusion, nausea and vomiting, malaise, confusion, seizures, non specific diffuse abdominal pain, ileus, a tendency to bleed (so called 'lazy' platelets). 

Junior doctors and learned helplessness; a rant.

Pete Devesons's speech opposing the motion "This house believes that medicine is the best career in the world", recorded at the #BMJLive Big Debate in London on 23/10/15. Its been a rough ride for Junior Doctors but now lets take action, keep looking up. 

Optimism and how I'd rather just laugh

It's been a long day for me, I'm writing this on the 23:33 train from Luton airport to Bedford and feeling a little philosophical. Might be a pretty boring story so I recommend cutting to the final paragraphs for the point.

Woke up this morning on the bus to university, my morning routine a blur through sleepy eyes. Morning surgery starts at 7:30am, so as usual I was on the 7:18 bus to the hospital listening to the Joe rogan experience podcast. It was episode 764 with Duncan Trussell the comedian and good friend of Joe's. Duncan had a little crazy rant about how people get annoyed so easily and the pettiness of daily life. He was saying how optimism and positivity even for the little things would make life so much brighter.

I was lucky to get to spend the entire morning in the operating theatre, put some stitches did some ultrasound, love it. The last case was gruesome, transmetatarsal amputation of the foot, seeing a toe sawn off (and it's literally sawn off with an electric bone saw) is not terribly easy to watch but the surgeon did a great job (textbook, I read about the procedure before and he matched it point for point).

The afternoon was a rush of packing, lunch (pizza to say goodbye to Italy) and goodbyes (my korean flatmate and wonderful girlfriend). Before I knew it I was going through customs.

My phone buzzed after getting through customs, “you flight details have changed”. My flight was delayed 30minutes, shit. I had booked a train that left an hour after my flight touched down. This was the start of what could of been a very frustrating evening.

Airports are funny places, people from all over the world from all different backgrounds congregate briefly in the departures lounge while they wait for their huge steel transport to fly them away. (Ever thought about planes, how the flip do those things even fly, a 747 weighs 400 tonnes, there definitely some kind of magic going on there). Screaming kids, smokers in their tiny smoking closet, old, young, businessmen, stoners, they are all here like some kind of multicultural Royal rumble.

The flight delay meant I had exactly 40minutes from flight landing to the train leaving. As I passed the lady who checks boarding passes she said the plane was too full and my handluggage and others must go in the hold and my bag was whisked away, I just managed to pull my book out just before it was gone.

The flight was pretty uneventful, well at least compared to the flight where a window blew out I was on once (I'll post about that another time, it's a good story and ends with free pizza ha). The couple next to me were very much in love or something, they spent most of the flight making out. I think she had thing for ears, the guy would turn to read part of his guidebook now and then, but she would just keep kissing in his general direction, mostly in his ear, noisy stuff. The kids behind me must of confused my seat and the couple's as a drum set or punchbag. That was the only moment the lady next to me stopped inserting her tongue in mouths or ears, she turned and gave the two ‘little shits’ (her words not mine) an angry look and they stopped.

The flight landed on time (delayed time) and we bounced down the Luton airport runway to a typical Italian applause, well done pilot for avoiding a burning wreckage. As soon as the seatbelt signs flicked off I was up out of my seat and in front of the rear door, ready to run for my train.

Looking out the rear door window I couldn't see anything happening, the air hostess then told me after hearing my plight that sometimes they only open the front door. This now put me at the very back of the queue to leave the plane. Damn. The front door finally opened and everyone slowly shuffled off with me at the very back. After getting off the plane I sprinted to passport control only to be met by the biggest queue I've ever seen winding it's way left and right to fill the entire room (and it's a big room). With this long queue and the fact i still had to collect my bag and navigate from luton airport to the trainstation. There was no way I would make my train.

Through the airport WiFi (thank God for airport WiFi!) I managed to find out there was another train home leaving in around an hour. After just missing the aiport-train link bus by a second I eventually got to the station and the eight minute delay for the train seemed like nothing compared to my mad rush through Luton terminals.

This whole story is pretty boring perhaps even frustrating but I would like to get to the point now. Optimism. I could of easily have been pissed off with the various delays, the noisy neighbours on the plane, the fact I missed my trains, but I chose to except them and even laugh at them. By stepping back and accepting that there was nothing I could do, I felt so much more relaxed. Admittedly there was a brief surge of panic when I realised I may not be able to get home but focusing on the fact I would make sure I did, alleviated that. I am alot happier with this approach to life. I laugh at the obsurdity of situations and how easy it is to be annoyed in the modern world. ‘Living in the moment’ may sound like some hippy rubbish but there is certainly some truth to it.

Discussing this approach with a friend, an important point was brought up. You mustn't be completely passive with everything happening around you. If there is something wrong it should be dealt with but without the anger or aggressiveness that usually accompanies frustration.

Moral of this story to quote easyjet: ‘you should allow two hours after arrival before connecting trains or  flights’ ha.