Diabetic Ketoacidosis- Glucagon is the Problem!

Another common topic and also a frequent presentation to the ED is DKA. On the whole I think of this as straight forward ie bang up some fluids and insulin and it'll sort itself out! That being said when you actually read about it things are a little bit more complicated.

Your hospital will have it's own policy and approach, but a nice little guide has been produced by the Joint British Diabetes Societies Inpatient Care Group:

http://www.bsped.org.uk/clinical/docs/DKAManagementOfDKAinAdultsMarch20101.pdf

Let's start with some background to put things in perspective:

• It is potentially life threatening, although mortality rates have fallen in the last 20 years from 7.96% to 0.67%!
• Cerebral oedema especially in children and adolescents is the most serious complication.
• The typical fluid deficit in DKA may be 100 ml/kg!
• It is now possible to measure blood ketones at the bedside.
• The treatment of DKA has developed and will continue to develop as our understanding increases.

The rest of this post is about adults, there are key differences in the management of children/ adolescents.

Definition:

1. Blood glucose >11
2. Ketones > 3 (or 2+ on urine)
3. pH <7.3 or bicarb <15

Pathophysiology:

Its a lack of insulin, right? Well yes and no.

Type one diabetics have impaired insulin production and therefore cannot bring their sugars down, but Insulin also acts to oppose other hormones (glucagon). It is this lack of opposition that causes the metabolism of fatty acids which in turn produces the ketones. So it is good to think of it as unopposed gluconeogenesis: the production of ketones lowers the pH and therefore gives us the acidosis ie. not a sugar problem.

Bang up some fluids and give insulin:

Treatment is aimed at correct the abnormalities and these patients are certainly dry and in need of lowering their blood sugars, but actually we need to think of treatment goals as switching off the gluconeogenesis and ketone production.

1. Fluid resuscitation - the link at the top contains a bit of debate as to the fluid to give, but essentially 0.9% Chloride is the answer because you can add potassium when it is needed.
2. Insulin- fixed rate infusion based on weight (0.1 units/kg/hr) - this corrects the sugars but also suppresses ketogenesis!
3. Monitor K+ and add it to fluids given - remember insulin will push it into intracellular space.
• hypokalaemia is a complication of treatment.
4. Give glucose when blood glucose is <14 - DKA is not a sugar problem but the production of ketones driven by glucagon, what we don't want is the sugar to fall and the gluconeogenesis to begin again!!!

What should I be worried about?

Things to worry about are the complications mentioned above: cerebral oedema and hypokalaemia.

Other things that warrant a higher level of care (HDU/ ITU) include:

• pH <7.1
• bicarb <5
• cardiovascular compromise
• Blood ketones >6
• Hypokalaemia on admission
• Anion gap >16
• Reduced GCS

Question:

A 36 year old lady who frequently attends the department with diabetic problems presents with a three day history of abdo pain and vommiting. She ways 65kg. Her observations are as follows: HR 117, Bp 109/76, RR 30, Sats 99% (21%). The results of her blood gas are as follows:

• pH: 7.23,
• Pa O2: 10
• Pa CO2: 1.4
• HCO3: 11.2
• Glucose: 36

a) What are the diagnostic criteria for Diabetic Ketoacidosis (DKA)? (3)

b) Write an appropriate prescription for an insulin regime in this patient. (2)

c) Give three features that should trigger discussion with critical care? (3)

d) What would be an appropriate fluid regime for this patient? (2)

Clever Marks:

Another question could quite easily ask you to calculate the anion gap - I have left this out of the gas information as I intend to do another medical maths entry on this topic.

Bloodbourne Infections and Needlestick Injury

Needlestick injuries and other exposures are a risk that all healthcare workers are exposed to. Out of hours they may easily present to the ED and are therefore on the syllabus for CT3 - they have also appeared in part B. Questions around rates of seroconversion, vaccinations and risks could easily appear in part A.

The Syllabus includes the following:

The health protection agency have a useful tutorial/ elearning http://www.health-protection-update.org.uk:8100/tutorials/needlestick/

Points to consider:

Risks:

Donor - Known blood HIV, Hepatitis B/C or High risk group - IVDU/ High prevalence Country

Fluid- Blood/ CSF/ Peritoneal or Pleural Fluid/ Breast Milk

Mechanism- hollow needles/ visible blood/ needle that has been in vein or artery/ deep wound/ not --------------------- through gloves/ injection of contaminated material

Disease Specifics:

The risks of transmission differ for the 3 main infections:

Hep B (30%) > Hep C (3%) > HIV (0.3.%)

Management:

It is necessary to take a relevant history including the risk factors and the vaccination status of the patient. The main point of management is to make a risk assessment and decide of post-exposure prophylaxis (PEP) is needed - you will have a local policy for this and it may well involve your oncall microbiologist. Follow up will be necessary however this is likely to be by occupational health rather than the ED.

• HIV - PEP available to high or unknown risk - many side effects and interatctions to consider
• Hep B - need to know immunisation status - immunoglobulin available
• Hep C - no PEP available

Acute Kidney Injury (& Hyperkalaemia)...

Whilst revising this I couldn't stop myself seeing how easy it is to turn into a part B question, the stem could begin with an ecg and ask you to describe the changes and give the diagnosis. Then ask you to list causes and describe the treatments. Alternatively you could be given a blood gas result including a sodium, potassium and glucose with an Addissonian picture and be asked to list what changes you would look for on the ECG, then to describe your management. Worst case scenario could even be to define an Acute Kidney Injury. Given it lends itself so well it is little wonder that it is a previous part B question!

Acute Kidney Injury:

Definition:

Stage 1: 
- creatinine rise >26 from baseline over 48 hrs
- creatinine rise x1.5 from baseline over 1 week
- Urine output <0.5 ml/kg/hr for 6 hrs

Stage 2:
- creat 2-3x baseline
- urine output <0.5ml/kg/hr for 12 hrs

Stage 3:
- creat >3x baseline
- <0.3ml/kg/hr for 24 hrs or anuria

The Causes are summarised in the following diagram borrowed from the wonderful Sketchy medicine

Investigation in the ED can help pin down the cause: protein on urine dip suggests glomerular disease, blood on dip think TINS (Trauma/ infection/ neoplasm/ Stones). However by far the commonest cause is pre-renal ie poor perfusion (sepsis/ hypovolaemia/ etc).

Management in the ED involves: catheter and hourly urine output, IVI bolus and response monitoring, treat the cause!

Hyperkalaemia

The most significant complication of AKI from an ED perspective is the potential for an increased serum potassium, as this can by imminently life threatening!

• Mild: 5.5-6 mmol/l
• Moderate 6.1-6.9 mmol/l
• Severe >7 mmol/l

See raised K+ think ECG:

• Tall t-waves (easy)
• short QT
• prolonged PR
• wide QRS
• flat p waves
• VT  (may be pulsed)

Treatment:

1. Calcium Chloride 10mls 10% IV - cardioprotective
2. Insulin - shifts potassium intracellular (remember to give with glucose!)
3. Salbutamol neb.

Clever Marks:

Marks may be available for recognising an addisonian crisis (hyponatraemia, hyperkalaemia and hypoglycaemia) and treatments including hydrocortisone.

Bad to Worse... SIRS, Sepsis and Shock...

The bread and butter of Resus, there are certain things you will see at work time and time again and this is one of the them. However it is not always something we manage as well as we should. Here is a three step approach to recognising sepsis:

Step 1:

The first concept you have to get your head round is the the Systemic Inflammatory Response Syndrome (SIRs)... Which requires two or more of the following:

• Hr >90
• RR >20
• Temp >38.3, <36
• WCC >12 or <4

SIRs does not mean sepsis but it does mean the patient is unwell (seems obvious), however it just means the body is reacting to an insult. This could be trauma/ post surgery/ PE/ infection/ autoimmune. I find my self documenting explicitly the sirs criteria present before my diagnosis for all my patients and this makes it easier to remember the exact criteria.

Step 2:

Does the patient have an infection or do you suspect they might? This deliberately includes the suspicion of infection as you may not have proof straight away but this should not delay treatment. It obviously requires you to have examined the patient and consider basic investigation. If the answer is yes the patient has sepsis.

Step 3:

Is there end organ dysfunction? Easy ones to quickly measure are renal function (urine output) and brain function (GCS).  If the answer is yes the patient has severe sepsis. You can also measure liver function (INR), Lactate, etc.

The final thing to know is the definition of SHOCK- which is inadequate tissue perfusion given end organ dysfunction and this clearly overlaps with our severe sepsis definition. The magic number to remember is a MAP <65.

What Next?

Its all good and well recognising SIRs/ Sepsis/ Shock but actually that is only half the story as we need to be able to treat these patients as well. Guidance exists on this from the surviving sepsis campaign: http://www.sccm.org/Documents/SSC-Guidelines.pdf

This can be summarised into initial management steps and some physiological targets:

Decussation is the key to the infamous Brown Seqard...

Well this one always gives me a headache... spinal cord syndromes! No matter how hard I try I can't keep these in my head, however the video podcasts http://emergencymedicineireland.com/anatomy-and-em/ always make it easy to refresh my knowledge:

AFEM 06.1 - anterior cord syndrome
AFEM 06.2 - central cord syndrome
AFEM 06.3 - brown seqard

This is a pet topic made for exams as it includes anatomy and specific clinical findings matched to that anatomy, it can be linked to a variety of clinical cases/ images. It could also quite easily be tied into a question about c-spine clearance, management of suspected spinal injury or SCIWORA.

My summary of Brown Seqard is below (the colour scheme and concept are borrowed from AFEM):

Decompression, Drain or not to drain...

Tension pneumothorax... every one knows how and where to decompress (https://www.youtube.com/watch?v=PblI70wkpjg - you only have to watch the first three minutes but I recommend the whole episode).

However what if it is a primary pneumothorax, measured at 3cm and no features of a tension? Fortunately the BTS are there to help: http://www.brit-thoracic.org.uk/Portals/0/Guidelines/PleuralDiseaseGuidelines/Pleural%20Guideline%202010/Pleural%20disease%202010%20pneumothorax.pdf

The Takeaway points can be summarised in the following flow chart and diagram

Another nice easy stem would be to describe the anatomical landmarks for the safety triangle:

Question...

(this should be easy after reading the above)

A skinny 24 your old presents with shortness of breath and reduced air entry on auscultation of the left chest.

1) Describe your management of this condition.

2) What features would suggest a tension pneumothorax?

3) Give the land marks of the "safe ares" for chest drain insertion, and why is it "safe"?

4) List three predisposing factors for this condition.

5) What advice would you give before discharge?

DVLA and illness.

So you've seen a patient, sorted them out and now it's time for discharge... they take their car keys out of their pocket and then you remember does the DVLA have something to say about their diagnosis?

Never fear, the college has a nice little summary of conditions that lead to restrictions on driving.

CEM summary of DVLA fitness to drive medical standards

Conditions restricting driving:

Things that do

1. Seizure- 6 months
2. LOC with high risk factors- 6 months unless cause identified
3. Cough syncope- 6 months
4. CVA - 1 month
5. Angina- driving must stop with symptoms at rest/ emotion/ at wheel
6. Arrhythmia - stop driving if arrhythmia incapacitates
7. Diabetes- only if awareness of hypoglycaemia is lost
8. Attacks of disabling giddiness - stop driving

Things that don't

1. Hypertension
2. Single episode of syncope.

Copycat or Inspired By...

Inspired by the previous post about sketchy medicine I have scanned in one of my revision "post-it" notes that I have up around my desk. It's my summary of common organisms causing illness in adults...

Brilliant little find...

I stumbled upon this little gem of a website with fantastic cartoon summaries of various topics... perfect for a quick revision bite...

http://sketchymedicine.com

Also some of the images are for sale on etsy.

Here's an example for toxidromes:

Baby on Board

The majority of pregnancies don't need the ED, but sometimes things don't go to plan, therefore a working knowledge of physiology in pregnancy and certain presentations are common MCEM questions.

For Part A

For Part B

Pre-Eclampsia affects around 5-6% of pregnancies. It is a triad of...

1. Hypertension 
2. Proteinuria
3. Oedema

1-2% of patients with pre-eclampsia will develop eclampsia. Eclampsia is marked by the development of seizures.

For Pre-eclampsia:

• Obstetric input
• Consider left lateral position - see physiological changes in pregnancy
• Control BP - labetalol/ hydralazine
• Limit fluid input.
• Consider magnesium
• Delivery is the definitive management. Notably pre-eclampsia can develop for up to several weeks after delivery!

For Eclampsia:

• ABC!
• Magnesium 4g IV over 5-10 mins to treat seizures.

Further Reading:

• http://www.rcog.org.uk/files/rcog-corp/GTG56.pdf 
• http://www.nice.org.uk/nicemedia/live/13098/50416/50416.pdf

B is For... Books and a tip for Burns management

There aren't many books specifically for MCEM

For Part A:

Question books - never underestimate the benefit of practicing MCQ's

• Get Through MCEM Part A: MCQs (Get Through Series) - AKA the Red One
• Divided into sections on specific areas covered by the exam such as anatomy, physiology,   pharmacology, microbiology, etc.
• As well as 3 mock papers.
• Gives answers and good depth of explanations.
• Recommended by most and is of similar standard to the exam itself.

• MCEM Part A Practice Questions (Oxbridge Medica's Revision Series) - AKA the Green One
• Again divided into key topics for each chapter, the chapter sizes seem weighted to reflect the exam.
• What I like the most is that answers are on the reverse of the same page as the question. This means you can use the book in short spells, or even in the rare event of spare time on the shop floor.
• This one seems harder to get hold of via the internet (amazon/ ebay

• Practice Papers for MCEM Part A - AKA the Blue One
• 8 practice papers back to back.
• Seems to be similar standard to the exam, my scores prior to taking the paper reflected my final score in the paper.
• The smallest book in terms of physical size but given its structure it doesn't lend itself to "quick" bites. Better to sit and practice as mock exams.

Other Books:

• Revision Notes for MCEM Part A
• Essentially the syllabus but annotated with bullet points, is also as you would expect a little bit bulky. Notably contains a few errors, but there really aren't any alternatives based on the syllabus directly.
• Can be useful for a quick dip on specific topics, but leans towards specific facts rather than explanations of base principles. Useful when used with other book.

• Basic Medical Sciences for MRCP Part 1, 3e (MRCP Study Guides)
• This might not be specifically for us but with the degree of overlap of basic sciences this is a book worth a read. Anecdotally the content seems to correlate with some common Mcem questions
• It is also worth having your favourite anatomy text and a specific microbiology book.

For Part B:

• Revision Notes for MCEM Part B
• My goto book at the moment, covers the whole syllabus in good depth with common exam topics and tips flagged up.
• Includes example SAQ's based on each chapter and previous papers.
• Get Through MCEM Part B: Data Interpretation Questions
• About to start this one and will update it as I work through it, but it written by some of the team behind the Bromley courses so has some credibility.

For Part C: - I'm not quite here yet so watch this space...

AND Finally...

For those who have made it to the bottom of this post a bite of information...

Parkland formula for fluid requirements for the first 24 hours in burns:

Burn Surface Area (BSA) x Weight (Kg) x 4             BSA x W x 4 (8/16)

Notably the clock starts at the time of the injury and half should be given over the first 8 hours, the second half over the next 16 hours. If a patient arrives 1 hr post injury you have 7 hours to give the first half.