Bronchiolitis update 2018

#KYJ Bronchiolitis in 2018

Bronchiolitis
Dispelling the myths that we should do what we do because it’s the way it’s always been done.

Background.
The smallest airways are bronchioles. They connect the big airways (bronchi) with the air sacs (alveoli) where oxygen and CO2 do-si-do .

Bronchioles have mucous coated meaty walls with abundant smooth muscle .  They actually constrict and relax to change diameter and regulate air flow. Remember that pearl- we will use that later on.

When inflamed (Bronchiolitis) they swell and constrict, which results in restricted air flow, causing the person to have an increased work of breathing.   That is ok in mild bronchiolitis in fit older children or adults, but in babies or toddlers, these wee tikes get exhausted (the struggle is real).  Apnoea or respiratory arrest is the feared complication in severe bronchiolitis.

Now it comes in two flavours.   Allergic bronchiolitis, and infective bronchiolitis.  Both are swollen restricted airflow. Both cause increased work of breathing.

Infective Bronchiolitis is the most common reasons for babies to be admitted to hospitals in our region (Aust/NZ).  As the name implies, infective Bronchiolitis is caused by a pathogen, almost certainly viral, but far more rarely, bacteria.

With allergic Bronchiolitis the trigger is some substance other than a pathogen.  It might be milk, egg, pollen, dust mite, or any number of triggers.  This stimulates an immune response where histamine is released, swelling and mucous is produced, and unique to Allergic Bronchiolitis (Asthma by another name - but don’t call it that prior to the 3rd birthday), unique to this pathodrome is the feature of dominant bronchospasm.  Remember those smooth muscles?  Yeah, they constrict, strangling the bronchioles worsening air flow.

Ok...  still with me?

48% of infants admitted to Australian hospitals with bronchiolitis receive treatment that has no evidence of benefit (Davis , 2018).
You may know Tessa a Paediatrician who runs a great paeds SoMe called
#DontForgetTheBubbles

She writes that the PREDICT network have conducted a systematic review to produce Australia’s first bronchiolitis guideline .

Investigations
Recommended
•Urine M/C/S (if under 2 months old and febrile)
•Monitor Sats (spO2)
•Monitor work of breathing

Not recommended
•Routine blood
•Routine urine testing
•Viral swabs

Treatments
•Hydrate the kid.  Oral,NG or IV
•Oxygen in children sating at or below 91%

Not recommended
•Oxygen if Sats are >91% (prolongs stay)
•Salbutamol- May worsen
•Steroids eg Predmix
•Saline nebs
•Adrenaline nebs
•Nasal saline drops
•Antibiotics -more harm than good

 Now let’s look at these #CageRattlers.
A common feature of allergic bronchiolitis is bronchospasm, but that is not a common feature of chest infection, so salbutamol, adrenaline or other bronchodilators are not helpful.   In viral chest infection, antibiotics are only effective when it if the child gets an opportunistic bacterial infection on top.  And to suppress their immature immune system using steroids is asking for bacteria and thrush to come to the puffer-party.

So the key here is differentiating between an Asthma like presentation where steroids and salbutamol are indicated, and an infective bronchiolitis where they aren’t recommended as routine.

All in all an interesting summary with a bit of dogma busting along the way.

For a more comprehensive look
Click here: Davis, T. Bronchiolitis guidelines, Don't Forget the Bubbles, 2018. Available at:
http://doi.org/10.31440/DFTB.17023

Liver Falure blood tests

#KYJ - Transaminitis

Pesky liver enzymes.  You’ve had patients who have had blood tests looking at liver function.

When running biochemistry on patients suspected of being in liver failure, a number of enzymes and other proteins are measured.  In this knowing your jargon blog post I’ll take you through the basics in a way you’ll understand, and be able to share with your patients.

There are many, but the rock stars are:

ALT and AST

Albumin

Prothrombin Time or PT.

Let’s start with the Acute /current liver injury ones.

Alanine Transaminase (ALT) and Aspartate transaminase (AST).  These enzymes are in your liver cells.  Locked up like a prisoner in a cell.   There roles are complex and outside the scope of this post, and frankly unimportant for the purpose of measuring  acute liver disease.  

Let’s just say that they are inside liver cells and during acute damage, trauma, infections or cancer of liver tissue, they leak out like myoglobin from damaged muscle cells, or troponin from damaged heart cells.

It stands to reason that when you injure your liver with one too many Yager bombs or a wild night of Beer-pong, you can expect to have released some ALT/AST into your blood stream where it can be measured on biochem blood tests.

ALT/AST is a sensitive marker for acute damage where a big number of liver cells died.  In chronic liver failure, cells die off slowly, so these enzymes leak or leach slowly into the blood.  For this reason, ALT/AST is aun reliable in Chronic disease like cirrhosis or cancer.

An acute injury and subsequent inflammation is termed transaminitis rather than hepatitis which is usually associated with infective inflammation.  Both cause ALT/AST rise.

PT

Prothrombin time or PT is a measure of function of the liver’s role in coagulation.

You know that your liver makes proteins for coagulation. These are called Factors.  Factors 2,7,8,9,10 (and 1&5), all undergo manufacture and activation using Vitamin K .

In acute and chronic liver failure, these proteins (factors) are not made efficiently or in big enough quantities, so the TIME it takes for blood to coagulate is slower.

Measuring Prothrombin Time (PT) allows a measure of hepatic function on coagulation.  

If it normally takes 10 sec for a blood sample to convert Prothrombin into Thrombin, it may take 20seconds in someone in liver failure.

PT is also measured as a blood test called an INR.  It means International Normalised Ratio.

A way of standardising the measure of PT all over the world.

A PT of 10sec roughly equals an INR of 1.0.  PT of 20sec = INR of 2.0 and so on. 

Adequate vit K in the diet allows the liver the ingredients to make those coagulation factors .  Not enough VitK and coagulation (PT/INR) will get longer.  This is why warfarin (a VitK antagonist) makes it longer for people to coagulate.  So... in liver disease, coagulation suffers, and bleeding / bruising can complicate patient symptom sets.

Finally Albumin.

A hugely important protein called Albumin is made in a functioning liver and released into the blood.   It acts as a water magnet and carrier protein of many drugs and other substances in the blood.  After being secreted into the blood by the liver, it has a half life of about 20days. 

If you went into acute liver failure today, we wouldn’t really notice a change in your serum Albumin for a few weeks.  So Albumin reduction is a marker for chronic liver damage.

Well that is it.  A wordy but simplified overview of the stuff they are looking for in liver function tests. 

Raised ALT/AST = acute liver damage

Slowed PT = acute and chronic damage

Reduced Albumin= chronic damage.

More?? Consider coming to one of our fun nurseing/paramedic seminars.   We love our Jargon.

Courses:

Www.Ect4Health.Com.Au/whats 

#KnowingYourJargon

Urobilinogen in Urine

#KYJ - Urobilinogen.

Ward test urine is such a common nursing assessment.

Occasionally I go through some of the urine values seen in abnormal urine tests, but one often poorly understood urine value is urobilinogen.

To understand this substance in urine we need to go back to the origin.

Red blood cells are born in bone marrow, and after 120 days, they are killed off by your immune system.  Components of the dead RBC are recycled, and processed by the liver.

RBC bodies become unconjugated bilirubin, which is processed into bilirubin and further into Bile. There,  bile is secreted to the Gall bladder to be concentrated and stored, waiting for your next fatty meal.

Once fat in your meal is detected by your gut, bile is secreted into your duodenum to mix with food, assisting lipase enzymes to break the fat down into triglycerides for absorption.

The reminant bile passes with undigested food into the large bowel and is acted on by intestinal flora .

This bile is converted into stercobilin, a dark brown pigment that gives faeces it’s colour, and urobilinogen a water soluble waste that is reabsorbed from the faeces.

Now stay with me:

All gut reabsorption of urobilinogen passes into your liver where it is converted into urobilin, and released into the blood stream so the kidneys can excrete it.

It is a light yellow colour and gives the urine it’s hue.  The more urobilinogen and subsequent urobilin you have the yellower your pee.

So it’s in there and it’s normal.

But...

There is a limit! If urobilin on dip stick is reactive (too high) it can represent one of two things.

More bilirubin than the liver can metabolise or hepatic failure.

1- RBC destruction

Haemolysis is the break down of RBCs.  In gut bleeds, haematomas or haemolytic anaemia ; even after a blood transfusion (massive), the sheer numbers of RBCs that are being broken down, and producing bilirubin overwhelms the liver’s capacity to convert to bile, so the liver converts it directly to urobilinogen where kidneys excrete what it can.

2- Liver failure. 

In hepatitis, liver disease like cirrhosis or liver Cancer, or any other liver disease; the conversion of bilirubin fails.  It therefore fails to be utilised adequately, and must be renally excreted.

Symptoms to check your patient for, when there is positive urobilinogen in their WTU, include 

Jaundice or skin yellowing 

Itch, or pruritus. 

Yellowing of the sclera.

Pale/ fatty /offensive faeces

Altered Liver Function Tests.

Coagulation issues leading to bleeding/bruising.

It is not too often that we get a chance to review the little physiology tips and pearls .  So our KYJ (#knowingyourjargon) blogs are one small way I contribute to Free open access medical-education. (#FOAM).

Check them all out on our website. WWE.ect4health.com.au

#KYJ - Why are ECG waves called PQRST and not ABCDE

#KYJ -Why are ECG waves called PQRST and not ABCDE?

In short, the first ecg was ABCD.

So to answer the question we need to go back to the late 1800s. Electricity was a new thing and we were still understanding ways to measure it.

The first ECGs waves were measured by a Lippmann capillary electrometer device that measured current in liquid mercury rising and falling in a fine glass tube.   There were actually only 4 waves and rightly called ABCD.

But the mercury was heavy and subject to friction in the glass tubes where it fluctuated with current, so Einthoven in 1895, devised the precursor of today’s ECG.

He used a more sensitive technology called a String Galvanometer, that demonstrated a more mathematically correct 5 distinct waves.  Naturally these were different to the Mercury Glass system and the ABCD needed to be replaced.

So why PQRST?

These go back historically to Descartes.  Where a set of variables were grouped XYZ if there was 3 ; ABCD if there was 4, or PQRST if there were 5.

Einthoven therefore named his 5 ecg waves of the normal sinus rhythm, PQRST.

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Bruising v Eccymosis

#KYJ- Bruising vs Ecchymosis

Bruises change colour, but why?

So I’m in Mt Isa today teaching a plaster/trauma slab workshop,

(Yes your facility can book one- but more on that later), and one of the discussion points is eccymosis and bruising associated with trauma.

Eccymosis is the external bruising that results from skin vessels rupturing and bleeding into the layers of the skin.   Eccymosis can be called a bruise, but not all bruises are eccymosis.

If you rolled your ankle- inversion injury results in stressors places on the ligaments that hold your ankle together.  The Fibula, the Tibia, the Talus. 

Should a ligament rupture (tear) occur- this is called a sprain (as opposed to ‘strain’ which is muscle or tendon).... anyhooo....

The commonest site of these ankle sprains is the ligament binding the Talus to the fibula head( the nobbly bit on the outside of your ankle (called the lateral malleolus).  There is three ligaments there, but it’s the one in front (Anterior  Talofibular (ATFL) ) that cops 70% of injuries.

That ligament and structures surrounding will bleed when torn.

Initially this will cause swelling into soft tissues around the ankle, but in the surface of the skin, redness may not be immediate.  In 24 hours the classic bruising emerges from deep tissues, and is seen as ankle discolouration.   Now over the next week or so, this bruise fades from Deep Purple (purpura) to greenish yellow/brown and fades with time.  This is bruising.

Eccymosis is bruising from external trauma, like a blunt impact.... see the difference?

Significant- probs no- but can imply an injury mechanism like indirect internal trauma (bruise) and direct surface injury (eccymosis).

The colour of the bruising can indicate time since injury occurring.   Be wary of a child presenting with an orthopedic injury reported to have happened this morning, when the bruise is coloured like a 2 day old injury.   Delayed presentation is a red flag for SCA&N .... but that’s a whole other post. 

#KYJ- Goitre and thyroid hormones

#KYJ -Goitre

Questions continue to come in about Thyroid symptoms and medication.

Here is a selection:

“Rob, you mentioned Goitre in a recent post, what causes it? And how is it linked to iodine“

Goitre is a common term used to describe the typical swelling of the thyroid gland (and surrounding tissues) when it has become inflamed or overactive.   

The causes are :

Autoimmune flares (Graves’ Disease or Hashimoto’s) or inflammation of the thyroid (Thyroiditis).

Iodine deficiency- thyroid uses iodine to manufacture its two hormones (T3 and T4), so in iodine deficiency, the thyroid gland will become over active in an attempt to convert T4 into T3.... more on that later.

Physical manipulation/massage or trauma of the thyroid, 

pituitary or thyroid tumours, 

Hyperthyroidism – This condition refers to an overactive thyroid gland, or one that produces too much hormone. 

Hypothyroidism – This condition refers to an underactive thyroid gland, or one that produced too little hormone. The diminished activity can also result in goiter. Hashimoto’s disease, another autoimmune disorder, is one manifestation of this.  

Thyroid Nodules – Sometimes, the thyroid develops benign nodules. This results in an enlargement of the gland as a whole.

Being a woman - Pregnancy and Menopause– Hormonal changes can affect the thyroid, resulting in enlargement.

Age is a factor(>40).

The thyroid gland used Iodine to make two hormones in response to a chemical signal from the Pituitary gland.   The pituitary regulates most endocrine organ functions by secreting stimulating or inhibiting hormones to regulate metabolism.   In the case of thyroid function, the pituitary gland secretes TRH Thyrotropin regulating hormone  and TSH- Thyroid stimulating hormone.

In response, the Thyroid manufactures 

T3- triiodothyronine (remember T3=Tri), 

and it’s quarter strength cousin Thyroxine (T4).

The low potency T4 Thyroxine is released into circulation as a precursor.   It is converted by the thyroid into the active T3-triiodothyronine, where it attaches to receptors on most tissues to upregulate/or stimulate their function.   Thus, T3&4 increase metabolism, heart rate, fat mobilisation, temperature, etc.

If you had a condition where you were deficient in TSH from the pituitary gland, or a problem with your thyroid gland, then your thyroid function would be poor.   

This is treated with administration of Thyroxine (T4) supplements.

For people with zero thyroid function still intact, a synthetic T3 -triiodothyronine can also be given.

Remember, T4 needs some functioning thyroid gland to convert Thyroxine into triiodothyronine the active metabolic hormone.  The liver can act as a T3 to T4 converter, but not as efficiently as a piece s of intact thyroid gland, so for post radical Thyroidectomy patients a T4 supplement is usually prescribed.

Common brand name of T4 supplement is called Liothyronine.   It is ready to go Thyroid super juice.  Needs no conversion and though 4 times more potent than Thyroxine, only has a very short half life.

Hope you have enjoyed your little thyroid refresher... fueled by questions from page followers.

I tried to answer 5 questions in this post.. I hope yours was there.😉.

#KYJ -Thyroid

Brought to you by the letters T and the the numbers 3 & 4.

😂😂

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#KYJ- Exophthalmos

#KYJ- Exophthalmos

Kelly, a third year nursing student writes: “Rob, my mum has had a throat infection resulting in an inflamed overactive thyroid, and as a result, developed bulging eyes... can you explain the link between thyroid and eyes?

Today’s #knowingYourJargon  word of the day is Exophthalmos.

Say it... “Ex-opf-thal-moss”

This is the noticeable bulging eyes seen in 30-40% of patients with Graves Disease or Autoimmune hyperthyroidism.

In this condition, the thyroid becomes inflamed and hyper-secretes Thyroid hormones.

Patients become tachycardic, hypertensive, hyperthermic and hyperactive.  When it occurs over weeks to months, there is frequently sleeping disturbance, and quite profound weight loss.   Thyroxine up-regulates metabolism and fat burning.   When inflamed, the thyroid can over secrete, causing all these Red Bull like hyped metabolic effects.  There is often an enlarged thyroid on palpating, or inspection.   This swollen football like throat swelling is noticeable and called a Goitre.

Fluid and Sodium shifts also occur causing the interstitial tissues behind the eyes to become profoundly oedematous, pushing the person’s eyes out in a bulging characteristic symptom.  

This is called Exophthalmos , and sadly, is usually a permanent legacy of a long term untreated thyroid over-secretion.

The common initial treatment follows when clinical symptoms (goitre, throat tenderness and tachycardia leading to Atrial Fibrillation) manifest, serum TSH, T3 and T4 levels (Thyroid Function Tests (TFTs)) and Ultrasound to scan the thyroid looking for cancer, nodules and any other thyroid abnormality, are performed.

Thyroid destruction drugs like Carbimazole are usually first line when an acute thyrotoxic storm occurs.  In these emergency situations, the inflamed thyroid gland releases T3, and T4 (Thyroxine) which causes hyper metabolic effects.  Occasionally hypertensive crisis, and AF can occur.   Symptomatic treatment and cardiac protection with beta blockers or Calcium channel blockers is common.

After treatment or surgery to remove the thyroid, the patient will be reliant on daily Thyroxine supplements.

Many of your patients are on Thyroxine for one of two reasons.

Hypothyroidism which is usually age related degeneration.

A bit like post menopausal HRT.

And then there is the hyperthyroid (Graves Disease) patients, who had too much Thyroxine, it was stopped with surgery or Carbimazole, now they are permanently living in the hypothyroid state, and need supplemental Thyroxine.

As nurses you should know that not all brands are the same.  They must be stored differently.

Eltroxin is not the same formula as Oroxine and Eutroxsig. Oroxine and Eutroxsig 

Must be refrigerated right up to administration.

Taken first thing in the morning immediately after waking, on an empty stomach, with a glass of water only- Then Wait at least 30 – 60 minutes after taking the dose before breakfast.  

Other medications, vitamins/minerals herbal medicines and supplements should not be taken at the same time , and the Australian Thyroid Foundation mandates an interval of at least  4 hours after taking Oroxine/Eutroxsig before taking other medications.

Storage of Oroxine and Eutroxsig

It is essential to refrigerate blister strips not yet in use of Oroxine and Eutroxsig between 2 – 8 Degrees Celcius (refrigerated temperature).  Recommendation is to keep all the script of tablets in the refrigerator, all of the time and retrieve the daily dose immediately before administration. It is rapidly destroyed at room temp.

Storage of Eltroxin

Eltroxin does not need to be refrigerated.  Eltroxin should be kept at room temperature below 25 degrees celsius.   Please note Eltroxin is not the same formula as Oroxine/Eutroxsig.  They can not be used interchangeably.

Remember Cold tablets, empty stomach,  no other drugs for 2-4 hours post.  Damn near impossible to achieve given the state of polypharmacy we deal with.