Hypodermoclysis - subcutaneous rehydration

#KYJ- Hypodermoclysis

Do you have much experience with this procedure? Let's break it down.
Hypo = below
Dermo =skin
Clysis = to flood or inundate with fluid.

Hypodermoclysis is commonly called Subcutaneous rehydration.
It is a simple procedure that requires the insertion of a cannula (usually a butterfly) into the subcutaneous space, then infusion of an isotonic fluid eg normal saline or Hartmann's.

It was developed for use to rehydrate vomiting children, but has been used in all ages so successfully that it is a common rehydration strategy in debilitated elderly.

As an alternative to IV the other rock star is Intraosseous (IO) infusion; so why would you use Hypodermoclysis over IO?
It's all about  speed.  If fluid resuscitation is urgent then IO is your alternative to IV; but in the stable mild-moderately dehydrated patient, too nauseated to keep down oral fluids, subcutaneous infusion at 20ml/kg over an hour is a fair approach.

In children Insert 25 Butterfly into subcutaneous tissue between the shoulder blades.  In adults, the abdomen is a good site.
There is no hard and fast rule but the age old saying , "pinch up an inch" suggests that anywhere you can pinch up an inch of tissue, AND secure the butterfly safely,  is fair game.

Don't go bigger than 25g.  The sc tissue absorbs fluid at a rate that is constant, so a bigger gauge cannula won't achieve anything- it doesn't hydrate them faster and just causes swelling to increase discomfort.

Premed ?
Topical anaesthetic creams like EMLA or Angel cream are kind and effective.

Some clinicians use a premed of Hyaluronidase  150units S/C.
This temporarily dissolves (painlessly) the connective tissue glue membrane (Hyaluronic acid) that bonds skin to fat.  It accelerates fluid absorption up to 5 times faster.  Consider it.

What to expect.
Inflammation is expected, so some swelling and pinkish penumbra around the injection site are normal.  It shouldn't be hot to the touch, or itchy or painful, so if these latter  symptoms are present, then consider resiting.

Rate- 20ml/kg over an hour is well tolerated and once rehydrated , and nausea/vomiting eases, reattempt oral rehydration.

Secure with occlusive film dressing and leave it in up to 24 hours if needed.

Lactulose and why we give to Liver failure patients

Quick question from a nurse:
Why do we give our liver failure patients Lactulose?

Let's start by understanding that as we eat protein, it is broken down into AminoAcids which when processed in the digestive system form poisonous Ammonia.
Your healthy liver detoxifies this brain poison into a water soluble Urea so the kidneys can excrete it.

If ammonia builds up- brain damage.
So a healthy liver prevents this.  In hepatic failure patients - hepatic brain damage called encephalopathy occurs.
Lactulose prevents ammonia compounds being absorbed from the gut, reducing the workload of a failed liver, and thus prevents that brain damage.

It is an osmotic laxitive so diarrhoea is expected as a consequence of administration, but nurses asked to give it need to know what the rationale is for its addition to the medication orders. If it's for hepatic encephalopathy, then it should not be withheld.

#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?
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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
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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!