Wednesday, 27 November 2019


Pain management is something we're really bad at doing, and even worse at documenting!

Use a pain scale, or a pain ruler

Remember that pain has an emotional as well as physical component. When you catch your thumb in a door you shake it and look at it. If it does not bleed too much but still wiggles and the pain goes quickly, then that is mostly "red" - physical. However the longer a pain lasts the more the emotional component becomes part of the problem.
The emotional component is made up of three aspects. There is anxiety and worry and typically we worry about two things. We worry about the "meaning" of the pain, why is it there, what is causing it, what is going on. Then we worry about the future and how the pain will affect us and our lives and our work and relationships.
Pain also makes us unhappy, although not necessarily depressed. This typically occurs in three ways. It affects us directly to make us miserable. It commands our attention, both consciously and subconsciously so we are listening for the pain thus hearing it louder and more often. Finally it isolates us socially.
The final aspect of the emotional component is the frustration that accompanies it. We become frustrated that it does not go away, that promised cures do not work, and that that life gets worse.
Thus, the physical component can be viewed as the transmission of the message up to the brain and the emotional component can be viewed as the unpleasantness experienced. Of course the degree of disability and the behavioural changes are subsequent phenomena.

Pain is felt, and travels up the spinothalamic tract to the thalamus.

Use WHO analgesic ladder
Combining two weak opioids isn't considered good practice.


Use the WHO analgesic ladder

Tuesday, 26 November 2019


Awake and Conscious Patient 
Assess symptoms:
Put the temperature on the gas machine
Look for J waves (osborn). The upward deflection of the terminal S wave (at the junction of the QRS and the ST segment) occurs at or near 32 C. It is first seen in leads II and V6.

Rewarming - consider bypass in cardiac arrest, haemodynamic instability and a core temperature below 32°C, frozen extremities and rhabdomyolysis with hyperkalaemia.
Treat electrolyte disturbances - being careful of hypokalaemia as potassium will increase with re-warming
Remember coagulopathy is common
Haemocrit will rise.

Treat with 40 degrees water, aspirin

In cardiac arrest 
Don't give up too soon. Watch this great youtube video. It's true!

Further Reading

Wednesday, 20 November 2019


BNP is produced by cardiac myocytes in response to stretch which occurs in impaired diastolic or systolic function. BNP may play an important role in acute cardiac failure. BNP assays can supplement clinical judgment when the cause of a patients dyspnoea is uncertain. Results should be interpreted in the context of all available clinical data. The role of BNP in chronic heart failure is, however, well established for diagnosing, staging and risk stratifying patients.

BNP has reasonable sensitivity and therefore can be used to rule out heart failure as a cause of a patients breathlessness (in a primary care setting for example) but it is not very specific and therefore not useful for ruling the diagnosis in. BNP rises due to sepsis, renal or liver failure, hypoxia, myocardial ischaemia, tachycardia as well as many other reasons. In hyperacute or flash pulmonary oedema or acute mitral regurgitation the BNP level may not be elevated initially.
NT-proBNP is useful in differentiating between respiratory and cardiac disease in infants. It may be a good cardiac marker. May be useful for pneumonia prognostication. Can help risk assess PEs, although troponin is probably more sensitive so it's generally not considered useful.  It is a marker of secondary myocardial injury.

Interestingly: *Low risk patients do not need specific right ventricular (RV) functional assessment but where RV dilatation has been identified on CT or Echo in patients otherwise suitable for outpatient management, consider measuring BNP, NT-proBNP and hsTnI or hsTnT. Elevated biomarkers should prompt inpatient admission for observation. Incidental elevated troponin requires senior review and consideration of an alternative cause to the elevated troponin.

Probably adding noise to an already uncertain baseline. Sensitive but not specific.

Wednesday, 6 November 2019

Gout, Pseudogout

Clinical Features
Coffee is protective against gout, but intense exercise and microtrauma can precipitate
For rheumatoid rather than reactive, symptoms must be >8 weeks.
Ask about skin (ank spond linked to psoriasis), butterfly rash in the heat (SLE), morning stiffness (RA has atleast an hour), diarrhoea, blood, eye signs, miscarriages
If it's 1st MTP - gout most likely
There can be RA accelerated atherosclerosis

Red, hot, shiny joint is likely to be gout
95% of nodules are gout or RA.

10-40% have a normal urate during flares

NSAIDs - topical or oral
Rheumatoid - conside steroids 10mg for 3days
Stop DMARDs if infection - for up to two weeks - they have long term not short term effect

May be a manifestation of systemic illness:
Systemic lupus erythematosus (SLE)
Behcet’s disease
Reiter’s syndrome /Reactive arthritis
Hypertrophic pulmonary osteoarthropathy (HPOA)
Ankylosing spondylitis (tends to affect axial skeleton)
Familial mediterranean fever
Amyloid arthropathy
Rheumatic fever

Tuesday, 5 November 2019


There are many causes of hypoglycaemia. Contrary to popular belief, hypoglycaemia is not caused by diabetes- hypoglycaemia is caused by the treatment of diabetes.
Whipple’s triad:
Symptoms of hypoglycaemia with abnormally low plasma glucose concentration, and relief of the symptoms after glucose concentrations normalise.

Overdose of insulin or oral hypoglycaemics
Drugs—ethanol, MAOIs, haloperidol, sulfonamides, salicylates
Insulinoma or islet cell hyperplasia
Adrenal insufficiency (Addison’s disease)
Hepatic failure, hypothermia and sometimes sepsis.
Increased exercise
Decreased calorie intake, or missed meals or snacks.

Signs and Symptoms
The signs and symptoms can be split into two categories – neuroglycopenia and adrenergic response. The adrenergic response is perhaps the one we are most familiar with, and precedes the neuroglycopaenic symptoms.

Adrenergic response
Catecholamines are released. How much catecholamine is released is inversely proportional to the sugar level, not the rate of drop. Symptoms include:

This occurs over 1–3 hours:
Headache, diplopia
Difficulty in concentrating, hallucinations
Confusion, irritability
Focal neurological deficits

Lab Values
Hypoglycaemia is a blood sugar of less than 4.0mmol/L.
There is individual variation in the BGL required to produce symptoms, but it is generally regarded as <2.5 mmol/L.

Eating + Drinking:            Sugary sweets like Percy Pigs or jelly babies. Chocolate is bad because the milk needs to be digested before it can be used to provide sugar. 10g of glucose is available from 55ml Lucozade, Ribena 19mL, Coca-Cola 100mL, 2 tsp sugar and 4 sugar lumps.
Once you have given a short acting sugar, remember to follow it up with some complicated carbohydrate like a sandwich.

Not Eating And Drinking:
Glucagon 1mg    IM injection        Glucagon causes transient insulin resistance for <2 hours, so BMs might rise. Glucagon may stimulate vomiting, so consider use of glucagon carefully.
IV Dextrose        20% IV dextrose is the treatment of choice. 50% dextrose is no longer available, as it causes a lot of inflammation. 5% dextrose is not helpful in treating hypoglycaemia. 10% glucose is acceptable.
Glucagon stimulates insulin secretion, and glycogenolysis so is less useful in type two diabetes. IV dextrose also stimulates insulin release, and can trigger rebound hypoglycaemia. Glucagon tends to produce a steady rise in glucose levels.

Insulin is very dangerous, and a cause of many medical errors. Be aware of long and short acting insulins.

Saturday, 2 November 2019

Heparin Induced Thrombocytopenia

Hypercoagulation Symptoms: MI, stroke, limb and organ ischaemia, DVT, PE
Bleeding Complications
Fever, chills, flushing or the skin

4Ts: Thrombocytopenia
   Timing of Platelets fall
    Thrombocytopenia from other causes

Type I Immune Mediated - platelets normally between 100 and 150. Self limiting. 2 days after heparin administration.
Type II Immune Mediated - Platelet IgG (which cause release of pro-coagulant factors and acute inflammation) complexes removed by splenic macrophages. Thrombocytopaenia >50% in 5-15 days of heparin adminstration.
If someone has had heparin before, this happens quicker.

Fundaparinox induced HIT is rare.

Thursday, 24 October 2019

Mental Health Presentations

AMTS (Abbreviated mental test score)
1. How old are you?
2. What’s your date of birth?
3. What is the year?
4. What is the time of the day?
GIVE ADDRESS to remember (42 West Street)
5. Where are we? (What building?)
6. Who is the current monarch?
7. What was the date of the 1st world war?
8. Can you count backwards from 20 to 1?
9. Recognise two people
10. Can you remember that address?

Mental state examination
All Sane Men Think That Pizza Is Italian
- Appearance and behaviour
- Speech
- Mood
- Thought form/process
- Thought content (e.g. delusions)
- Perception (e.g. hallucinations)
- Insight
- IQ (cognitive function)