#KYJ - Hold breath while pulling CV lines

#kYJ -  Valsalva during removal of tubes

I was sent this question:

Rob can you please explain the rationale of holding breath for 10 seconds during removal of CVC!

I understand this action minimizes risk or air embolus .... But how?

...

You may know that this is a common instruction given to patients when we remove CV lines and chest tubes.  We do it to minimise the risk of air entering the thoracic cavity when pulling out the tubes.

Ok so here is the physics.

To understand the rationale you must understand 4 concepts. 

1 Atmospheric pressure 

2 intrathoracic pressure

3 intrapulmonary pressure

4 Pascale's principle

But First, a refresher on the pressures.

All pressure (air pressure, blood pressure, intracranial pressure etc) can be measured using different pressure units.

In medicine we use 

Centimetres of water(cmH2O) or millimetres of mercury (MmHg) also called "torr" but only nerds say Torr.  Eg blood pressure might be 120/80 MmHg.

Car tyres use pounds per square inch (PSI) or kilo pascals (KPa). Eg  a full tyre may be pumped up to 36 psi or 250kpa.

Atmosphere and weather reports use Bars or pascals.

1 bar = 1000 millibars=100000 pascals.

(100 KPa or 1000hectopascals)

Thus a millibar is also a hectopascal.

It's confusing and looks like a horrible highschool maths nightmare but just know that all units of pressure can be converted into each other.

1 Atmospheric pressure is the pressure of air that we breathe.  At sea level it is 760mmHg.  If you saw it on the evening weather forecast map they would say 1013 hPa.

This atmospheric pressure is all around us and fluctuates slightly.  A tropical low might be reported at 1004hPa and a cyclone reported as 890hPa.

1013 hPa converts into 760MmHg

I will use MmHg because we are speaking in the medical context.

Just know that seal level pressure is 760. 

2.  Intrathoracic pressure is the total pressure inside your thorax.  Predominantly influenced by the changing pressure in your lungs as you breathe. This brings us to intrapulmonary pressure.

3.  Intrapulmonary pressure is the pressure inside your lungs.  As you go to breathe in, your diaphragm contracts, drops, and creates a vacuum or negative pressure change inside you lungs.  The pressure in your lungs is less than atmosphere so considered to be a relative negative pressure when compared with the atmosphere.  The change is small, only 6-8 MmHg, but enough to allow the atmosphere to rush into your lungs to equalise pressure inside.  We call this breathing in, or negative pressure ventilation. 

On inspiration

Atmospheric pressure 760

Intrapulmonary pressure 752

A relative vacuum.

Now breathing out is the opposite. I must push air pressure inside my lungs to blow air out to the world.  Diaphragm relaxes, rises and puts the lungs under higher pressure than the world.

On expiration

Atmospheric pressure 760

Intrapulmonary pressure 765+

Air rushes out.

Stay with me we have nearly answered the question.

Inside the chest wall, the pressure emulates the fluctuation of the inside of the lungs.  Thus intrathoracic pressure rises on inspiration and falls on expiration. This close relationship is described by Pascal's principle which suggests that a pressure increase in one area of a confined space (thorax) is equally transmitted across the whole confined space. I know... Boring!!! 

Back to holding your breath.

Take a big breath in now and hold it. Hold it!  Hold it!

Feels full hey?  Ok breathe normally.  

When you held your big breath (valsalva manoeuvre) you held pulmonary (and thoracic pressure) at its highest point relative to the atmosphere.

Your thoracic pressure while breath holding was perhaps 770mmHg, and thus higher than the word. It would be impossible for air to enter your lungs or chest cavity through surgical holes, because the pressure inside you was higher than atmospheric pressure.

Asking the patient to hold their breath during tube removal then makes it impossible for air to invade the hole before you seal it with an opsite or other occlusive dressing.

The pressure inside was too high.

Now the consequence of air getting in through the CVC site is an air embolism.  A very small risk, and even if air did get in it enters the venous network and bubbles flow into the right atrium.  Bubbly blood is then pumped to the lungs, where most bubbles are filtered out. 

In the context of a chest drain tube; well they are sitting in the pleural cavity not a central vein.  The tiny bit of air that can get in while pulling out a tube is insignificant and reabsorbs in a hour or so... But safe practice implores you as a nurse to take steps to avoid this introduction of air into a chest when pulling out tubes, drains and CV lines.

Just get them to hold their breath.

Pressure 

Should we reduce fever?

Fever

So I found myself banging on about kids and fever again last week in a trauma course of all platforms.

The message is slowly getting the through, but where literature focuses on efficacy of paracetamol and ibuprofen, it conclusively agrees on two key points:

1.  that these drugs should be reserved for pain and discomfort .

2.  There is no evidence that they will prevent a febrile convulsion. 

In 2010 the RACGP (college of GPs ) in Australia released a paper redefining what a fever was. Previously a patient was considered to have a fever when there core temperature rose above 37.5 degrees of Celsius. Now it is 38.0.

This was also coupled with the notion that fever should not be treated until at least 39.0. 

A common ignorance in health care providers is that at the slightest hint of a fever, some over the counter antipyretic would be given. The medical world is calling for this nonsense to cease. But it is so hard to sell this message to "out of date" parents, doctors and nurses.

Here it is - as blunt as I can put it. Stop treating fever like it is a bad thing!!

Recognise that fever is the body's normal natural response to fighting an infection.

After invasion by a virus or bacteria, phagocytes coming into contact with pathogens release signalling chemicals called pyrogens which stimulate prostaglandin release. These prostaglandins alter the body thermostat in the hypothalamus. As long as phagocytes are active in killing pathogens, they will release these chemicals to keep the temperature high. It aids in proliferation of immunity compounds and cells to the site of invasion. Fever cures infection .

Now paracetamol, and ibuprofen acting as antipyretic medicines, inhibit these prostaglandins, thereby inhibiting the natural immune response. By reducing the fever, they can mask sinister symptoms and prolong an infection

Reserve these drugs for pain and discomfort associated with illness. They don't prevent febrile convulsions, and there is NO evidence that they improve the illness. 

Just Stop treating fever!!! Fever is your friend!

Share this with your parents, colleagues and anyone you know sucked in by advertising that tries to sell a message that "Brand N" or "Brand P" is for pain and fever. 

FEVER IS YOUR FRIEND!!

This 2011 article is just another paediatric journal that refreshes the notion that antipyretics are to be reserved for discomfort.

http://pediatrics.aappublications.org/content/pediatrics/127/3/580.full.pdf

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#KYJ - Hyperkalaemia

#KYJ -  Hyperkalaemia 

High potassium in the blood.  Potassium is expressed by the chemical symbol "K".  It stands for Kalium which is the Medieval Latin word for potash, a mineral used for hundreds of years as a fertiliser, and a natural potassium salt formed millions of years ago when ancient seas dried up.  Burning plant matter in iron cauldrons (pots) yields high concentrations of potassium which in English, is termed potash.

Literally, Hyperkalaemia means high(hyper)-Potassium (Kal)-of the blood (aemia).

...

In our bodies potassium is abundant inside our cells.  It is a positively charged ion (electrolyte) termed K+.

In blood and other extra cellular fluid, it's concentration is very low relative to the high intracellular concentration.  The principle of diffusion predicts that it will leak out of our cells to balance (equilibrate) with extracellular fluid.

In converse to K+, sodium (Na+) is abundant outside cells and does the same as potassium, in that it attempts to ooze into cells. 

Normal blood potassium ranges from 3.5-5 mmol/L.  Should potassium rise beyond 5.5 then it is called Hyperkalaemia.  This is life threatening, and exerts its effects on muscle action, particularly cardiac muscle.

Elevated potassium leads to cardiac arrest. ... Badness! 

Given potassium is normally abundant inside cells, it stands to reason that when cells are damaged, destroyed and die, their potassium leaches out and increases levels in the extracellular (interstitial fluid and blood) fluid.

Under normal circumstances, your kidneys remove excess K out of your blood and some of it is transported back into cells (influx).  

Causes of Hyperkalaemia

Too much in, cell destruction or not enough excretion are the main causes.

Too much.  

When we eat foods rich in potassium, it is rapidly absorbed via our gut and enters the blood stream. It is then either transported to cells where insulin is responsible for facilitating its movement into the cell as glucose is transported into cells for energy production. 

In condition of tissue damage (burns, crush injuries and a muscle breakdown called Rhabdomyolysis), damaged cells leak massive amounts of K into the blood.  The bigger the trauma, the bigger the potassium rise.

Not enough excretion. 

If your kidneys fail, you can't excrete potassium.  It accumulates.  Remember it is continually leaking into your blood, so your kidneys need to be continually functioning to regulate potassium levels in blood.  In renal injury or failure, accumulation is swift.

Diagnosis and suspicion

Muscle weakness especially after strenuous exercise (??rhabdomyolysis)

Lethargy,

Reduced urine production

ECG abnormalities eg tall tented T waves and s widening QRS complex=badness.

Serum K (blood test) is the fastest way to definitively assess Hyperkalaemia and is part of a routine test called U&Es (Urea and Electrolytes).

Treatment

Driving kidneys to excrete is the simplest strategy.  By giving IV Normal saline, and or adding a diuretic, the patients kidneys can excrete more potassium.  The common choice is a loop diuretic like Frusemide (Lasix). Naturally these are not appropriate if the cause was renal impairment.

Insulin and glucose infusions

Insulin acts like a swipe key that open channels (gates) in the cell membranes to let glucose into cells. When this occurs, potassium molecules are moved into the cell with glucose.   Therefore an effective treatment for critically high potassium levels is an insulin infusion (with glucose).

• 10-20 units IV Actrapid insulin  and 25-50g IV glucose.
• Starts working in 20mins
• Will reduce potassium by 0.5- 1mmol/L 

Salbutamol.  

Yep you read right. Salbutamol or Ventolin either IV or Nebulised (10-20mg) causes potassium to influx very effectively. This is the preferred option in renal disease patients when diuretics are useless and mucking around with glucose and insulin is a risky gig.

Salbutamol is as quick as the insulin, 20-30 mins and strips about 1mmol/L.

Resonium

Speaking of renal patients.  A slow but relatively effective treatment for Hyperkalaemia is using oral or rectal Resonium resin.  This old school treatment binds with potassium in the bowel and facilitates its removal in faeces. 

It relies on gastric motility, so it is slow to onset, but gets the job done in the non acute patient.  It is given as a 30-45g dose usually mixed with a laxitive (to really get things moving) - sorbitol is a favourite.

When things are Critical!!

If the patient has dangerous potassium levels (>8.5) then dialysis is the game changer.

Capable of stripping K+ at a rate of 1-2mmol/L over a two hour treatment, this intensive treatment is a proven lifesaver.

So there we have it.  A very basic overview of hyperkalaemia .  I hope you enjoyed my latest #KYJ. 

#KYJ- Asthma Metered Aerosol actuations are 30% greater in quantity than the number stated on the packaging, but we don't know if it is drug or just propellant being delivered.

Introduction

Salbutamol sulphate metered inhalers are frequently observed to be able to discharge (puff) many times after the listed actuations on the product. 

This leads to confusion in patients and clinicians as to whether the device is delivering therapeutic doses of Salbutamol or just the gas propellant.  This paper reviews two common brands of salbutamol metered aerosol products to document how many total activations are possible from new.

Context 

People experiencing asthma are at risk of acute exacerbations known as flare-ups (previously "Asthma Attacks")(National Asthma Council Australia, 2015).  The pathophysiology involved frequently includes an immunoglobulin E mediated immune response to an allergen, like smoke, dust mite, foods and fragrances.  Alternatively exercise, stress and ambient temperature/humidity fluctuations may lead to a flare up (Kim and Mazza, 2011).

Regardless of aetiology,  the disease is characterised by cough, bronchiectasis, bronchospasm, and bronchiole luminal narrowing from oedema. This triad significantly causes increased work of breathing manifesting subjectively as 'shortness of breath' and chest tightness, and objectively as dyspnoea, accessory muscle use, cough and wheeze (Holgate, 2008).  

A short acting beta-2 receptor agonist (SABA) delivered as a metered aerosol (MA or "puffer"), nebuliser is common initial treatment (Asthma Foundation, 2015;Australian Resuscitation Council, 2010).  In most countries the medication of choice is Salbutamol (North America - Albuterol) often referred as "blue reliever medication".  

It is an observation by many clinicians in emergency practice, that patients using their SABA, are unaware of the correct use, correct dose and remaining drug in their MA.  Irrespective of the brand of Salbutamol, the metered aerosol delivers 100micrograms, and reports 200 doses.  Despite this, a  common observation is that long after 200 actuations, the device is capable of being discharged many more times.

This may cause concerns with those individuals that, during a flare-up, diligently self administer their SABA, believing it to be discharging drug, when it may be void of anything but propellant gas.

Some other metered aerosol products include a counter device that informs the user of doses used, or doses left. Salbutamol MA products available in Australia don't have this feature, so the user is required to keep a tally.  There is no way of knowing if the MA is drug depleted. 

Question

Despite advertising 200 metered doses, how many times will a salbutamol MA discharge before it stops actuating?

Methodology

A simple experiment was designed where six (6) metered aerosols (three of two different brands) of salbutamol  were discharged to extinction.

To minimise expiry dates, ambient temperature, atmospheric pressure or humidity being a corrupting variable, all discharges of the medication were performed on  new stock, on the same day, same time,  and at the same location.

Data

Ambient temperature was recorded at 23 degrees Celsius.  Altitude was sea level .

The brands of salbutamol sulphate included were Ventolin (GlaxcoSmithKline) expiring 4/2017 and Asmol (Alphapharm) expiring 2/2017.

The experiment was conducted at the end of September 2015 so all medication had a minimum of 16 months prior to its expiry date. 

Medication was discharged to exhaustion of propellant. One discharge per second in blasts of 10 puffs (barrages), followed by 4 shakes of the device between each barrage.

Asmol 1- totalled 276 discharges

Asmol 2- totalled 275 discharges

Asmol 3- totalled 273 discharges

Ventolin 1- totalled 272 discharges

Ventolin 2- totalled 274 discharges

Ventolin 3- totalled 274 discharges.

Results

From this small experiment it is apparent that the two brands were similar in the total number of unit discharges.  Range of variance 272-276 

Mean 274, mode 274, median 274.

It is fair to report that salbutamol sulphate metered aerosols deliver 274 +/- 2 actuations.

Discussion

Whilst it is clear that the MA devices assessed in this experiment discharge their advertised actuations, it is concerning that at a mean discharge rate of 272, this represents 72 puffs more than the reported doses.  Given this premise it was outside the scope of this study to assess the content of each discharge.

It is not known if after 200 actuations the remaining 72 puffs contain drug or just propellant gas.  A common observation in emergency departments is that a patient reports that their "puffer" is not "working" despite the apparent discharging.  This could be poor technique, out of date medication or indeed use of a MA that is drug depleted yet continues to discharge gas.  If the later is true, this represents a patient teaching opportunity, and nurses/doctors and pharmacists in a position to offer patient teaching should be informing their clients of the need to tally their MA use.

Limitations

The study was limited by a small sample of MA devices (n=6) and only two brands of salbutamol were included.  A more statistically powerful experiment could be conducted to assess a larger number of units, and include a larger number of brands.

A second limitation is that despite advertising only 200 doses on the labelling, this study did not analyse the content of each spray, so can not surmise that all sprays were delivering a full 100micrograms of salbutamol, or only the first 200 actuations.  A robust content analysis of the full 272 (+/- 2) sprays  would allow conclusions to be made as to whether manufacturers over compensate and include more than 200 metered doses, or whether, as advertised, each device only delivers 200 doses, and any excess is merely propellant.

Conclusion

Six metered aerosols of salbutamol sulphate were discharged to exhaustion to assess  quantity of actuations. All devices (n=6) discharged between 30-36% (272 +/- 2)  more times than advertised.  It is not knows if the mean 72 extra actuations contain any drug, or just propellant.

Author concludes more research and content analysis is needed, and a practice application reinforces the ongoing need for clinicians to provide education to their clients to keep tally on their salbutamol use.

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Refs

National Asthma Council of Australia

http://www.nationalasthma.org.au/handbook

Asthma Australia

http://www.asthmaaustralia.org.au

Australian Resuscitation Council.

Www.resus.org.au

HOLGATE, S. T. (2008), Pathogenesis of Asthma. Clinical & Experimental Allergy, 38: 872–897. doi:10.1111/j.1365-2222.2008.02971.x

Kim, H and Mazza, J. (2011), Asthma. Allergy, Asthma & Clinical Immunology, 7(Suppl 1):S2. 

KYJ- Takotsubo cardiomyopathy

#KYJ - Takotsubo 

It was 1976 when Sir Elton John sang those famous words..."don't go breaking my heart"; to which Kiki Dee retorted, "I couldn't if I tried".

Well Elton, a broken heart is easier than you think. Broken heart syndrome or more correctly, Takotsubo cardiomyopathy is a stress induced apical ballooning and reshaping of the left ventricle, caused by stress.  Under periods of extreme stress, brought on by tragedy, life events, loss, and anxiety inducing stimuli, the myocardium undergoes a remodelling of shape. It is induced by high concentrations of stress related hormones, eg adrenaline, norepinephrine, and cortisol, released at times of stress.  Not new, this stress induced cardiomyopathy presents as an acute heart failure that mimics an Anterior MI with typical pain, and ECG changes.  It is thought to be a silent contributor to 1.5-2.5% of ACS.  

Made up of two Japanese words, "Tako" means 'octopus' and "tsubo" means trap or pot.  Literally Takotsubo means octopus pot, and it is so called because when observed the patient's heart takes on the shape of an ancient pot that the Japanese fishermen in sea side villages, used to catch octopus for food.

It was first described in the 1990s so is really a relatively new syndrome.  It was seen women, who in their 60 & 70s, lost their husbands.  Proving to be such a stress inducing life event, a statistically significant number of widows died in the months following from what was originally called Broken hearts, then stress cardiomyopathy.  On autopsy their hearts had taken on the reshaping appearance of a Takotsubo, hence its renaming.

More?? ... 

http://m.circ.ahajournals.org/content/124/18/e460.full

#KYJ - Inflammation symptoms - Swelling- 2 of 5

#KYJ - Inflammation symptoms part 2 of 5

.

Inflammation has 5 cardinal symptoms.

Redness(rubor)

Heat (Calor)

Swollen (Tumour)

Painful (Dolor)

Loss of function. (Pathy)

In the first episode we took a look at pain.  Tonight we review swelling.

Swelling or oedema is a common symptom of inflammation and represents the proliferative stage of inflammation's cascade.  After initial vasoconstriction caused by platelets and injured tissue cell releases of phospholipids, and other inflammatory mediators, the next group of cells in tissues to activate are the Mast Cells. 

Mast cells are specialised white blood cells that reside along side capillaries in tissue.  A type of basophil that is classified as a granulocyte (a cell containing granules).  Mast cells are rich in granules of Histamine a potent vasodilator and leukotriene which is a chemical attractant for blood borne white blood cells to migrate towards the site of damage.  When released histamine causes capillaries to enlarge increasing blood flow to the damaged area, and also allows them to open tiny pores in the capillary walls.  Ultimately this increase in permeability allows large white blood cells (neutrophils and monocytes) to squeeze out of the pores and start fighting bacterial contamination, and clean up cellular debris.  Trouble is that when the capillaries pores open, they leak plasma and plasma proteins like Albumin into the interstitial spaces.  This is called oedema or swelling. 

It starts inside the first hour, and maximises in 24-48 hours.

Remember the last sprained ankle you saw, or burn, or even a minor injury that you experienced... Swelling is a common feature of inflammation. 

This link is a short video I did to talk about oedema. 

http://youtu.be/sdWhUmUuWqc

Asthma or vocal cord dysfunction? Would you know the difference

Vocal cord dysfunction vs Asthma flare up. 

The patient comes in, breathless, panic stricken coughing and has a wheeze, audible from the doorway.  She is pale, distressed and clutching at her "puffers" claiming they are not working.

The usual approach to managing this "Asthma Attack**" is to sit her upright, and administer a battery of doses of salbutamol. 

Standard dose is 4 puffs via her metered aerosol using a spacer device.  

One puff-4 breaths

One puff-4 breaths

One puff-4 breaths

One puff-4 breaths

Wait 4 minutes and repeat.

But for many people suffering an asthma flare up (** new term for asthma attack), the routine use of a SABA (short acting beta agonist) like Ventolin, will be ineffective.

It is estimated that up to 75% of asthma flares could be vocal cord  dysfunction (VCD).

Where salbutamol exerts its effectiveness, is on the smooth muscle in the lower airways. During VCD the dyspnoea is caused by the closing of the vocal cords, and unlike asthma which is allergic or hyperresponsiveness to a trigger, VCD is often psychogenic.  It responds not to drugs, but calm breathing, and relaxation.

Now we are not saying "don't give salbutamol", but there is immense value in adjuncting breath coaching during assessment and management of what may be asthma, but might just be VCD.

So how would you differentiate the two?  Three fairly simple assessments.

1. Asthma wheeze is primarily on expiration. It is a low airways disease. Auscultation of a wheeze in lung fields should exclude a throat wheeze (called stridor).  In VCD there is no lung noise, it is all upper airway.

2 Asthma cough is the first symptom to manifest, it is associated with over production of white to cream sputum from the Goblet Cells lining the bronchial tree.  In VCD the secretions being coughed are watery, spittle and salivary. It lacks the viscoelastic lustre of true bronchial sputum.

3 Desaturation is usually not present in VCD.  Being all laryngeal obstruction, alveoli gas exchange impairment, and gas trapping is not a feature, as it is in Asthma.

Anxiety is the dominant feature in VCD. I know all you asthmatics out there will say "not being able to breathe does make you anxious... And it does!! But this is a Chicken or the egg scenario.

In Asthma, real asthma, a physiological trigger is the norm, leading to a flare up then anxiety follows. Asthma is bronchial restriction

In VCD anxiety is the trigger which crescendoed into a worsening Shortness of breath.

VCD is often idiopathic. It is all in the vocal tissue.

And while it causes asthma-like symptoms. It is all too commonly misdiagnosed as an asthma attack. When you treat VCD as an assumed asthmatic with oxygen and bronchodilators, and you find these modalities have very little to no effect and may even exacerbate anxiety and symptoms, a focus on anxiety reduction is key.

In these patients, stay with the person, and have them focusing on their breathing.  Talk them down, and offer encouragement.

Oxygen is not indicated for either condition unless O2 sats are <93% ( <95% in kids). 

Gram Negative or Gram Positive -what does it mean

#KYJ gram negative bacteria vs gram positive bacteria.

In this episode of #KnowingYourJargon we discuss bugs.  Not just any bugs, but bacteria.  Thousands of types of bacteria are found in and around us.  Some are friends that offer some protective or digestive function and often called "Normal Flora", others cause infection and disease, these are collectively called pathogens.

Two of the largest groups of bacteria are called Cocci, and Bacilli.  They differ by their shape.  Cocci are spherical, whereas bacilli are rod shaped.   Bacteria are classified as neither an animal nor a plant, they exist in their own group that hovers between both.  As such their cell structures are more similar to plants because they have tough cell walls made of complex sugars (carbohydrates) whereas animals have cell membranes made of lipids (fat- cholesterol actually).

Now I know you have heard of Gram negative and Gram positive organisms, but what does it mean?

In the mid 1880s a Danish bloke, Hans Christian Gram developed a method of putting a Crystal Violet Dye on bacteria cultures to stain them for microscopy.  While performing autopsies in a German morgue, he discovered that some bacteria would absorb the dye and therefore would be easily visible under microscope.  

Gram calked these his Gram positive bacteria.  Those bacteria that didn't take up the dye were therefore calked Gram Negative.  A common great example of a gram negative bacteria is E-coli found abundantly as normal flora in your gut. And the pathogenic Typhoid bacillus where Gram first discovered that some bacteria wouldn't pick up his violet stain.   

Rock Stars in the gram positive world include staphylococcus, streptococcus and some types of mycobacterium.

So, perhaps not the most interesting if information, but I bet you've wondered why some are called gram positive and some are called gram negative.

Now the application of this information became more important later in medicine.  Gram just used his stain to see the bugs more clearly in the tissues he was studying.  

Fast forward 45 years and we find ourselves in the final years of 1920s, the party and glitz of the Gatsby years is drawing to a close and the great New York stock market crash is imminently about to plunge the western world into depression.  A brilliant young Scotsman called Alexander Fleming, a (biologist) discovered that  in a bacterial (staphylococcus) culture on an agar plate, there was a spot of  green mould that seemed to exude a substance that killed the bacteria around it on the culture.  Penicillin had been discovered.  12 years he failed to get this discovery recognised as a medicine, then at the beginning of WW2 that Florey and a mob of doctors developed into a pharmaceutical grade product to treat infections.  The dawn of the Antibiotics had begun.

So ... Great Rob!  Now connect the dots for me...

Penicillin (and other Beta-lactam) antibiotics are large molecules. Penicillin was found to be very effective on Gram positive bugs, but not so good on gram negatives.

It was later discovered that the "tough to kill" gram negative pathogens, possessed a ring of lipid (fat) around their sugary cell walls. Like a condom acting as a barrier preventing the large penicillins in. It was at the same time discovered that this same barrier prevented Gram's violet stain from sticking to the sugar wall.  Where gram positive bacteria had no lipid barrier, the crystal violet stain can stick to the sugary cell wall... Thus these visible bugs are called Gram positive, and we know that both the stain and the penicillin can get in and destroy the inner workings of the pathogen.

...

Blank face??

Well I find it interesting!!

More... Pre register for our newest seminar on drugs and how they work.  "Rusty Pills" is coming to a location near you.  Expressions of interest to admin@ect4health.com.au

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Aspirin- chew or swallow.

#KYJ - Aspirin for Chest Pain

For as long as I can remember the mantra for chest pain management was MONA. Standing for Morphine, Oxygen, Nitrates and Aspirin, MONA has largely gone unchallenged for 25 years. The exception is the deemphasis on using Oxygen, and a 2011 report challenging the use of morphine in Acute cardiac failure but that is a whole other post.

In this episode of #KnowingYourJargon (KYJ) we explore the rationale for Aspirin.

Aspirin or Acetyl Salicylic Acid (ASA) is an ancient non-steroidal anti inflammatory drug (NSAID) used originally as a tooth ache remedy when the bark of the Willow tree was chewed by tribesmen and women. 

It has so many great uses, but is not with out its problems.  It can initiate asthma flare ups, so caution in these patients is needed.  Gastritis and epigastric pain is a common concern, especially if taken on an empty stomach.  In the 60s and 70s parents giving aspirin to febrile children discovers that some children developed a rash, vomiting, liver and brain damage, and died.  The collection of symptoms was termed Reyes Syndrome, and for this reason, aspirin is not recommended for children under 13.   At around the same time aspirin powders marketed under the trade names Bex and Vincent's powder, were a housewife favourite that resulted in a spike in kidney failure in much the same way that we are seeing a current increase in incidence of kidney disease from ibuprofen and other NSAID over use, but I digress.

Aspirin exerts an anti-platelet function.  Platelets secrete a surface protein which is a prostaglandin chemical that signals other platelets to clump together, and form a clot.

Aspirin (like other non-steriodal antiinflammatories) acts by inhibiting these prostaglandins from forming. It permanently disables the platelet, rendering it useless for the rest of it's life (7-10days).

In chest pain of cardiac cause, the ischaemia is usually due two mechanisms; vessel spasm, and clot formation.  Enter the use of Aspirin. If we give aspirin, we disable the platelet, resulting in inhibited clot formation.

150-300mg chewed or dissolved and given orally is indicated for chest pain patients as soon as possible.  It should be stated that this is standard chest pain protocol, but only if not contraindicated. Active bleeding, allergies, and hypersensitivity would all be reasons not to administer aspirin as a routine.

Because aspirin inhibits prostaglandin production, it also inhibits protective prostaglandins like those that protect the stomach from erosive gastric juices.  This is the link between gastritis and aspirin.

Aspirin is a versatile drug, and in chest pain, is a life saving intervention with its anti platelet effect.  More and more , it is used with an adjunct drug called Clopidogrel.  This also works on the platelets surface inhibiting their ability to stick to each other causing a clot.  This process is called platelet activation, and together aspirin and clopidogrel are a great team in inhibiting the thrombus formation and snowballing.

"Rusty Pills" our newest Pharmacology refresher seminar is coming soon.  Check out our upcoming courses including Rusty Pills here

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Concussion in sport. When to get back on the field

#KYJ- Concussion. What is it, and what are the implications for future play.

Sitting on a freezing footy field in a mid June Toowoomba Saturday covering first aid for Rugby, may be your idea of Hell, but once the grizzling is done, I actually like it. 

First Aid is where I started in the world of Emergency medicine all those 35 years ago.

I thought I'd dedicate this post to a common sports injury.  The concussion.

Concussion is a closed traumatic brain injury that is graded from an insignificant mild Concussion where the person did not loose consciousness, through to the worst of persistent vegetative States (PVS) caused by a severe Diffuse Axonal Injury or DAI.

For the stock standard concussion that you see at sporting events on most weekends, the presentation of a "Classic Concussion"  has sparked debate and controversy in locker rooms and clubs the world over.

A classic concussion is one where a traumatic blow to the head causes transient (5 seconds or more) of unconsciousness.  Headaches, nausea, fitting and vomiting are common, as is ataxia (wobbly walk) and confusion of varying degrees.

A classic concussion used to be a normal inevitability of contact sport, and as such was often seen as a badge of honour.  Perhaps more sinister was the false held belief that concussion was harmless, and never caused permanent brain injury.  We now know that to be wrong.  If someone sustains even one classic concussion, the neurosurgical community are now calling for an end to that victims contact sport career.  Yes... One concussion.  With overwhelming evidence to disprove a myth that CC was harmless, with newer sensitive scanning technology, we now know that permanent damage is done, and that the victim is now more susceptible to further and worsening extension if they receive another blow.  Try selling that to coaches, and aggressive parents on the sidelines, and players hellbent on ignoring the science!!! Not easy.

With the improvement in mandatory rest periods, clever head protection, and rule manipulation, the risks of injury and permanent debilitation are minimised, but we need to be champions that teach the parents, players and coaches of the Weekend contact sports arena, what we now know is true.

They shouldn't play again.  But selling this to the sporting community is like asking Americans to give up their guns.

At the very earliest is a recommendation to stay off the field for a minimum of 14-21 days.

In concussion, Axonal fibres (tails of brain cells) are stretched and or damaged in sudden head strikes, or torsional rotation mechanisms.  These fibres, like all damaged tissues release inflammatory chemicals that start the process of secondary injury and cerebral hypoxia through a sudden rise in intracranial pressure. The shock wave of energy may render the player unconscious, or knock the "silly" into them.  Any degree of an alteration in neurological function is seen.

The factor in level of, and duration of consciousness, is the extent of energy from the blow, and or the extent of neuronal damage.

Nerve cells regenerate with such a slow regrow that a large concussion may leave permanent deficit.  We've all seen a "punch drunk" old boxer, or footy player.

The symptoms that follow, are almost  certainly caused by the swelling local to this injury.

The big risk of playing again is referred to as ‘second impact syndrome’ and it is due to a repeated head trauma.
It occurs rapidly after single head impact in most published cases.  Rapidly means, weeks or months, not hours or minutes. 

Pathophysiology may involve disordered autoregulation, that causes lack of blood flow to healthy areas of brain.

30% of concussion results in a post concussive syndrome when the patient may suffer from head ache, dizziness and confusion +/- personality, memory and concentration problems for up to 3-4 months post injury.

A cross-sectional study in retired football players showed a 2–3-fold increase in relative risk of clinical depression.

Concussion is not a harmless consequence of a contact sport. It is a poorly respected medical phenomenon that needs to have its awareness shared.

Do your part and share this post. 

A paper last year that is a great go to for some RACGP refs, here http://www.racgp.org.au/afp/2014/march/sports-related-concussion/