#KYJ - Troponin rise in kidney disease

#KYJ Troponin in renal disease.
 An all too common question in my cardiac courses relates to a common (up to 70%) situation where a patient with chronic kidney disease (CKD) returns a positive Troponin .
So
Why does my renal patient have an elevated Troponin level in the absence of an acute MI?
...
Let's recap some basic cardiac sell physiology.
Inside heart muscle cells (cardiomyocytes) exists tiny molecular protein machines called sarcomeres. They look stripy under the microscope which is why heart tissue is often called striated muscle.  Striated means stripe like.

These sarcomeres contain complex protein filaments that change shape (shortening and lengthening) in shape when electrically stimulated.
Called Actin and Myosin filaments, the action of shortening is what causes the muscle cell to contract.

Now actin and myosin are glued together with a protein called Troponin.  Three types, Troponin I, T and C
.
Troponin T and I are cardiac muscle specific.

Now visualise this. The sarcomeres with all these Troponin, Actin and Myosin proteins are "locked" away inside heart cells.  Not in blood/serum, but inside cells.

If you think of them as the yoke of an egg.  The only way a yoke can leak out, is if the egg breaks.  Likewise, the only way Troponin can leak out is when the cardiac cell is damaged.

Enter a myocardial infarction (MI).  As heart cells die and break open like eggs, they leak their contents onto the interstitial fluid, then, because the cardiac tissue injury causes inflammation and subsequent increase in capillary permeability, the large troponin proteins diffuse (leach) into the blood stream.  Hence, a Troponin rise is detected in serum.  It is not quick, it leaks slowly into the blood stream, and peaks at about 9 hours after injury to heart cells.

Measured in nanograms/L or micrograms/L depending on the path lab at your facility, Troponin rise it diagnostic when recorded to be greater than 15ng/L (on newest assays), or 0.04mcg/L on older assays or IStat machines.

Commonly clinicians report false positives.  In patients who live in areas where there are high rodent numbers (esp mice), these individuals can have developed anti-mouse antibodies due to high rodent exposure.  Their rodent antibody rich blood can cross react with the various Troponin assays in the lab, returning false elevated Troponin values.

Commonly, renal patients with CKD will have elevations in Troponin in their blood which can confuse the diagnostic value of a CKD patient's chest pain presentation.  But why?  Why if there was no acute cardiac damage, could Troponin leak?

Well it does.  Chronic kidney disease patients often have a chronic elevation in Urea in their blood.  This uraemia is damaging to cardiac and other muscle tissue.  Slow chronic insidious erosion of heart tissue allows troponin to continually leak like a dripping tap, elevating the baseline level of Troponin.  A sharp rise is still diagnostic, but a one off elevation that is slightly over the threshold of 0.04mcg is not diagnostic of an acute event in these renal patients.  We'd admit for serial cardiac Troponin levels to watch for rise over the 9-12 hours.

We cover all this interesting stuff in our #Cardiac, #ARRR #PirateSeminar, and #AcuteDeterioration
Seminars.  Check them all out here www.ect4health.com.au/whatswww.ect4health.com.au/whats 

Restrictive versus Obstructive airway disease

#KYJ-  is it Obstructive Airway disease or Restrictive Airway disease?

We've all cared for a patient with a chronic lung disease. Words that we add to the jargon soup include chronic obstructive pulmonary disease or COPD, emphysema and asthma and chronic bronchitis and pulmonary fibrosis and pneumonia and pulmonary oedema.  All these are terms that we associate with both acute and chronic conditions that often manifest in shortness of breath.
At times we may confuse the terminology and when  nursing patients with respiratory diseases, two terms seem to dominate.
Obstructive airways disease and restrictive airways disease; these are different.

Obstructive Lung disease

An obstructive airways disease, as the name implies, is a disease characterised by a patient's inability to breathe out the predicted volume of air from the lungs.  Obstructive diseases also cause a restriction in the flow of air while breathing out, and as a result, are sometimes confused as restrictive airways disease.
Take a typical COPD patient, they tend to be able to draw breath but when they go to breathe out, the volume exhaled is less than normal (forced vital capacity (FVC) is diminished), and the outward flow of expired air is slower than normal.  This can be measured by a spirometry test called the Forced Expiratory Volume in one second or FEV1.
Say for example you were expected to be able to breathe out 4 litres, but when a spirometry test is performed, you can only breathe out  3 L; this would mean that you have only exhaled 75% of what was predicted.  Likewise you would expect to be able to breathe out a minimum of 70% of your entire lung volume in the first one second but on your test you might of only be capable of blowing 50% of your lung volume in that first second (ie 1500ml at 1 sec).  This would represent and obstructive picture, where you have both an obstruction to be able to blow your entire volume out (FVC 70% of normal) and an obstruction to the airflow, making exhalation slower (FEV1 50% of normal) .
Typically these are diseases like asthma, emphysema and chronic bronchitis, The three conditions that make up COPD.  The hallmark of these obstructive diseases is trapping of gas, altering diffusion and oxygen/CO2 exchange.

Restrictive Lung diseases
So what is a Restrictive lung disease?
People with restrictive lung disease are said to have a restriction preventing them from fully expanding their lungs.  They cant fill their lungs with air.

Have you ever munged out on a buffet so much, that you were so full you couldn't breathe?  Well imagine you did; that is an example of airway restriction.

With restricted airway diseases, there is a mismatch between ventilation and perfusion (VQ). Normally a adult lung will bring approximately 4 L of their into contact with 5 L of blood making a ratio of 4:5 displayed as a VQ=0.8 (4:5=4/5=0.8).  
When somebody has a restrictive lung disease, blood still circulates through the lungs in the same fashion, but it comes into contact with less air over a given point in time.  This reduction in VQ ratio, is often called a shunt, and results in poor gas exchange, and at its worst, respiratory failure
Restrictive lung diseases usually result from a condition causing stiffness in the lungs themselves, or in stiffness or weakness of the chest wall; think muscular dystrophy.

Other causes of restricted lung disease include the lungs physically filling with exudate or fluid such as ARDS, severe pneumonia, pulmonary oedema.

Physical body shape and chest architecture can have a restricting impact. Especially morbid obesity, severe kyphosis (hump back) and scoliosis (lateral spine curvature).

If a person suffers spinal cord injury between T2-T8 there may be poor neural control of the intercostal muscles which support chest expansion, deep breaths, sigh and yawning.

You can now probably think of a number of conditions that give rise to Restrictive pulmonary diseases.

Fibrosis causing diseases like post chemo, pulmonary fibrosis, cystic fibrosis, asbestosis, silicosis, anthracosis and its ugly spawn "Black lung or coal miners lung" (pneumoconiosis).

Space occupying lesions like cancerous tumours, will take up valuable thoracic realestate.  And another example could include a large pleural effusion, empyema, pneumothorax, or haemothorax.  They all take up space restricting a persons ability to fully filled the lung. These are just some examples of diseases that result in airway restriction.

In summary
Obstructive airways disease is characterised by not being able to empty a predicted volume of air
Restricting airways diseases are characterised by not being up to fill the lungs due to lung stiffness, poor muscle function or something occupying space.

Well that's it for this quick KYJ (Knowing your Jargon).

Catch more breathtaking respiratory education at one of our seminars. #ECT4Health #Respiratory

~breath easy - Rob. Www.ect4health.com.au/courses

Questioning Routine oxygen on PCA patients

#CageRattler
Should patients on Patient Controlled Analgesia (PCAs) be given oxygen routinely?

In this first of our dogma busting #dogmalysis posts, I wanted to review the evidence supporting the use of supplemental oxygen when a patient is attached to an intravenous PCA.   But couldn't find any.

Let's review the typical scenario.   Mavis has just undergone a total knee replacement surgery and returns from PACU (recovery) with a Patient Controlled Analgesia infusion.  She is receiving supplemental oxygen at 2lpm via nasal prongs.  It is estimated that she is getting 24-28% oxygen.

She is easily roused from dozing comfortably with a respiration rate of 14. A heart rate of 72 and is normotensive at 115/70.  she has good pink colour, her oximetry sats are 99% with a good reliable pleth wave.

Two questions come to light from this.

1.  Why is she getting oxygen?
2.  Does she need it?

The first question typically is answered : "because  policy states all patients on PCA must receive supplemental oxygen"
The second question's answer is No.

There is no evidence for supplemental oxygen in patients on PCA.  Oxygen use historically came from its use in patients in respiratory failure, where the treatment of desaturation was oxygen delivery.  It still is the cornerstone of managing respiratory failure.  Different jurisdictions have different thresholds for application of oxygen, but it is widely accepted by the AHA and Australian Resuscitation Council that oxygen should be used when sats drop below 94% (lower in COPD patients).

Here we have a well saturated post operative patient on a narcotic infusion.  She does not meet criteria for oxygen delivery until an assessment of her saturations on room air (21%) has taken place.

So why is she on oxygen (other than an outdated policy), what clinical indication is there for supplemental oxygen?   Respiratory depression risk?? Nope- let's look at this.

Narcotics (mostly) bind at the Mu , Kappa, and Delta receptors in the central nervous system.  All three receptors are like switches that, when flicked on, interpretation of pain is dulled.
The Mu receptor, when stimulated, also causes euphoria in low doses, and sedation in large doses; pinpoint pupils, slowed gastric motility and large (bigger than sedative doses, depresses the respiratory drive.

It's this respiratory depression that we fear, and rightfully so, because respiratory depression causes CO2 retention, and subsequently, as CO2 accumulates, respiratory acidosis.   We breathe (in part) to regulate our acidity of blood. This is where the post might get a bit sciencey.

Blood pH is kept in a tight range of 7.35-7.45.  A drop in pH below 7.35 is termed acidosis and the deeper the acidosis is, the less capable is the red blood cell's ability to carry oxygen.  In early acidosis, no desaturation occurs, but once a threshold is met, and acidosis reaches a critical stage, haemoglobin dumps oxygen, causing a desaturation event.   Slow shallow breathing reduces the "blowing off" of acidic CO2 gas which, when built up, drops pH into acidosis.   Because this is regulated by breathing rate and depth, this form of acidosis is called Respiratory Acidosis.

So your post op patient develops respiratory depression.  Her respiratory rate drops to 6. She is difficult to rouse, but isn't turning blue because she has been receiving supplemental oxygen via nasal prongs, yet her CO2 (if you'd measured it is sky high, and she has acidosis).  But sats are looking ok, because desaturation is a late sign of respiratory depression and it is delayed by unnecessary over oxygenation.

Now what?    Her acidosis worsens to the extent that her blood now can't carry oxygen. This sudden desaturation point has been met, and your patient decompensated into respiratory failure.

Now what do you do?  You hit the blue button on the wall!
In the crisis you see her sats hit 80% so it seems reasonable that you'd put high flow oxygen on, but the cause of this patients desaturation is not a lung disease (COPD, pneumonia, OE) it is acidosis, and acidotic blood won't carry oxygen.

Mavis needs stimulation, narcotic reversal (Naloxone), and to be bagged up to blows off CO2.   Her acidosis is what is killing her, and you must correct her acidotic blood before oxygen will have any effect.

Oxygen has no evidence based rationale as a supplement in post op patients on PCA.  You want to review sedation scores and respiratory rates, but saturation monitoring is of little use because by the time you see saturations that sink, your patient is too sick for its use to be of value without correcting acidosis first.

By all means have oxygen handy, but know this.  Oxygen does not prevent respiratory depression in PCA patients.

Look into your policies, see what they say. Challenge the dogma, generate a culture of practice from evidence.

If you find research that supports use, please let me know. I can't

#cagerattler

Therapeutic Hypotension- Trauma

Fluid resuscitation in Haemorrhage : Therapeutic Hypotension

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Caution : serious spoilers for Game of Thrones Fans

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Did Arya do The Hound a favour when she left him to die  from his wounds on that mountain?

The premise of allowing someone to bleed to death is one that may be viewed as a barbaric act, but evolutionary biology would demonstrate to us that profound hypotension seen in hypovolaemia (from blood loss), facilitates both clotting and its spawn, coagulation.  Could it be a survival tool?

A caveman gored by some would be assailant had no fluid resuscitation.  He dropped, unconscious, and dies or wakes some time later, miraculously.  Perfusion has returned supporting consciousness. Slowly he returns to health to hunt mammoth with Ogg, Uhg and his other mates.

Here is the spoiler:  the Hound lives.

It begs to ask how? And it may even allow us to question the time old practice of prompt fluid replacement.

So What are we doing in fluid resuscitation ?

As a TNCC instructor some years ago, I always preached the doctrine of 

"If we don't water the veggies, they'll die".

Two large bore IV cannula and 2 litres of warm crystalloid straight in.  So important was this intervention, that it was a dogma that became indelibly etched into every emergency nurse's trauma primary survey.

We have come a long way since the mid 1990s, and in these 20 short years we have seen the removal of routine oxygen from chest pain protocols, removal of spinal boards and stiff collars from spinal protocols, the removal of routine antipyretics from febrile children management, and the introduction of countless new procedures and trauma techniques.

Included in the new wave, is therapeutic hypotension.  

The concept of permissive hypotension in trauma resuscitation is not new. What is more novel is the change in paradigm from "Permitting" hypotension as though it was previously considered to be naughty, to one where recognising that the bleeding patient's systolic blood pressure hovering at 70mmHg is actually desirable for 1-2 hours before intervention to fluid resus.  This shift from permitting it, to valuing it, as a therapeutic device is a cage rattler.

Therapeutic hypotension utilises the notion that hypovolaemia from haemorrhage leads eventually to hypotension so low, that the  bleeding patient's hydrostatic pressure allows small arterioles to adequately constrict, and a clot to form.

Even the ALOC that ensues with this drop in mean organ perfusion pressure (MAP), is beneficial as oxygen demand plummets, allowing what little perfusion and blood left to retain survival.

So how is this applied in the context of a modern emergency trauma setting.  Two words burn bright.... 

"Just Wait"!!

Clearing safely, assessing haemorrhage, Airway, breathing, circulation , level of consciousness; have long been and continue to be priorities.  As are interventions to stop haemorrhage, secure airway, augment oxygenation and ventilation, and of course intravenous access.  But hold off on that massive whole blood transfusion, or crystalloid bolus.   The suggested 60-90 minutes should pass before fluids in most circumstances.

Your one job in haemorrhage is to stop the bleeding.   It is not to immediately replace blood.  Stop the bleeding with digital compression on a bleeding point.  And if you can pack the hole, then you pack that hole.

Many companies manufacturing procoagulant impregnated gauze will try and convince you that they have some magic property but compression on the bleeder is by far the sovereign intervention. 

Where direct (and I mean direct pinpoint) pressure doesn't work, crank out that tourniquet for limbs, or a surgeon for the torso and neck.  But pressure is the boss, and this non-science love affair we have had with pouring in fluids when someone is still bleeding is just lunacy.  

When the time comes for blood or fluids (and it will), the patient should have had time for a clot to form, and reconstitution of what volume they have to adequately distribute.  We have an incredible ability to store clotting factors, water and red blood cells in reserve for those days that we get stabbed, or cut.  In fact, most adults can loose 20% (1000-1500) of blood and not skip a beat, because of this compensation.

Now think about all those times that we have taken a shocked Hypovolaemic patient, nearly drowned them with saline or Hartmann's in some inane quest to get elevation in their blood pressure (a poor indicator of perfusion).   Inevitably we have haemodiluted the life out of the blood.  Washed out the red cells to the point of anaemia, washed out platelets and coagulation factors to the point of coagulopathy, washed out white cells and immunoglobulins to the point of immunocompromise and finally filled their vascular highways with pressure exacerbating rebleeding.  

Now one thing has always rung true:  your first clot is your best clot. Say it out loud. Own it!  

Your first clot is your best clot!

So this is where therapeutic hypotension (permissive hypotension) is a game changer.   Holding off on aggressive fluid resus early, stopping bleeding, allowing natural clotting to occur, then introducing (ideally) blood, but if not small titrated aliquots of crystalloid in 100-200ml boluses to achieve a systolic pressure of just 80-90 is best practice.

As these are given the best measure of perfusion is not peripheral capillary refill, but etCO2 if your patient is ventilated.  If not, it's respiratory rate which is a barometer for acidosis.  It is complex and deserves a post all of its own, but to return CO2 to the lungs to be blown off, the patient needs to be perfusing tissues where CO2 is collected.  Hypoperfusion = reduced CO2 production = low etCO2 .

Anyhow we digress.

Stop bleeding- and don't be too keen to get that BP to normal.  Hypotension is a life saver in haemorrhage an the sooner we practice from what we have learned from cavemen the better off our bleeding trauma patients will be. 

You need to listen to this awesome podcast on the topic. https://itunes.apple.com/au/podcast/emergency-trauma-management/id634332324?mt=2&i=361877809

The Hound lives. 

Plasmids and antibiotic resistance

#KYJ -  Superbugs, Plasmids and Genetic mutation.

Make a note of " MCR-1 ".

It is a buzz term that you will hear more about.  We start our explanation of this, with a  a basic review of microbiology.... 

Hello.... Hello??  Are you still awake?  Stay with me.

Bacteria a living cells with cell walls made of carbohydrates (cellulose- a complex sugar).

Some have a fatty (lipid) membrane coating around the cell wall. 

Inside, are most of the goodies that other cells have, organelles like mitochondria, cytoplasm, lysosomes, and nucleus to name a small familiar sample.

Inside the nerve centre of the bacteria is genetic material (genes) arranged in to long protein strands called chromosomes.  This is where the bacteria gets its instruction to function and reproduce.  

Unlike animals and plants that must mate with a male/female combination to reproduce, bacteria are asexual; boring I know, but true none the less.  To divide into two identical copies of its self (producing offspring called Daughter cells), bacteria copies its chromosomes, then simply splits down the middle to form two new cells. 2 become 4 become 8 become 16 and so on ( look up you year 8 maths books , or have a chat to any Amway dealer to see how effective the power of duplication becomes.)

Anyhow I digress... 

Given that bacteria make absolute clones of them self, you would think they can't change.   But we know they do.   They become resilient, and adapt to new environments.  They mutate.

Enter the plasmid.

A plasmid is a rogue speck of genetic material that lives in the cytoplasm (watery juice) of the bacteria.  Plasmids are genetic coded proteins that can become altered when a bacteria is exposed to an antibiotic (that should have killed it) but survives.   Plasmids change, replicate on their own and translocate genetic information with genes inside the nucleus.

Now this surviving bacteria passes on this information to its daughter cells creating a bacteria that is now resistant to the antibiotic that previously would have killed its grand parents.

Are you still awake? 

Ok.  So plasmids don't just mutate and affect the host bacteria, but they can also share genetic information to other bacteria, even other species of bacteria.  A Strep can share its resistance recipe with a Staph, or an E.coli with an Enterococci, or a Bacillus with a diplococcus.

Frightened yet?

Recently, an E.coli strain was discovered in a urine sample of an American woman with a UTI.  This infection is resistant to every antibiotic.  EVERY ANTIBIOTIC.   

This drug resistant E.coli strain has a gene called MCR-1 which is harboured in the E.coli's plasmid.  

This E. coli bacteria with the mcr-1 gene could pass its plasmid and gene  to another superbug with other mutations-- creating a truly super-superbug that resists all known antibiotics.

The bio surveillance role that nurses and doctors have was always important, but this is going to have implications on infection control practices going forward.  

I'm off to wash my hands ... again! 

Adenosine

#KYJ.  Adenosine.
Have you ever given this IV drug to a patient?
It is used to cause a complete block through the AV node, in patients experiencing a Junctional Tachycardia (previously and more commonly called Supraventricular Tachycardia (SVT)).

Its use is common, and when given correctly it is very effective.  In the past you may have been taught to give it as a neat push IV.  But more recently it has become popular to dilute the required dose up to a 20ml volume and rapidly push in a largish (18g) IV cannula in the antecubital fossa, and quickly flush with a 10-20 ml saline

This drug has the effect of stopping the heart.  Thankfully it has a very short half life of 4-7 seconds (requiring the rapid push). Like a computer that is playing up, you get the sense that this drug is like a cardiac "Reset button", like someone said "have you tried turning it off, then on again?"

Vials come in 6 mg but it is very common (almost expected) that we start at 9mg.
A common regimen is
3 x 2 minutely doses starting at
9mg - 9mg - 12 mg.

If it works on dose 1, the other two are not needed.

Doses are expected to work in 5-10 seconds so as you give the push, the patient needs to be attached to the cardiac monitor.  You are watching for the SVT to deteriorate into a severe bradycardia or asystole (flat line).

Their heart stops.... Then in 3-5 seconds it automatically restarts, hopefully into a normal sinus rhythm .... It's a reset button.

Patients often experience fear, and altered consciousness as their brain oxygenation ceases for that few seconds.  Many describe a sense of doom, or near death phenomenon like a Tunnel of light, out of body experiences or a peaceful place of comfort and warmth.  Some report an experience of meeting their deity or previously deceased loved ones.  Rarely this experience is one of terror, and there are documented case reports of Post traumatic stress disorder.  This drug is excellent but has some issues.

Nurses should comfort the patient and prepare them for a sensation of "passing out". Tell them that you will stay with them and keep them safe.  Hold their hand.  They are often very frightened.

Have you had a patient on this drug?  Tell us your story.

#KYJ - HbA1c in Brief

Understanding HbA1c (#knowingyourjargon)

Smooth RBCs  are kind to your blood vessels, but sugary sticky ones damage the walls stimulating the inflammatory system that initiates cholesterol to be sent out from the liver to repair the damaged walls.

Red blood cells live 120 days.  During that time they slowly accumulate glucose and the haemoglobin protein (most famous for transporting oxygen) becomes glycated.

This glycated haemoglobin is measured as a percentage (old measurements) or in mmol/mol

The test for this stickiness of red blood cells is called HbA1c

As a percentage less than 6% is normal.
More modern tests measure in mmol/mol where less than 42 is considered normal.

Diabetes is commonly diagnosed with HbA1c levels above 6.5% or 48 mmol

Unlike a random BSL, the A1c test looks at glucose control over a period of 3 months, and is accurate as a control monitoring test for diabetics.

ACE inhibitors- why they cause cough

#KYJ - #KnowingYourJargon

ACE inhibitors and that nasty Cough.

With many classes of blood pressure drugs on the market, it can be a mind storm navigating them all as nurses.

A common first line antihypertensive is the humble ACE inhibitor.  It's main side effect is cough and it drives patients and their partners crazy.

... But why? 

How does it cause cough?

Well let's understand ACE.

Angiotensin Converting Enzyme.

ACE is created in lungs and there, it has a role in destroying inflammatory chemicals called Bradykinin and Substance P.   These pro-inflammation proteins cause lung tissue irritation- notably cough (tussis).

ACE also notably converts Angiotensin into a vasoconstrictor that raises Blood Pressure.  It stands to reason if I inhibit ACE then I can't convert Angiotensin.

Hence its valuable role as a blood pressure lowering drug.

BUT....

If you give an ACE inhibitor, and prevent the breakdown of bradykinin and substance P (Inflammatory chemicals), there is an accumulation of these protussive mediators (coughing stimulants) in the respiratory tract. 

This side effect is not dose-dependent and often precludes the use of all agents within the drug class.

Common offenders are Lisinopril, Perindopril, and a new one released after March and before May called April😆😆😆.

No seriously.  ACE inhibitors cause cough and often this means that the patient needs a new approach to BP control.

 

Polypharmacy and drug interactions

#KYJ - Polypharmacy
www.ect4health.com.au/rustypills/
Interesting term, but one we need to know more about.   Polypharmacy is defined as 4 or more concurrent medications.  The issue is drug to drug interactions that occur when a person takes two or more drugs that are metabolised by the same enzyme systems in the liver and other tissues.
Many medications use a system called Cytochrome 450 enzymes(P450).
If drug A and drug B are both metabolised at the P450, then metabolism of both drugs can be impaired or delayed, rendering both inactive or toxic.  These interaction can make one or both medicines overly potent.

The issue compounds with every extra medication a person takes. In fact if your patient takes 5 medications, there is a 50-80% chance of an adverse effect.  What's worse, is that the risk increases 12-15% for each extra drug in that little dosette box.

Take Lipitor (Atorvastatin) the worlds most prescribed drug.  It has over 250 drugs that interact with it to cause adverse effects.
Common medications  causing issues in combination with Lipitor include:
amlodipine
aspirin
atenolol
Cymbalta (duloxetine)
Fish Oil
gabapentin
hydrochlorothiazide (Enduron)
Lasix (frusemide)
levothyroxine
lisinopril
metformin
metoprolol
Nexium & omeprazole
Plavix (clopidogrel)
Synthroid (levothyroxine)
Vitamin D3 (cholecalciferol)

These drugs are hard to get our head around, but the issue of polypharmacy being linked to dementia, falls and muscle atrophy in elderly is one that is on the rise, and needs clinicians to be wary and hyper vigilant.

Our latest Rusty Pills seminar discusses this issue and many others.
Check out http://www.ect4health.com.au/rustypills/

Post concussive symptoms in children

Concussion in kids

Concussion is divided loosely into two categories.
Mild concussion is a bang on the head where the patient was not knocked out.

Classic concussion is when a person was knocked out.

When assessing patients after a closed head injury, nurses and doctors often use a multitude of tools and questions about the event.  On average about 30% of adults who receive concussions, go on to have persistent symptoms of headache and concentration loss, memory disturbances and dizzyness for months.   This is called Persistent post concussion syndrome (PPCS).
Predicting who will have PPCS is difficult, but one team of researchers in Canada have just published a paper that summarises the process in children.

They state that  "clinician prediction is no better than a coin toss".

In assessing long term risk of PPCS in children the research team found some surprising things.

Where we as clinicians have long thought that loss of consciousness and vomiting post head injury were somewhat prognostic for post concussion symptoms, these researchers consider these as less predictive.

Using a 12 point scoring system the researchers looked at some 3000 five to 18 year olds,
Higher scoring data (2 points) Included
Gender=female
Age >13
Fatigue

Points are also allocated for
Headache
Previous concussion
Slow to answer questions
Sensitivity to noise
History of Migraine
Poor balance
For

A score of 9-12 correlated with a 93% incidence of prolonged post concussion symptoms.

Ref:
Zemek et. al  2016
Clinical Risk Score for Persistent Postconcussion Symptoms among children with acute concussion in ED
JAMA. 2016;315(10):1014-1025.
 doi:10.1001/jama.
http://jama.jamanetwork.com/mobile/article.aspx?articleid=2499274

Breath Sounds -part 4. Ergophony and whispering Pectoriloquy

Breath Sounds -part 4

Whispering to a Goat??

Ergophony and Whispering Pectoriloquy.

In this short mini-series, we look at the basics of auscultation of lung sounds.

Few things are cooler than listening to a sick patient's chest and hearing the classic sounds that highly suggest a specific diagnosis.

Pneumonia (lobar consolidation), is one such diagnosis.  With alveoli collapsed and congested under the strain of pus, and other inflammatory debris, the way sound is transmitted becomes characteristically different.  If reading about this for the first time, you will be itching to give this a go.

Ergophony

Assume Mr Chester in bed 6 has a diagnosis of Right middle lobe pneumonia. He is admitted on the ward for IV antibiotics and supplemental oxygen.  As part of your routine assessment, you auscultate his lung sounds.  

You ask Mr Chester to repeat the letter E, over and over while you listen the the resonance of his voice, through your stethoscope, at different locations on his chest.  Across his left chest you hear the familiar sound of him chanting "Eeeee, Eeeee,Eeeee...." Over and over.

But as you place your stethoscope over the consolidated region of his right chest, the sound changes to a muffled "Aaaahhh, Aaaahhh, Aaaahhh..." sound.   It sounds to you like the bleat of a goat or sheep.   This is called Ergophony and literally means "voice of the goat".  It is caused by changes to the sound waves as they travel through different densities of lung. When transmitted through pus filled dense pneumonia lobes, the Eeee resonates to Aaahhh.

Whispering Pectoriloquy

Say it out loud :

"Peck - tor- rill- oh- Kwee"

Apart from being a cracking scrabble word, this funky phenomenon is another one that can be heard in patients with pneumonia.

Normally if I listen to your lung fields with my stethoscope while you are whispering, I wont hear your words.  The light air filled matrix of your ventilating lung filters out whispered sounds, rendering them inaudible on auscultation of a normal chest.  However, when Mr Chester has pneumonia and an area of consolidation, sound is transmitted well through more dense tissue.  

Start by asking your patient to sit upright and chant through the alphabet or count to 100 but only whispering.  As you listen to the healthy areas of his chest you'll not hear his whispers, but when the stethoscope is placed over pneumonia consolidation of lung masses, you will hear the whispered words through your stethoscope. This is called whispering pectoriloquy, and is a symptom of consolidation.

Well that is it for part 4 of our breath sounds .  Stay tuned for part 5 where we discuss some other adventitious noises.

If you missed our other KYJs in this series click them here.

Www.knowingyourjargon.blogspot.com

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Breath Sounds -Part 3- location

Breath Sounds -part 3

Continuing on with our series on breath sounds. Today we look at stethoscope position.

First, knowing your stethoscope. The  flat disk like part of your stethoscope is called the diaphragm, and is the surface that is used for high pitched sounds. Lung auscultation and bowel sounds are examples.

If your stethoscope is a dual head, with the cone shaped bell, then low pitched sounds are heard best through this part of the scope.  Heart sounds can usually be heard better with the bell.

Anatomic placement

Listening to breath sounds is as simple or as complex as you want to make it.

Start with anterior (front of chest) for a quick listen for normal.

Location 

2nd intercostal space in the mid clavicular line.  Listen left then right in a patient sitting upright.

Then 5th Intercostal space in the mid axillary line (same spot you place the V6 lead on an ECG).

Again listen left then right.

You are listening for equality between two anatomically opposite locations. Read that again.... It's important!

R=L at the 2nd ICSMCL

R=L at the 5th ICSMAL

Listen to a couple of breaths in and out with the patient breathing through their mouth.

Focus on the duty cycle (time taken to breathe in vs out, focus on the equality between left and right and listen for abnormal sounds like wheeze or crackles.

Record any adventitious sounds or inequality.

These two locations complete a basic respiratory auscultation.  If a comprehensive assessment is needed (usually not) then the patient should be propped forward and auscultation is performed on the back.

This allows you to hear the largest portion of lung fields.  The posterior chest is called the base, which is often erroneously confused with the inferior aspect of the anterior chest.  More alveolar area is in the base of the lung.

Now say out loud... "2,4,6,8,10"

Did you say it? Are people looking at you funny? 

2,4,6,8,10.

These are the intercostal spaces.  Either side of the vertebral column, you listen at the 2nd ICS left then right 

4th ICS left then right

6th ICS left then right

8th ICS left then right

8th ICS at the Axillary line .

10th ICS left then right

Then finish at the 10th ICS out on the widest part of their chest - the posterior axillary line.

Don't be daunted by these 6 sites.  You are only listening to compare Left to right at each spot. 

Practice these locations on your partner or kids. Listen to normal chests to get your ear in for the nuances of normal.

Know normal so you can recognise abnormal sounds as they arise.

Next episode we will discuss classic consolidation/pneumonia and the funky sounds you can experience to identify a pneumonia in your patient. 

#KYJ Wound care series - part 4 Venous Insufficiency

Wound care series part 4.
Venous insufficiency.

In this #KYJ episode we look at venous insufficiency as a cause of leg ulcers and as an inhibitor to healing.

To begin to grasp the impact that venous disease has, we must understand a few truths about leg circulation.  Arteries in legs transport oxygenated blood to the tissues of the legs and feet. Arteries deliver nutrients to the capillary beds that perfuse tissue.  I like to think of arteries as a garden hose, and the capillaries as that soaker-hose weaved around the garden bed.  There is a blood pressure gradient that is highest as blood leaves the heart, that reduces in arteries and almost zero by the time that blood reaches the legs capillaries.
To return that blood to the heart, the veins and muscles of the legs are structured to "pump" blood back.
Three types of veins are featured.
Superficial
Perforating
Deep veins

Superficial veins are often seen as swollen inflamed spiderweb like varicose veins on the feet and ankles of people with venous congestion.  They drain their blood into communicating veins called "Perforating veins" , that take blood from the superficial veins and direct blood flow into the deep veins located deep in the muscle fascia.

Blood is forced along the length of the vein by the action of leg muscle movement.  If there is no leg exercise, this blood pools and congestion occurs, forcing the pressure inside veins to rise.

To ensure blood travels in one direction through veins, veins have one way valves. As congestion and pooling occurs, these valves fatigue and fail.  Venous insufficiency is a combination of high venous pressures from congestion & pooling of blood, and the valves no longer being efficient at transporting blood in the Leg to Heart direction.

Pooling of blood is called 'stasis'. In veins it is referred to as venoustasis.  If there is one thing that pooled blood loves to do, it's coagulate...Badness!

Venous pressures are strongly influenced by gravity.  Standing and sitting for long periods are the leading cause. Once we walk or contract leg muscles, the pump like action promotes momentum of pooled blood and the congestion eases.  This is true for healthy legs, but in patients with long term valve failure walking does little to alleviate pressure.

So what is the link between this venous disease and wounds?  Wounds need a constant clean flow of blood delivering nutrients to the wound bed.  Congestion seen in patients with valve disease or venoustasis slows or stops momentum, stops removal of waste and hence; stops healing.

In many patients with venous insufficiency, their disease actually causes ulceration.  Always on the lower leg and almost always on the medial ankle (malleolus) or anterior shin.

Patients with venous disease often have classic tell tale symptoms.
Ankle swelling
Superficial varicose veins
Spider veins on the inside of their ankle.
Discolouration to their skin ranging from red to rust to purple.
Occasionally slow healing wounds

As congestion increases, red blood cells are forced out of capillaries and fracture in the superficial skin.  The iron in red blood cells oxidises to iron oxide (rust).  It is called haemosiderin and is a permanent rusty discolouration of patients with advanced venous insufficiency .  Sometimes this is called venous eczema .

Next wound care episode we will look at compression as a treatment.

Stay tuned...
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Breath Sounds part 2 - Wheezes

#KYJ -Knowing your Jargon

Breath sounds part 2. 

Wheezes.

In part one http://knowingyourjargon.blogspot.com.au/2016/02/breath-sounds-part-1.html?m=1

We looked at the concept of pitch in breath sounds. In that episode we discussed the two major groups of abnormal (adventitious) lung sounds. We focused on crackles.

In this episode we look at the other group, the Wheezes.

Wheezes are a sound produced by air being squeezed through narrow swollen oedematous bronchi/bronchioles.  They can occur during inspiration (stridors) or expiration (wheezes).

Like crackles, wheezes are pitched differently, depending on the area of lung affected.  High pitched wheezes are heard in the periphery of the lung, whereas low pitched wheeze come from larger airways.  Like crackles, wheezes are termed differently depending on the area they originate.

High pitched wheeze is called a sibilant wheeze.   Sibilant is a whistle like sound of high frequency (high pitch). It is characteristically heard in asthmatic flare-ups.

Low pitched wheezes originate from bronchi and trachea, and sound like snoring.  In fact this is exactly what they are called, "snorous wheezes".  In older texts, you may hear these called Rhonchi (pronounced 'Ronk-Eye').

Typically these wheezes are heard in multiple areas of the lung field.  For this reason it is not uncommon to hear multiple different pitches.  Wheezes of this nature that demonstrate both snorous and sibilant qualities are frequently documented as widespread polyphonic (many voices) wheezes.  Asthma is a classic presentation.

Listen carefully to a wheeze; especially if the patient has cardiac or hepatic history, and after any rapid IV fluid infusion.  If crackles can be heard along side a sibilant wheeze, then a diagnosis of acute pulmonary oedema (APO) needs to be excluded.

So similar is an acute asthma wheeze and an acute pulmonary oedema wheeze, that at one time APO was called "Cardiac Asthma".

So that is it for this short episode. Next edition we look at where a stethoscope is placed.

Check out our blog site for all the KYJs you've missed. Www.knowingyourjargon.blogspot.com

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Breath sounds part 1- crackles

#KYJ- knowing your jargon
Breath sounds, part 1.

Rattles, rales, crackles n creeps, Wheezes, and Rhonchi.

When I teach nurses about breath sounds, I always ask who does them, and who does them confident in the knowledge that they can name them.  In an average class of 25 nurses, 5-7 put up their hand indicating they auscultate chests, but only 1-2 of these (about 5-8% of all nurses) attending my nursing assessment classes, or respiratory nursing classes, agree they can identify different breath sounds.

Here is my simplified version of the terminology (our biggest hurdle).

Pitch (highs and lows)
Let's start with a beautiful pipe organ in a cathedral.  You know the ones I mean, huge gilded pipes arranged artistically around a dual layered keyboard and foot pedal system.  When a low note is struck, deep, chocolate vibrating sound emanates from the largest pipes.  When a high note is played, the tone bursts from the smallest pipes.

Lungs are similar.  As air rushes through them, the pipes (bronchi and bronchioles) vibrate producing noise audible with the diaphragm (flat surface) of the stethoscope.  Large airways towards the centre of the chest produce low pitch deep notes, and fine tubes on the outer periphery of the lung fields produce a higher pitch sound.... It's just like the pipe organ.

The first concept is this one of pitch. Low pitched sounds over the middle of a chest, high sounds in the outer reaches of the respiratory tree.

Next to master is the two major categories of abnormal sounds produced by diseased lungs.  Abnormal lung sounds are often called "Adventitious sounds".  They are lumped into two types.

Wet and squeezed.

1.  Wet sounds (crackles)
Wet sounds are produced as air moves through pipes filled with water and thin mucus. Typically heard in pulmonary oedema, wet sounds resemble that bubbly noise you made as a kid, sucking the last dregs of a milkshake through a straw.  Don't lie, I know you did.

Wet sounds are collectively called crackles, and depending on where in the lungs they are, they will produce a different pitch.

In smaller peripheral airways, the sounds are high pitched, so these crackles are called creps or fine crackles. Typical in pulmonary oedema, pneumonia, and chest infections.

In larger bronchioles and bronchi, the sound is lower pitch.  Still wet bubbling sounds, but lower in tone.  These crackles are commonly called Rales, or simply coarse crackles.  Typical of bronchitis.

If the wet sound is audible with no stethoscope, the gurgling sounds like comes from the back of the throat, it is fluid in the main bronchi, or trachea.  These sounds are called Rattles.  The gurgling death rattle common in an frail dying patient is a classic example.

Next episode we look at squeezy wheezes.
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#KYJ - Wound care series- Hydrogel dressings

Hydrocolloids. 

These dressings have been around for 30 years.  They are generally a thin film that has a thick rubbery adhesive which , when contacting a moist wound, creates a gel against the wound surface.

Some hydrocolloids  contain an alginate (seaweed base) to help with wound exudate absorption. Different hydrocolloids dressings come with many shapes for "difficult to attach" areas, and different thicknesses so the nurse can tailor the dressing to the amount of exudate.  The hydrocolloids dressings often stick to the wound's healthy skin margin with a water resistant film type adhesive.  

So how do they work?

Being water occlusive,  they provide a moist healing environment and heat insulation.  In episode one we discussed the need for a moist and warm wound bed.

These dressings also encourage a process called autolytic debridement.  This is where the gel from the hydrocolloids attract moisture from the wound like a sponge, and in doing so, promote the release of protein and debris dissolving enzymes from tissues.  These dressings clean the wound, not just cover it.

Pros

• Water resistant keeps bugs out.
• non stick to the moist painful wound surface, so gentle when being removed.

• Easy peel and stick application that can be used under compression stockings or lymphoedema bandages.

• Can and should stay on for days.  Many products report 3-7 days with the familiar mantra "leave it a week or till there's a leak"

Cons

• Never on infected wounds, and they are not great on heavily exuding wounds.  Venous ulcers and some diabetic ulcers are notoriously oozy.

• extreme caution on diabetic feet!!  Only safe if the wound is superficial with no signs of infection, there is low to moderate exudate, there are no signs or symptoms of ischemia, and dressings are changed frequently.  This last point negates the value of a dressing that is designed to stay on for days. 

Diabetic wounds crash in hours when they crash, and you want to be there when that starts.  You don't want to pull off a dressing to find 2 weeks of healing undone overnight!

• unlike film dressings which are clear and transparent, hydrocolloids are opaque.  So you can't watch the wound.
• notorious for dislodgement if wound is too wet, and they curl or roll at the edges, potentially trapping bacteria.
• some patients (and nurses) complain that they are a bit on the nose.
• can cause wet maceration to healthy skin (all those trapped enzymes in the Slough )
• May cause trauma/injury to fragile skin upon removal... That prednisone abused nana skin is so paper thin!
• hypergranulation can be a problem leading to scaring

When to use

A hydrocolloid dressing is appropriate for these situations:
• necrotic or hard capped eschar covered wounds (lifts the dry nastiness)
• dry wounds
• partial- or full-thickness wound
• protection of intact skin ( but watch for maceration ) or a newly healed wound.

Frequency of dressing changes

• depending on the product specifications, dressings should be changed every 3 to 7 days.  This of course depends also on exudate.

How to apply a hydrocolloid dressing .

Gloves on and remove the soiled dressing (noting the date it was applied) - contaminated bin is wise, irrespective of colonisation.
Deglove, hand wash, reglove
Clean the wound with warm normal saline or warm tap water.
There is no evidence that chlorhexidine or other antiseptics are safe, or necessary or helpful.
Use gauze to pat dry the foot edges of the wound margin where the adhesive should stick.
Apply liquid barrier film or moisture barrier to the periwound area.
For deep wounds, apply wound filler or packing materials as indicated/ordered ( a whole other post).

Warm it by holding it between your hands to increase molding and adhesive ability.
Remove the paper backing from the dressing.
Bend the dressing (sticky side out) and apply it from the center of the wound, smoothing it outwardly like putting contact on the kids books.
Hold the dressing in place for a few seconds, warming it with your hands to improve molding and adhesion.
The dressing should be at least 2cm larger than the wound. 

Our next instalment will take a look at hydrogels.

Check out our Webpage for education opportunities.

Www.ect4health.com.au

#KYJ - Wound care series- Hydrocolloids dressings

Hydrocolloids. 

These dressings have been around for 30 years.  They are generally a thin film that has a thick rubbery adhesive which , when contacting a moist wound, creates a gel against the wound surface.

Some hydrocolloids  contain an alginate (seaweed base) to help with wound exudate absorption. Different hydrocolloids dressings come with many shapes for "difficult to attach" areas, and different thicknesses so the nurse can tailor the dressing to the amount of exudate.  The hydrocolloids dressings often stick to the wound's healthy skin margin with a water resistant film type adhesive.  

So how do they work?

Being water occlusive,  they provide a moist healing environment and heat insulation.  In episode one we discussed the need for a moist and warm wound bed.

These dressings also encourage a process called autolytic debridement.  This is where the gel from the hydrocolloids attract moisture from the wound like a sponge, and in doing so, promote the release of protein and debris dissolving enzymes from tissues.  These dressings clean the wound, not just cover it.

Pros

• Water resistant keeps bugs out.
• non stick to the moist painful wound surface, so gentle when being removed.

• Easy peel and stick application that can be used under compression stockings or lymphoedema bandages.

• Can and should stay on for days.  Many products report 3-7 days with the familiar mantra "leave it a week or till there's a leak"

Cons

• Never on infected wounds, and they are not great on heavily exuding wounds.  Venous ulcers and some diabetic ulcers are notoriously oozy.

• extreme caution on diabetic feet!!  Only safe if the wound is superficial with no signs of infection, there is low to moderate exudate, there are no signs or symptoms of ischemia, and dressings are changed frequently.  This last point negates the value of a dressing that is designed to stay on for days. 

Diabetic wounds crash in hours when they crash, and you want to be there when that starts.  You don't want to pull off a dressing to find 2 weeks of healing undone overnight!

• unlike film dressings which are clear and transparent, hydrocolloids are opaque.  So you can't watch the wound.
• notorious for dislodgement if wound is too wet, and they curl or roll at the edges, potentially trapping bacteria.
• some patients (and nurses) complain that they are a bit on the nose.
• can cause wet maceration to healthy skin (all those trapped enzymes in the Slough )
• May cause trauma/injury to fragile skin upon removal... That prednisone abused nana skin is so paper thin!
• hypergranulation can be a problem leading to scaring

When to use

A hydrocolloid dressing is appropriate for these situations:
• necrotic or hard capped eschar covered wounds (lifts the dry nastiness)
• dry wounds
• partial- or full-thickness wound
• protection of intact skin ( but watch for maceration ) or a newly healed wound.

Frequency of dressing changes

• depending on the product specifications, dressings should be changed every 3 to 7 days.  This of course depends also on exudate.

How to apply a hydrocolloid dressing .

Gloves on and remove the soiled dressing (noting the date it was applied) - contaminated bin is wise, irrespective of colonisation.
Deglove, hand wash, reglove
Clean the wound with warm normal saline or warm tap water.
There is no evidence that chlorhexidine or other antiseptics are safe, or necessary or helpful.
Use gauze to pat dry the foot edges of the wound margin where the adhesive should stick.
Apply liquid barrier film or moisture barrier to the periwound area.
For deep wounds, apply wound filler or packing materials as indicated/ordered ( a whole other post).

Warm it by holding it between your hands to increase molding and adhesive ability.
Remove the paper backing from the dressing.
Bend the dressing (sticky side out) and apply it from the center of the wound, smoothing it outwardly like putting contact on the kids books.
Hold the dressing in place for a few seconds, warming it with your hands to improve molding and adhesion.
The dressing should be at least 2cm larger than the wound. 

Our next instalment will take a look at hydrogels.

For ECT4Health information and courses
Www.ect4health.com.au