Assessing Pain

Are you assessing pain ?

One of the most neglected skill sets of a clinician, is pain assessment.   Much has been written over the years but two themes reign supreme.

1- pain is what the patient says it is.

2- we are not good at assessment of pain.

As a subjective phenomenon, it is difficult to measure. So, do you use a system?  Have you got a template or a mnemonic you use when assessing a patient for pain.

I like OPQRST

O -Onset 

Asking about what brought the pain on.  Was it sudden, or a chronic ache that has been there long term. This lets the nurse drill down on any acute change in the pain .

P-Palliation /Provocation

Palliatition is easing or symptoms and provocation is worsening.  So ask your patient what makes their pain better or worse.  Has positioning, analgesia at home, or hot/cold pack made any differences?  Is the pain worsened on movement, palpating, or position? In chest /abdo pain, dies deep breathing alter the pain?  In leg ulcer patients, is their pain worse when they hang their legs down (venous congestion) or worse when elevating (arterial)- called claudication; this is the difference between venous or arterial disease.

Q-Quality

Asking the patient to describe pain.  This can be difficult for the patient to articulate, so I use this question like a multi choice question.  People might identify if you say others describe their pain as “sharp, dull, stabbing,burning, shooting, electric, heaviness, aching, pressure, throbbing, spasming, cramping etc”. Is there altered sensation like numbness, pins n needles or intermittent tingling? Can you think of others?

R-Region and Radiation

Where exactly is the pain at its worst? Can they pinpoint the pain by pointing to where it hurts most?  Some is vague regional pain eg abdominal or cardiac pain, others are isolated pains like fractures, and epigastric pain.

Ask the patient if the pain radiates or spreads from a focal point to somewhere else.  Typically, cardiac pain radiates from the centre of the chest into the neck, jaw, teeth and arms (L>R).  Some abdominal pain can radiate to the shoulders, and some back pains can send electric shooting pain down the buttocks and back of the legs (sciatica).  

S-Severity

Pain scores have been around for a long time in visual (Wong-BakerFace scale, slide rule descriptor) and numeric 0-10 scoring systems.  These are hard for many patients to interpret and the most inaccurate part of a pain assessment.  Part of the problem with their use is inconsistency that nurses and paramedics apply the pain score.  

0 is no pain.  10 is the worst pain experienced.  It is finite, it is recognisable and it is something that the patient needs to reflect on NOT imagine.   You can not imagine a pain you have never felt, so stop expecting a patient to do this.  Never say.

“10 is the worst pain imaginable”. It isn’t.   10 will only ever be the worst they’ve remembered.  So should your patient suggest they have never experienced pain worse than this pain right now; then take them at their word, and record it as 10.

Soon you will intervene to ease the pain, so you will want to reevaluate the score after positioning or giving analgesia.

0= no pain:  10 is the worst they’ve ever experienced.

Even if they are laughing or won’t get off their phone!!  Frustrating I know, but it’s not a number they need to get right, nor one that you should judge them on.

T-Time 

Get a time line on the patient pain.  How long have they had this pain, is it there now? If not when was it there, and for how long?  If it is intermittent, how long is each episode?

Now the data is collected, a physical inspection or palpation may be valuable to aid your assessment.  Use range of movement assessment to put limbs through their paces.  Observe patient posture, positioning and any self protective guarding.   Look for inflammatory signs - red,hot,swollen.

And obtain a tidy medical history, including medications the patient is on.... I use AMPLE and I’ll look at that in the next blog.

So that’s it.  OPQRST.  In a simple template you can follow every time you’re assessing pain.  I hope it was a helpful refresher. 

I’d love to hear your thoughts and opinions, tips and tricks.

ECTopics 18: Thyroid and its hormones

ECTopics 18: Thyroid and its hormones

ECTopics :17 Claiming CPD

Do you know how to diarise your CPD? In this short podcast, I discuss the standard reflection. Get through your next CPD NMBA audit with my Rule of Threes.



ECTopics :17 Claiming CPD

ECTopics: 15 Knowing Your Jargon - Cardiac Terminology

ECTopics: 15 Knowing Your Jargon - Cardiac Terminology

Ectopics :12 Comedian Georgie Carroll **Explicit Language and adult content**

Ectopics :12 Comedian Georgie Carroll **Explicit Language and adult content**

Had a great chat with Adelaide nurse, and Standup comedian Georgie Carroll. 

Born and raised in Manchester, England; now a proud Australian. Georgie Carroll is a Comedian, Nurse, Wife and Mother. 

This combination of Nationalities, home life and hospital has provided a 24/7 training ground that has nurtured Georgie’s naturally funny bones. Her bluntness and charm coupled with razor-sharp wit, give her a broad-spectrum appeal that can be put into any room and shine. 

this podcast features a free flowing (mostly) unedited fly on the wall type ear, of our chat that lasted the best part of 40 mins.   Like some Nurse to nurse conversations had in the privacy of comfortable company, there is a language disclaimer and some dark and risque content.  But all in all , its just fun chat with talented nurse, mother, and all round great conversationalist.

Catch Georgie's own Podcast called THE SWAB  on all your fav podcast apps.

Or flick over to her webpage -https://www.georgiecarroll.com/

42mins

#georgiecarroll #TheSWAB #ECTopics  #ECT4Health

A 5th category of Shock: Pneumogenic

A fifth category of shock - Pneumogenic

Are we missing a vital category of shock? 

Forever- we have had shock classified into 4 main categories, but is there a fifth?

Hypovolaemic - that is a reduction  in blood volume. 

Cardiogenic- that is a reduction in cardiac output

Obstructive - which is an obstruction to venous return and this preload.

And Distributive which is a venous dilation which causes a maldistribution of blood between arterial and venous capitance.

The point is- they are all shock which can be defined as Global Cellular Hypoxia- Lack of oxygen to all cells is the fundamental definition of shock.

So with shock being one thing (global hypoxia), why wouldn’t Respiratory failure contribute to shock?   It should.

I think the clever books have missed a category.

So I’m advocating a 5th category - Pneumogenic shock.

All tissue /organ oxygenation starts with delivery of oxygen via the arterial network.

The right heart receives blood from the tissues, pumps it into the lungs, to be oxygenated, receives it into the left heart, then pumps this oxygen to tissues- thus completing the circuit.

Traditionally in shock we have categorised every step in this circuit, except the glaringly obvious issue to oxygenation of blood inside pulmonary vessels.

The world of respiratory medicine goes to great pains to highlight the importance of understanding the physiology of VQ ratios, PF Ratios and A-a gradients, but stop short when translating this hypoxaemic discourse of respiratory failure to the concept of shock.

It therefore seems rational to add a unique category into the age old shock paradigm.  I propose “pneumogenic shock” to describe an aetiology of profound  global hypoxia born from a respiratory failure, not a cardiovascular failure.

Definition - Pneumogenic Shock, is a syndrome of hypoxaemic hypoxia caused by pathophysiological conditions that prevent adequate oxygenation of blood  (external respiration).

Pneumogenic shock would be classified as pre-pulmonary or extrinsic, and intrapulmonary (intrinsic).

Extrinsic Pneumogenic shock (EPS)

EPS occurs when a person is exposed to a reduction of oxygen in the gas mix being breathed.  EPS could manifest with toxic gas inhalation, or hypoxia environments.  It’s estimated that Fio2 of less than 0.15 (15%) is not sustainable for life at sea level barometric pressure.

Therefore breathing a smoke filled toxic gas environment where partial pressures of oxygen are too low would be considered to constitute EPS.

Prepulmonary Pneumogenic shock would manifest as a factor of airway obstruction, or restriction.  Foreign body airway occlusion (FBAO), mechanical suffocation, strangulation/hanging, and upper airway, larynx, tracheal or bronchial oedema, are all examples.

They may be manifestations of trauma, infection or other triggers of inflammation to the upper airway.  Fundamentally, shock caused by this subcategory are not associated with low Fio2, or alveolar dysfunction.

Intrinsic Pneumogenic Shock 

This Pneumogenic shock is intrapulmonary.  Where gas exchange occurs in alveoli, a mismatch of VQ ratio leads to an A-a gradient that is incompatible with survival.

In instances of severe pulmonary oedema, pulmonary embolism, low airway injury, ARDS or acute lung injury; gas exchange may become so impaired that hypoxaemia is critical.  

 A measure of PF ratio and V:Q would be assessment data that differentiates Pneumogenic shock from other syndromes.

I’m Rob Timmings a nurse educator.

The thoughts on this page are my own.  Not the position of ECT4Health, it’s directors or employees.  Rob Timmings is open to discussion on the content in this article.  It exists as a discussion paper.

Rob@ECT4Health.com.au

ECTOPICs-Nurses podcast

ECTOPICs-Nurses podcast

Ectopics :10 Wound Care Basics. Stage/ Grading a pressure Ulcer? - An Interview with Kim Kaim

Ectopics :10 Wound Care Basics. Stage/ Grading a pressure Ulcer? - An Interview with Kim Kaim

COVID19 update- ECT4Health

#ECT4Health. .. An Update.

There are currently 1,098,456 confirmed cases and 59,162 deaths from the coronavirus COVID-19 outbreak as of April 04, 2020, 02:52 GMT.

When the government predicted 6 months selective shutdown which finishesin August, we had to reinvent how we deliver quality seminars.

We are game ready for face to face courses from July onward. Remaining optimistic !!!

That said ,  our programs in this “down time” are being revamped and updated to 2020 standards.

We are also converting them into online webinar versions (just like our HICCS-COVID19 Seminar booking currently.  You’ll have choice of online live, purchase a seminar series, or attend face to face.

I guess what I’m saying is - we will get through this and reclaim our territory as a popular option for face to face seminar delivery.
But the web space opens a whole world (literally) to our seminars.

Stay connected.
Do you want to stay in the loop?
Consider our free e-newsletter.

The new virus free ECT4Health will rise, and we are taking bookings right now.

* QuarterDose” is our new e-newsletter coming out quarterly .
Get on the list: admin@ect4health.com.au 

* webinars through Zoom . All our seminars are being converted to web delivery for access right now.

* Whatson page is our real time e-calendar of dates (www.ect4health.com.au/whats  )

* Bundled Subscriptions
For a low $9.90/week (early bird $6/week) you can doin our collaborative subscription service.  Each week there will be a number of items for you to access.  From 3D or VR educational video lectures, to topical podcast episodes, to blogs/blogs, and all using the innovative delivery via Virtual Reality.  In 3D you can participate in clinical scenarios and simulations right from the comfort of your bedroom or lounge.  Upgrade your subscription to $25/week and you’ll own your very own state if the art VR headset with a fully integrated 3D Anatomy software loaded into the head gear.  
You’ll be able to join live classes with us and dozens of nurses or paramedics around the world in real time virtual seminars hearing from world class speakers.

* Imagine putting on a VR head set and being transported to a tranquil rain forest or deserted beach to do a 30 min interactive yoga or mindfulness session.
All this and so much more with our exciting partnership launching in just 4 weeks. Click here for this Bundle of Rays Check our the sample

* ECT4Health blogs (>150 up for you now) are regularly written as a response to questions in our seminars.  There is hours of Free CPD there for your reading pleasure- 5 minute grabs on my blogger page :www.knowingyourjargon.blogspot.com

* YouTube Channel.  All the little videos I’ve recorded in one place on our  YouTube channel 

So so much going on people.  Please spend a bit of time looking around our Whatson page-  I really would love to see you in one of our seminars. But in the mean time .  Let the CPD world get a shake up from ECT4Health and our collaborative approach to innovative health care professional education.

We will rise from this.
~Rob

EKA and Gliflozins

Why do these drugs cause EKA?

#kYJ Euglycaemic KetoAcidosis (EKA)

With the introduction of *Gliflozins as a strategy to target hyperglycaema, and insulin resistance, there has been for the first time real promise that perhaps, we can reverse Type 2 Diabetes.

These drugs (like all) have costs and benefits. They cause increased incidence of UTI as now, sugary urine is a virtual fertiliser for bladder bacteria.
They also cause a rare ketoacidosis where the blood sugar isn’t elevated- euglycaemic KetoAcidosis.
Why??   Read on.

Unlike the older sulphonylureas, Metformin, and even incretin mimics, Januvia and it’s DPP4 inhibitor cousins, the Gliflozins are novel.

These drugs (empagliflozin, dapagliflozin) shut off a protein in your kidneys (SGLT2) responsible for reabsorbing glucose back into the blood.

Block SGLT2, and you pee your glucose out, dropping your blood sugar, and subsequently your insulin secretion.    Less sugar=less  insulin= improved insulin sensitivity.... T2 diabetes fixed (... ok not that simple, but treating Insulin Resistance (IR) is the goal in T2DM.

So ... remember that insulin reduction in blood results from blood glucose reduction.
...
Now insulin.   To fully understand insulin, you need to rearrange what you previously knew about this little hormone.

Insulin is a growth hormone.  It grows fat.
The more insulin a person has, the better they grow fat.

Insulin takes glucose and offers it to cells.  When fat cells are offered glucose, they say “Yes please!!!”, and takes in glucose in to convert it with free fatty acids, to fat.

Now if there is lots of insulin,there is lots of storage.

The FAT house
Think of a house with an open doorway where glucose is streaming in. Insulin keeps that door open, and glucose flushing in.
If insulin is absent or low, then instead of glucose flooding into fat cells, fatty acids flood out.  
Low insulin= free fatty acids  (FFA) released into blood.
...
Are you with me?
...
Insulin = fat cells grow
No insulin = fat cells melt.

Now , when this happens, the FFA, circulated to the liver which converts these FFAs into a group of acids called Ketone Bodies, or just, Ketones.

An accumulation of ketones can only happen when :
Fatty acids are converted to ketones, and this can only happen when insulin is too low.

Summary: low insulin- fat melts-ketones produced.

Now-  back to the side effect of Gliflozins...Euglycaemic KetoAcidosis.
Work it back...
The blood is acidotic because too many ketone acids in the blood.
Ketones are made because fat cells are melting FFA into blood.
Fat is melting because insulin levels fell.
Insulin levels fell because glucose levels fell.
Glucose fell because Kidneys pee all the glucose out (glucosuria)
Glucosuria occurs because
The Gliflozins block glucose reabsorption back to blood.

Less glucose=less insulin= fat melt= ketones and acidosis (Ketoacidodis).

I need a chocolate!

How Vaccination works

How does a vaccine work?

Do you ever remember tasting something or smelling something that takes you back to a childhood memory?

Perhaps it was a tune you heard, and you recognise it from the past.   Well,when you were first exposed to it, your brain chose to store a memory of the taste/smell/sound.

Well it’s not just your brain that remembers stuff.   Your immune system does too.  Special White Blood Cells (leukocytes) called lymphocytes have an incredible capacity to remember chemicals that they’ve been previously exposed to.   Every living and even non living thing is made up of matter that is unique to itself.   

Think of an orange- it looks and tastes and smells like an orange.  An apple looks and tastes and smells like an apple.

To your lymphocytes, they remember how a bacteria,  virus, or parasite/fungus/allergen smell/taste.

On the surface of these organisms, proteins or sugars are present which act as a unique fingerprint called an Antigen.

Once your immune cells have been exposed to an antigen, your lymphocytes remember it for a while.

Lymphocytes that are born and mature in the bone marrow are called B Cells.   They remember the antigens and produce memory jogger chemicals called Immunoglobulins (we commonly call these Antibodies).

Now floating around your blood stream are these Antibodies, and as soon as that virus, or bacteria or threatening allergy producing thing comes into contact with your body again, your immune system can remember it; remember what a threat it was, attack the invader to protect you.

This is happening every minute of every day.  Constant surveillance and defence.  Some diseases are so dangerous (measles, Flu, polio, tetanus (the list goes on)), that it isn’t safe to allow ourselves to be exposed to it.  Your lymphocytes must have first come into contact with the disease before it can make those memory jogging Antibodies.  So vaccination is the strategy.

When vaccination occurs a tiny dead (in the case of bacteria) , attenuated (weakened) or inactive virus sample is introduced into the body, stimulating your lymphocytes to learn to recognise it, and make those memory jogging Antibodies.

Now the immune system has been exposed, so should you come into contact with the wild live/active disease, your immune system can whoop it back to primordia.

Memories fade,and so do some antibodies, which is why some diseases need booster shots to remind the immune system what to be vigilant for.

Some organisms mutate so rapidly that they change their antigen.  Kind of like getting a fake ID.  So for diseases like these (Influenza is a great example) we often need an annual immunisation.

Hope this was in some way helpful.   Get your shots!

~Rob.  #ECT4Health 

We cover this stuff in our Fevers and Sepsis sessions 

Check out the website for more details www.ect4health.com.au/whatswww.ect4health.com.au/whats

Virus- alive or not

Is this alive or not?

Coronavirus

News out this week that Australia has “grown” the nCoV virus in a lab and is now “observing the ‘live’ virus in the laboratory to see how it ‘behaves”.

The biocontainment  security facility at CSIRO in Geelong is set to offer valuable information on the Coronavirus.

I thought I’d touch on a bit of misinformation on the internet about this and other viruses.

Point - Viruses are not alive.

The term live virus is a figure of speech that indicates the virus is able to be active or functional.

It is not a living thing,nor is it dead.   It’s undead.   It is a particle of proteins (amino acids) and sugars.

Think of an egg, or a piece of chocolate; it’s not alive or dead, it just ... is.

Now stay with me,

Take a glass.   The type of glass you drink from.  Not alive or dead (because is was never first living), yet that same glass can hold water.

It functions as a tool to hold liquid.  If you think of a glass as a virus, it isn’t living, so you can’t kill it.

In biology something that is living is called ‘biotic’.   A biotic, possesses the ability to reproduce through cell division (mitosis and meiosis).  Viruses are not cells, they can’t reproduce and therefore, are not biotic (alive).   This is the fundamental reason that antibiotics have no effect on viruses.  They’d have to be biotic, for an anti-biotic to have any effect.

So how do we stop viruses?

Well, come back to the analogy of the glass.    The glass functions to hold a drink; and it does this with no need to be living; but it does need to be intact.

If we broke a glass (say, by dropping it), the glass wasn’t killed, but it broke to pieces, so it ceases to function.   Now the same principle is applied to medications that we can use for viruses.   Antivirals break the protein shell that encapsulates a virus’s genetic information.  Alternatively, some antiviral agents break the genes inside a virus.

Currently we don’t have a magic drug available to destroy (break) the novel CoV virus.  The first step in knowing how to break this virus, is to understand the mechanism this virus uses to infect, and the behaviour of these proteins that it is composed from.

Interesting times ahead.   But for now you’d be more correct to think of a virus as active or inactive, rather than live or dead.

How a virus like nCoV works?

First -Out of China

There are concerning (unconfirmed) reports in news channels and social media leaks that Novel CoV has infected now 90000.  This disease first emerged as a new viral pneumonia in seafood market workers in Wuhan China.
The virus is infectious during incubation, and Chinese authorities are now suggesting that where previously this incubation was thought to be  less than a week, it’s now reporting up to 14 days .

Let’s do a recap on how this virus works.

Transmission- droplet and contact, and faecal.

If someone with nCoV sneezes in a shopping centre, like measles, the virus is aerosolised and breathed in or, the virus settles on a surface (eg escalators hand rail, elevator button, coffee table).   Someone touches it, and then touches their own face or eyes, and has at that point become infected.
That is called transmission.

Now the virus starts to invade cells lining the respiratory tree, lungs, throat and nose. It enters the cell using enzymes to invite itself into the cell.
The cell tries to defend itself, by dissolving the virus outer membrane (the envelope) but this is what the virus wants; now the payload is exposed- the genetic instruction sheet called RNA.
Like a recipe book, the lung cell’s own genetic material (DNA) is altered by the virus RNA which now reprograms these cells to to start to make copies of the nCoV .

When millions of copies are made- the new viruses then burst out of the slave cell, killing it, and showering a spread of millions of virus particles to neighbouring cells.
The process repeats until so many cells have been damaged that the immune system responds.
This lag from Transmission to symptoms is called incubation time.
In Flu it’s 1-3 days, but this nCoV is now believed to be up to 14 days.  All that time, a person is shedding and spreading virus, and has no idea they were even infected or infectious.

Mutation:
The concerning issue at hand is that this virus is thought to have mutated in to a second generation- meaning it can be passed from human to human.  Previously it was thought to be purely zoonotic, transmitted by an animal to human only in its first generation.

As a virus mutates, it undergoes minor changes called Drift, but major changes like second mutations, are referred to as Shift.  This causes the host (is in this case) to not recognise the virus from one mutation to another.   Very difficult to pin down this virus yo produce a vaccine.

#ncov
Official death toll (reported) is currently at 80.
Cases in China, Japan, France, USA, Australia and no doubt third world nations with limited capacity to contain or report.
Written at 8am on 27th Jan 2020.