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):

Can't Pee...

Another of the CT3 additional presentations:

Urinary retention is a fairly common presentation, but it is not the most glamorous of topics, there is however a CEM standard for its management and it easily could make an SAQ.

There is a nice summary article on the BMJ website http://www.bmj.com/content/318/7188/921

Question:

A 72 year old man presents with increasing lower abdominal pain and the inability to pass urine for the past 24 hours. He is in obvious distress and is tachycardic and hypertensive, a bladder scan is performed and shows in excess of 800mls. You successfully pass a urethral catheter and the patient is quickly relieved.

1) List 3 differentials for this man's problem. (3)

2) What clinical features would suggest a history of prostatism? (2)

3) Following insertion of a urethral catheter list three things you should document. (3)

4) Give two features that would require hospital admission. (2)

Blood Pressure is a GP thing right?

So we spend a lot of our time worrying about shock/ hypotension and are probably better at putting people's blood pressure up (white coat hypertension). Just occasionally though you will meet somebody whose blood pressure is too high and needs to come down.

What constitutes a hypertensive emergency? The section in the BNF is rather good for this and was my go to resource for part A.

Important numbers are 180/ or /110, the second step is to decide if there is end organ dysfunction:

1. Hypertensive encephalopathy
2. Acute LVF
3. Acute MI
4. Aortic Dissection
5. Intracranial Haemorrhage
6. AKI
7. Eclampsia

The presence of any of the above is hypertensive emergency.

Without them it is hypertensive urgency.

Remember BP = CO x SvR

Treatment options mostly cause some form of vasodilatation: sodium nitroprusside/ labetalol/ nitrates.

Another review of a course...

So I recently attended the Bromley Mcem Part B course (http://www.mcemcourses.org).

The course itself is two days in the clinical education centre of the Princess Royal hospital in Orpington. It includes 4 practice papers (with one sent out before the course) and lectures on some common topics that come up frequently.

The course faculty admit that they cannot cover the whole syllabus but they do try to flag up common things. It also includes so good tips on exam technique and how to approach the paper. I'm am not going to go into detail on what they say as I don't want to steal their content. However I will say I found the course useful and came away feeling better prepared to tackle the paper.

Another useful thing they encourage is to mark other people's papers to recognise how to make the examiner's life easier.

Their website's free resources include cases of the week, these make good practice questions.

All in all I would definitely recommend the course.

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?