#KYJ - Inflammation symptoms - Swelling- 2 of 5

#KYJ - Inflammation symptoms part 2 of 5

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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/

Bowel sounds in shock

#KYJ Bowel sounds.

Understanding bowel sounds in a trauma patient does not need to be a complicated process that is difficult to interpret. 

Here is the thing, smooth muscles lining the intestines require a healthy blood flow to continue peristalsis (movement).  When well perfused, the bowel rhythmically contracts to move food chyme through the digestive system.  As it does, the movement is heard using the diaphragm of a stethoscope in all four quadrants of the abdomen.  These sounds of squelching, are called bowel sounds.

In trauma or sick medical/surgical patients, shock may reduce bowel sounds through a simple process of redistribution of blood volume to more vital organs.  When this happens, peristalsis ceases, thus bowel sounds stop being heard.

So let's apply the typical assessment of a patient in shock. As blood loss worsens, the vascular system starts shutting blood flow to non critical  organs .

First is skin (pale, cold and clammy skin is the symptom)

Next is the gut. Poor gut perfusion ceases gut peristalsis and subsequent bowel sounds.

Loss of bowel sounds is not necessarily a gut pathology, but most commonly a significant indicator of shock.

Opiates and constipation

#KYJ - How Morphine causes constipation.

#KnowingYourJargon or KYJ for short is the #ect4health contribution of free open access nurse education (#FOANed).  As a teacher of nurses, I get lots of questions on drugs and their side effects.

Nurse Glenda writes:

Rob, I've noticed that a drug we give at work, Targin (oxycodone/naloxone) has both an opiate and its antidote in it.  Why is this? Wouldn't one cancel out the other?

Well this is a great question.  The answer lies in understanding the opioid's effects and side effects.

Oxycodone, fentanyl, morphine, codeine and other opium derivatives all act as pain killers by attaching to two receptors in the central nervous system.  The Mu and the Delta receptors.  When activated these receptors reduce the perception of pain impulses that the patient feels.  They still have the cause of their pain (Cancer, inflammation, injury) but the brain doesn't interpret it as pain.  The Mu receptors specifically initiate a sense of happiness often desired as a high, or a floaty euphoric sensation, sought after by many who are opiate addicts. Heroin is a perfect example.

Now naloxone antagonises this by competing at the Mu receptor and deactivating morphine/oxycodone's ability to stimulate the sensors.  Hence, naloxone is thought to be an effective "reversal" of opioid overdosage.

This brings us to the question of why you'd put naloxone in a combination treatment with an opioid like morphine or oxycodone.  At the simplest reckoning, you'd think that it would stop the opioid from working but it has little effect on the pain killing effects of morphine and more inhibition of the side effects which are euphoria, drowsiness, respiratory depression, nausea and constipation.

Targin, and other combo drugs like it allow the analgesic effects but limit the negative side effects.  Resp depression, and constipation are the big ones.

So how exactly does morphine and its cousins cause constipation.  The bum is a long way from the central nervous system and brain, yeah?

Well here is the thing.  Mu and delta receptors also line the intestines.  Opiates that stimulate these in the brain, also stimulate them in the gut.  When they are stimulated they have a few effects:

1- Gastric motility slows causing more transit time and dehydration of faecal matter- hence constipation.

2- strength of rectal muscles (those used to poo) is reduced, so dry faeces, is harder and more difficult for drug weakened rectal muscles to push out.

3- the nerves in the anus that detect a stool, are desensitised, causing a full rectum to be less of a stimulus to have the urge for number Twos.

So given these three issues, all leading to less moisture, weak pushing, and reduced urge, all roads lead to constipation as a major side effect of opiates.

Now let's bring back the question of adding naloxone into the analgesic... Naloxone inhibits the Mu receptor effects of constipation, yet allows the analgesic effect to still offer comfort.

If you are enjoying these #KYJs, please let me know, share this post or consider attending one of our seminars which are full of this sort of stuff.

 

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Inflammation - 1 of 5 Pain

#KYJ - Inflammation pain

Episode 1 of 5

In KYJ (#KnowingYourJargon) we explore those terms in health that we use commonly, yet often don't understand.

Think of KYJs as putting the science into your nursing artistry.

Inflammation

It starts with tissue damage and involves a storm of cellular chemicals that have 5 cardinal effects.

Dolor = Pain

Calor = heat

Rubor = Redness

Tumor = swelling

Loss of function = doesn't rhyme with the other four.

So let's look at why we see these symptoms.  In this episode- Pain

Pain is thought to be through multiple mechanisms.

Pain receptors (nociceptors) in your tissues fall loosely into two categories. 

Fast Delta-A fibres transmit sharp, burning pain messages to the spinal cord and brain for processing.

Slow C fibres transmit the dull ache of pressure/crushing, heaviness.  Pulsatile throbbing and crampy pain.

Both are stimulated directly by chemicals released during injury, but both are also stimulated by delayed manufacture of inflammatory chemicals made by the immune system eg bradykinin, and prostaglandins.

To start to understand inflammatory pain, let's explore what happens at the site of injury.  A cut or splinter.

Direct skin cell injury causes destruction of the membranes that encapsulate cells.  This membrane you will remember from grade 9 science, is made of fat (lipids).  It is actually a phospholipid that you know better by its common name Cholesterol.

That's right, all cells are lined by cholesterol and our liver makes this constantly to build cells and repair dead tissue.

But that is a whole other post.

So ... Cells are damaged, the phospholipid membrane leaks into the interstitial fluids (Extracellular fluid) around all our cells.

An enzyme present in this fluid is called Phospholipase (foss-foe-lype-aze). Any enzyme you read about inside our bodies will end with the suffix "-ase".

Now this enzyme breaks down the phospholipids released during injury, and it converts them into an acid called Arachidonic Acid.

Another enzyme present in extracellular fluid called cyclooxygenase or COX for short , now acts on the newly created Arachidonic acid, and converts it into a pro-inflammation protein called prostaglandin.

Many prostaglandins are responsible for stimulating those pain receptors, hence pain.

Application.  Recognising pain is chemically induced by this injury cocktail of substances, let's briefly look at the two big families of anti-inflammatory drugs used for inflammatory pain.

Remember pain is stimulated by the ultimate production of prostaglandins.

Steroid drugs 

These include hydrocortisone, methylprednisolone , Dexamethasone, fluticisone, betamethasone, Prednisolone, and others you are likely familiar with.

These "sone" steroid drugs stop Phospholipase from converting phospholipid into Arachidonic acid.  This stops further stages of inflammation occuring... Including pain.

The other family of drugs is the Non steroidal antiinflammatory drugs.

Abbreviated to NSAIDs, these drugs include ibuprofen, nurofen, aspirin, indocid, naproxen, diclofenac (voltaren).

These drugs inhibit the COX enzyme converting Arachidonic acid into prostaglandins that cause inflammation and pain.

Are we done?   Questions ?

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