Category Archives: Featured

Meningococcal sepsis – lest we forget

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Meningococcal sepsis and meningococcal meningitis

Meningococcal infections are something we don’t see often but we need to know about.  There was an outbreak in Suva, Fiji while I was there.

They may present with meningococcal sepsis, meningitis or both.  They may or may not have a rash.  They may or may not have neck stiffness.  They may or may not look sick.

When I was a young doc I almost sent a child home because who had a fever and purpura, but had no neck stiffness and was walking around looking fine.  Luckily the paediatrician I consulted decided to come in and see the child himself.

Papura can be easy to miss, especially in dark-skinned people: looks at the palms and soles for pupura and look at the conjunctivae and in the mouth, especially on the soft palate, for petechiae.

I treated one of the Suva patients myself.  She was a 22-year-old student from Vanuatu who had mild fever and myalgias the day before.  On the day of presentation she was found confused and hot and brought to hospital.  Her temperature was 38.5, HR 130, no palpable pulse, no BP, no sats reading, her neck was rigid and she had widespread purpura – but this was missed by a good local doctor.  She was alert but confused.  She did not vocalise or responding to questions.

She was given IV penicillin while we waited for ceftriaxone to arrive from pharmacy (consultant order required!).  Cefotaxime is the empiric therapy in some centres.  Neonates required different antibiotics (eg amoxycillin and cefotaxime) to cover maternal vaginal flora and those over 50 usually have ampicillin or amoxycillin added to cover Listeria.  Where there is a high incidence of penicillin resistant penumococcus vancomycin is usually added to the empiric antibiotics.

 

After 2L of IV fluid the local doc ultrasounded her: her IVC was not changing with respiration but her cardiac contractility was reduced.  He used M mode of the anterior leaflet of the mitral valve, see for example http://www.hindawi.com/journals/ccrp/2012/503254/ Minimum distance between the tip of the anterior leaflet of the mitral valve and the septum < 7mm represents good contractility, > 1cm shows poor contractility. She was started on an adrenaline (1mg in 1L of saline, running freely) while a noradrenaline infusion was prepared.  The noradrenaline quickly went up to 20mcg/minutes but the adrenaline wasn’t slowed for several hours.

She was also given intravenous steroids.  Hydrocortisone 50mg.  Starship Children’s Hospital recommends Dexamethasone 0.15 mg / kg 6 hourly for 2 days for children with presumed bacterial meningitis.

After about 4.5L of fluid she became tachypnoic and agitated – I thought we were going to have to ventilate – but there was no ventilator in ICU and no ventilator in ED and no ketamine. Fluids were slowed right down and luckily she settled.

Some would argue that once we saw her IVC was full we should of stopped the IV fluids and just used pressors, thus reducing the risks of volume overload such as ARDS.

A central line was placed.

Within 3 hours of arrival she was sitting up talking and saying thank you.

She was transferred to ICU.

She was transferred out of ICU approximately 24 hours after her arrival in hospital with no sequelae.

Last I heard there were 3 other meningococcal cases in the 6 bed ICU.

Here is some photos from one of them courtesy of Dr Krisneel Krishna

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Typically this is a disease of the young – preschoolers and young adults, but my mother-in-law had it in her 60s.  She was found confused at home, and had no fever, no rash.

In New Zealand we do blood cultures and meningococcal PCR to confirm the diagnosis.  LP in this setting is controversial. There is little utility to doing a lumbar puncture and there are concerns that the patient could “cone” if they have raised ICP from the meningitis. Starship Children’s Hospital says that an LP is contraindicated in a child with meningitis who is “sick or has a rapidly evolving rash” or “haemodynamically unstable” or “GCS < 13″.

CSF can be sterilised within an hour of giving IV antibiotics, so by the time your patient has had their CT to rule out raised ICP it is not that useful to do a LP.  Administration of antibiotics should not be delayed till after the LP.

PCR can not give antibiotic sensitivities.

We didn’t do an LP on the young woman.

 

Audio:

References

http://www.uptodate.com/contents/diagnosis-of-meningococcal-infection

http://www.uptodate.com/contents/initial-therapy-and-prognosis-of-bacterial-meningitis-in-adults

https://www.starship.org.nz/for-health-professionals/starship-clinical-guidelines/m/meningococcaemia/#Lumbar-Puncture

https://www.starship.org.nz/for-health-professionals/starship-clinical-guidelines/m/meningitis/

Music

Monach by Shapeshifter

A Beginner’s Guide to STEMI Thrombolysis: 5 Minutes Door to Needle

The Case

A 57-year-old man was brought in by ambulance with 1 hour of left shoulder pain, nausea and feeling faint.

He had a history of obstructive sleep apnoea and recurrent low back pain.

Paramedics had given aspirin and clopidogrel, obtained IV access and called us saying probable inferior STEMI.

He goes into a resus bay and the team pounce on him: monitoring, ECG, a second IV line, bloods including a troponin, a very focused history and examination.

He is pale but his obs are normal.

These was his first ECG in ED.

Inferior STEMI

It shows an inferior STEMI.  Note the reciprocal ST depression in aVL which helps to support the diagnosis.

See STEMI criteria.

We don’t have PCI so he needed thrombolysis.  Generally we will thrombolyse anyone who meets ECG criteria, has had pain for less than 12 hours and doesn’t have contraindications.

As always, if you are alone at night (or any other time) trying to make this big decision, scan and email, or text a photo of the ECG to someone else for a second opinion.

Contraindications to Thrombolysis

We quickly checked that he didn’t have any contraindications to thrombolysis. You can use a check list for this:

Absolute contraindications
History of any intracranial hemorrhage
History of ischemic stroke within the preceding three months, with the important exception of acute ischemic stroke seen within three hours, which may be treated with thrombolytic therapy
Presence of a cerebral vascular malformation or a primary or metastatic intracranial malignancy
Symptoms or signs suggestive of an aortic dissection
A bleeding diathesis or active bleeding, with the exception of menses; thrombolytic therapy may increase the risk of moderate bleeding, which is offset by the benefits of thrombolysis
Significant closed-head or facial trauma within the preceding three months
Relative contraindications
History of chronic, severe, poorly controlled hypertension or uncontrolled hypertension at presentiaton (blood pressure >180 mmHg systolic and/or >110 mmHg diastolic; severe hypertension at presentation can be an absolute contraindication in patients at low risk)
History of ischemic stroke more than three months previously
Dementia
Any known intracranial disease that is not an absolute contraindication
Traumatic or prolonged (>10 min) cardiopulmonary resuscitation
Major surgery within the preceding three weeks
Internal bleeding within the preceding two to four weeks or an active peptic ulcer
Noncompressible vascular punctures
Pregnancy
Current warfarin therapy – the risk of bleeding increases as the INR increases
For streptokinase or anistreplase – a prior exposure (more than five days previously) or allergic reaction to these drugs

 

So key screening questions to ask your patient:  Are you prone to excessive bleeding, have you ever had anything unusual happen to your brain like a stroke or head injury, does your pain radiate to your back, is it tearing, was it most severe at onset, have you been in hospital in the last 3 months, what medications are you on, could you be pregnant?

Check their blood pressure, check both radial pulses, listen for aortic regurgitation from a thoracic aortic dissection

Treatment Agreement

Discuss the risks and benefits with the patient.

Benefit: one life saved for every 43 people treated within 6 hours of onset of pain  (there are likely to be more who have no or reduced heart failure or angina due to treatment).

Harm: One in 250 recipients will have a haemorrhagic stroke – usually fatal.  2 of the patients I have thrombolysed have bled into their brains and died.  It isn’t pleasant.  There is also risk of other serious bleeding.  If the patient has any of the relative contraindications their risk of bleeding may be highter.

Thrombolysis

We usually use tenectoplase.  Some recommend streptokinase for the elderly as it is associated with a lower rate of intracranial bleeding.

For tenectoplase:

Tenectoplase

Inject the 10 ml of water from the syringe into the bottle with the powder then mix.

tenectoplase gear connected verticle

Tip the bottle and syringe upside down and draw out the required volume of the mixture.  The weight-adjusted dose is on the syringe. Our patient was over 90kg so he got the full 10ml = 50mg.

tenectoplase syringe verticle

 

Weight (kg) tenecteplase (IU) tenecteplase (mg) Volume of reconstituted solution (mL)
< 60 6,000 30 6
60 to < 70 7,000 35 7
70 to < 80 8,000 40 8
80 to < 90 9,000 45 9
90 and up 10,000 50 10

Give it as an IV push over 5 seconds

Other treatments

Give aspirin and clopidogrel if not already given.  Dose of clopidogrel with thrombolysis is controversial.  We currently use 300mg.

Give 30mg IV enoxaparin (omit if > 75 years old or known GFR < 30). Then 1mg/kg SC enoxaparin (0.75mg/kg if patient over 75, max 75mg).

Then we gave him small boluses of fentanyl.  I’m a little cautious with the opioids with inferior ventricular infarcts. They might have right ventricular infartion as well (see below).  I don’t want to venodilate the patient too much.  That would decrease his right ventricular preload and therefore his left ventricular preload.

After 40mcg of fentanyl he was painfree and back to a normal colour.  About 15 minutes post tenectoplase his inferior ST elevation had reduced to ~ 1mm.

Treatment Failure

If his pain persisted and 60-90 minutes post tenectoplase his ST elevation was still > half of what it had been at its largest this would count as failed thrombolysis.  Patients with failed thrombolysis are candidates for urgent transfer for PCI.  Some argue that all STEMIs in peripheral hospitals should be thrombolysed and flown urgently to a PCI capable centre so that they can receive PCI if thrombolysis fails.  This is not the practice in our region.

Door to Needle Time

I was a little disappointed our door to needle time was 5 minutes. We can do better,  eg we could have had the tenectoplase at the bedside before the patient arrived.

Supplementary ECGs

For interest, after thrombolysis, we also did a right-sided and posterior ECG.

We always do right-sided leads if there is inferior ST elevation looking for a right ventricular infarct. We do a posterior ECG when there is anterior ST depression looking for a posterior STEMI

His right-sided ECG (V4, V5 and V6 put on to the R side of the chest) showed ST elevation in V4R and V5R showing right ventricular infarction

RV infarct

The posterior ECG didn’t show any posterior ST elevation.  So this is an inferior and right ventricular STEMI.

Delayed ST Elevation

One last point:  If your patient has chest pain and a normal ECG, then develops ST elevation in front of you: thrombolyse, no matter how long they have had the pain.

Audio

References

Thrombolysis contraindications from UpToDate  http://www.uptodate.com/contents/image?imageKey=CARD/68784&source=graphics_search&rank=0&search=thrombolysis

Tenectoplase dose http://www.medsafe.govt.nz/profs/datasheet/m/Metalyseinj.pdf

Risks and benefits of thrombolysis from the NNT http://www.thennt.com/nnt/thrombolytics-for-major-heart-attack/

Whanganui Hospital ACS Guideline.

 

Music on podcast:  Release by Afro Celt Sound System

A Beginner’s Guide to Procedural Anaesthesia in ED

Procedural anaesthesia is providing IV anaesthesia to allow a painful procedure to be performed.  Very rarely it will be performed to rapidly control dangerous behaviour.

It has also been called conscious sedation or procedural sedation but usually we don’t want our patient to be conscious and we want them to be anaesthetised, not just sedated.  These terms are largely hangovers from the past when we had to pretend we weren’t really doing anaesthesia in ED.

We don’t usually count giving up to 70% nitrous oxide within the realms of procedural anaesthesia as there is very low risk of loss of airway with just nitrous oxide.

Generally the procedure is very similar to performing a rapid sequence intubation (RSI) just smaller doses of drugs are used, we don’t use paralytics and we don’t stick a tube in the trachea.  Otherwise the set up and monitoring is very similar.  This is a bit of over kill for procedural anaesthesia, but it ensures you have all the equipment, staff and drugs you need if anything goes wrong, and it’s good practice for the set up for RSIs so it keeps the team slick.  You can even use the first part of your RSI check list to set up for procedural anaesthesia, modifying it as required.

part RSI checklist

This will make sure you remember all the equipment and steps and will keep everyone familiar with your RSI checklist.

Written Treatment Agreement

Unless this is an emergency procedure eg unstable tachyarrhythmia, procedural anaesthesia requires a written treatment agreement or treatment request form (commonly know as a Consent Form).

You need to disuss and document the risks and benefits of the procedure and the anaesthesia. Risk of anaesthesia are: experiencing of pain, nausea, vomiting, inhaling vomit, confusion, hallucinations (depending on the agent used), allergic reaction to drugs, stopping breathing.  With any anaesthesia there is a tiny chance of death.   The benefits of anaesthesia is that it usually a pleasant, pain free experience with no recollection of the painful procedure.

You may want to make a pre printed treatment agreement form with all of the above alreay on it.

Place

Any bay with suction, oxygen and monitoring could be used.  In our hospital we use a resus bay as has all the gear in it already, and again it helps with team familiarisation with RSI procedures.

Team

Generally we like to have at least 3 staff for procedural anaesthesia.  An appropriately qualified doc to perform the anaesthesia and watch the patient.  A nurse as super can do everything person, helping with preparation, advocating for the patient and monitoring the patient.  They can help with the procedure being performed while keeping an eye on the patient.  The third staff member is usually a doctor performing the procedure itself.  You will need to check what your institutions rules are regarding how many staff are required and what the skill level required is. Generally the doctor performing the anaesthesia will be senior ED registrar (resident) level or above. ACEP allows just 2 staff members to be present, it does not require that 2 doctors are present.

If a consultant is performing the anaesthesia they may briefly help with the procedure while still closely watching the patient.

Medication

The choices of medication(s) varies with every consultant and often will vary depending on the patient and procedure.  Ask the team leader what they want.

For procedural anaesthesia we are aiming for that sweet spot where the patient is maintaining their airway, breathing spontaneously has a good cardiac output yet has no or minimal experiece of pain.

All medications need to be double checked and labeled (prefilled, prelabeled syringes of medication are ideal) and placed tidally in a tray.

Medication is administered by the doctor performing anaesthesia or by a nurse following the doctor’s direct instruction.

Some docs will push the whole predicted dose of anaesthetic, others prefer to titrate slowly eg asking patients to keep their eyes open or to hold one arm up in the air and stopping drug administration when the eyes close or the arm drops.  I prefer to push the predicted dose. Generally we will have more than the predicted dose drawn up in the syringe to allow for top up doses.  Doctor’s must make themselves aware of what is in the syringe.  We have had 2 episodes of doctors getting over excited and just pushing a whole syringe of the white stuff thinking the syringe contained the predicted dose only.

Propofol

Also known as Jackson Juice.  For a very brief procedure eg cardioversion, shoulder or hip relocation, often just propofol will be used.  eg 1mg/kg for a young person, down to 20mg for a 90 year old.

Propofol and Ketamine

For longer or very painful procedures often a combination of ketamine and propofol are used.  This may be in a fixed mg:mg ratio (know as ketafol) or titrated separately.

Ketafol

These drugs work well synergistically.  Propofol gives good anaesthesia and is antiemetic, it’s down side is that it can cause loss of airway reflexes, hypoventilation and hypotension.  Ketamine is very analgesic and dissociative anaesthetic usually with maintained airway, breathing and circulation but can cause unpleasant hallucinations and nausea and vomiting.  The combination allows lower doses of each agent and they negate each others negative effects.

As always doses need to be reduced in the elderly.  Good anaesthesia for cardioversion for an 89-year-old can be achieved with 20mg of ketamine and 20mg of propofol.

For a young person for a quite painful, longer procedure, eg MUA and plastering of a fracture, I will typically give 0.8 mg/kg of propofol and 0.8 mg/kg of ketamine.  If further doses of anaesthetic are needed I will usually just give boluses of propofol alone eg 0.2mg/kg, rather than giving further doses of ketamine to reduce recovery time and to reduce the adverse effects of ketamine.  But every patient is different and you need to be flexible titrating against respirations and response to pain.  It is reassuring that even when patients appear to be experiencing pain they only occassionally remember cardioversions but it seems they never remember the MUAs or I+Ds

I am not in favour of ketamine only anaesthesia.  I have had too many patients, even ones who said as they woke up “Wow, that was amazing”, stop me in the supermarket a week later and say “Hey doc, that drug was awful.”  One of our anaesthetists tells us of having ketamine only anaesthesia then spending the whole night hallucinating he was being repeatedly run over by cars.  A tad unpleasant.

I do rarely use ketamine only anaesthesia for rapid control of dangerous (to themself or others) patients eg ketamine 5mg/kg IM.

Antiemetic

Especially when ketamine is used it is good to add an antiemetic eg ondansetron 4mg or 0.15mg/kg.

Other medications

There are many other drug cocktails used.

Patient

AMPLE history

Allergies (especially to anaesthetic medication)

Medications

Past medical history (yes, I know that is redundant) especially anaesthetic history, family history of anaesthetic problems, obesity and reflux

 

obese

In my opinion this patient is not a candidate for ED procedural anaesthesia.  I gave him 100µg IV fentanyl and 70% nitrous but we couldn’t get his shoulder relocated.  He went upstairs.  (Turned out an anaesthetist with large gonads just gave him a truck load of propofol and face mask ventilated him while a very good ortho reg struggled for 15 minutes to relocate it).

Obese patients are our nemisis.  They occlude their airways at the drop of a hat, they are difficult to ventilate or intubate and they are high aspiration risks.  Just don’t go there for procedural anaesthesia unless it is emergent eg haemodynamically unstable arrhythmia.  Let someone else take that risk.

Last ate or drank, the patient does not need to be fasted according to ACEP, but we may modify things if we know he’s just had 10 beers.

Events: make sure you know the full story about this patient before you put them to sleep.  Is that dislocated shoulder actually attached to a broken neck?

Airway exam

Feel the neck, identify the cricothyroid just in case it all turns to custard.  Assess neck mobility and thyromental distance.  We want4 of the patients fingers (guestimate with your own fingers) between the top of the thyoid cartilage and the bottom of the front of the mandible with the neck extended.  Make sure the patient can protrude their lower teeth infront of their upper teeth and that the mouth opens wide (at least 3 of their fingers (again guestimate with yours if necessary), how much of the oropharynx can you see:

See Mallampati score

Is their anything on their face that would make them hard to ventilate with a BVM?

Positioning

If the patient is obese ramp them so their tragus is higher than their manubrial-sternal joint (blue line in the picture below)

If you are dealing with a lesion on the patient’s back put the patient on their side, not face down.

While you are positioning the patient refresh you memory regarding the bed controls: work out how to tip the patient head down if they vomit

IV Access

One good IV or IO line is enough for procedural anaesthesia.  Make sure it is well secured.

Cautionary tale: beware the IV line in the foot. Some of my colleagues in a land big and red were anaesthetising an elderly patient for a cardioversion.  They gave some propofol, then some more propofol, then some more.  Eventually all the propofol made it to her heart and brain and she had a PEA arrest.  They had the good sense to cardiovert her and give good CPR till the propofol wore off and she made a full recovery.

Some people have IV fluids running (which reassures us the IV line is working and can be used to flush drugs) others find this to be another tube that gets in the way and is probably unneccessary.  Ask your team leader.

Equipment

It’s OCD overkill time.

Size and have out on top of the resus trolley (or under the pillow) all of your airway equipment:

Suction – tested

Bougie

Oropharyngeal airway

Nasopharyngeal airway

Supraglottic device (eg intubating LMA)

Scalpel (I always keep one in my pocket while at work too)

ETT

Stylet

Bag-Valve-Mask (BVM)

Capnography tubing (we don’t routinely use this in our hospital for procedural anaesthesia as the powers that be have decided the consumables are too expensive, but have it out and ready to be used)

Laryngoscopes – tested

On the patient:

Nasal prongs oxygen running at 2L a minute till they are asleep then crank it up to 15L/min.

Non-rebreather oxygen mask with high flow O2.  3 minutes of preoxygenation.

Monitoring x 3 or 4  (depending on whether your hospital uses capnography (see above)

Audible oximetry (“the beeps”)

BP set to go every 2.5 minutes

ECG monitoring

+/- capnography depending on your hospital’s policy

The above rigmarole sounds complicated but takes very little time for a well trained team.

Push or titrate drugs

It’s finally sleepy time.

The anaesthesing doctor, or delegated nurse, pushes or titrates the anaesthetic drugs (see above)

Further top up doses may be required

Procedure, monitoring and apnoeas.

The patient is closely monitored and the procedure is performed.

Have a decent amount of chest and belly exposed so that you can watch the respirations.

Don’t panic if the patient stops breathing.  With the above preparation they will be able to tolerate a long period of apnoea.  If needed you can ask the doctor performing the procedure to inflict some pain or you can do a firm jaw thrust and the patient will usually start breathing again.  If not grab your BVM and start ventilating.  Use other airway adjuvants as needed.  Nasopharyngeal airways are very well tolerated and will sort out most airway occlusions.

Recovery

The anaesthetic is not necessarily over when the procedure is finished.  Especially if opioids or benzodiazepines are used this can be the most dangerous time for apnoeas – the pain has stopped but the drugs are still onboard.

The patient must have one-on-one observation until they are talking clearly.  Once they are talking take the oxygen mask off just in case they vomit.  Have a vomit bowl handy.  Once the patient is talking they should be kept on monitoring (reduce the BP frequency to  q 15 minutes) and watched by reliable family.

The patient is fit for discharge when they can walk independently (or the equivalent for their age and abilities).

Give them verbal and written advice not to drive or operate dangerous machinery until after a full nights sleep and to phone ED if they have any problems.

Images

Ketafol evolution http://eductionlanka.blogspot.co.nz/2013/03/academic-life-in-emergency-medicine_20.html

Facial piercings http://culturewarclasswar.wordpress.com/2012/06/13/the-itch-we-cannot-scratch-imprinted-to-tattoo-body-pierce-and-sun-bathe-in-prenatal-irritationrevulsion-21st-century-and-its-discontents-part-22/

Ramped patient http://crashingpatient.com/resuscitation/airway/airway.htm/

Contagious Calmness. Mindfulness at Work

By practicing mindful meditations we can find calmness within us and then bring this into our work.

We may find that the calmness starts to spread and appears in unexpected places.

Be the calmest person in the room no matter what is going on.

Focus on the people around you, patients, family, workmates, as a way to stay focused on the here and now, rather than lost in thoughts and worries.

Be patient with yourself. It takes time and practice to master these techniques.

Power of Now

The Power of Now is a great book for you, colleagues and / or patients.

Mindfulness for beginners

Some short guided mindfulness meditations from Prof Kabat-Zinn’s book Mindfulness for Beginners are here

 

Music from podcast: Lydia by Fur Patrol

Renal failure, hyperkalaemia, tachycardia. What’s going on?

 

 

Audio

 

A 67-year-old with a Hx of dilated cardiomyopathy, atrial fibrillation and obstructive uropathy presented after a collapse at home.  He said his urine has been white recently.

His temperature was 37.9 in the ambulance, 37.4 in ED.

He was tachycardic at 125, BP 90/60 (it had been 69/49 in the ambulance, in dropped again 81/60 again in ED).  He was euvolaemic.  He had no chest pain.

He had a large bladder and he was catheterised, he drained frank pus then clear urine.

U+E

Electrolytes

 

A flutter name erased

He was treated for urosepsis with IV cefuroxime and IV fluids and his BP improved.

What did the ED doctors miss?

[DDET Click for the answer]

Dig level

The patient was digoxin toxic.

This was picked up by the medical RMO.

Think about digoxin toxicity in any patient with AF who is unwell.  The ED doctor did not get a medication history for this patient.

Patients on digoxin who develop renal failure (in this case probably obstructive and secondary to urosepsis) often become digoxin toxic.

The combination of hyperkalaemia (digoxin blocks the ATPase Na-K pump causing hyperkalaemia) , renal failure and a supraventricular tachycardia with AV block (atrial flutter with variable block, misread as atrial fibrillation) is very suggestive of digoxin toxicity.

Probably anyone with a supratherapeutic digoxin level should be treated with digoxon FAB (antibodies that bind digoxin) eg digifab.  This patient definitely needed it.  He was prescribed digoxin FAB by ED (2 vials).  The admitting general physician cancelled the prescription as the patient wasn’t symptomatic, but was able to be convinced that treatment was a good idea.

Digoxin FAB is very expensive, but failure to treat may be life threatening and results in longer admissions – costing more than the digoxin FAB.

Keep the patient on telemetry for 6 hours.

Don’t retest the digoxin level – the test measures bound and free digoxin and so is meaningless and confusing after digoxin FAB

 

It is very easy to miss digoxin toxicity as elderly patients often have other good reasons for their hyperkalaemia and arrhythmias.

 

By the way, a posterior ECG didn’t show any posterior ST elevation.

 

Further reading:

Why I don’t like digoxin

Why Billy Mallon doesn’t like digoxin

 

Reference

Toxicology Handbook.  2nd edition.  Murray et al

 

Music on podcast 141 by Shapeshifter http://shapeshifter.bandcamp.com/track/141-4

 

[/DDET]

 

Burn this ECG into your brain

63-year-old male with 5 hours of central chest pain

 

Posterior inferior STEMI

What is the diagnosis?

 

[DDET Click for answer]

 

This is a posterior and probably inferior STEMI.

Anterior ST depression is a posterior STEMI (or a Sgarbossa +ve STEMI in the presence of LBBB) till proved otherwise.

To confirm that the anterior ST depression is the reciprocal changes from the posterior ST elevation, do a posterior ECG.

Move V4,5,6 to the posterior chest so they become V7-9 with V8 at the tip of the scapula.

Posterior leads posterior STEMI

The amplitude of the ST elevation on the posterior leads is not impressive – because there is lung between the heart and the posterior chest wall. Life in the Fast Lane says only 0.5mm of ST elevation is required to diagnose STEMI.

This patient was thrombolysed and did well.

And a reminder to document on the ECG the time your read it, your interpretation and your name legibly. DJM (the IIIrd) is not adequate.  Remember that the nurses need you to document the time you read the ECG to prove that they put it under your nose immediately after it was taken.

 

Audio

 

 

Reference:

Life in the Fast Lane. Posterior Myocardial Infarction

[/DDET]

 

The crashing intubated patient: DOTTS

R main stem intubation

Whenever a patient you have just intubated deteriorates, or a patient on a ventilator deteriorates quickly:

DOTTS

Disconnect and let them exhale:

This gets the ventilator out of the equation and simplifies things / reduces our cognitive load: we understand BVMs (bag-valve-mask), ventilators and circuits confuse and scare us.  It also stops ventilation for a few seconds and lets the patient exhale which will help with over inflation / breath stacking.  This is especially important in patients with asthma (see Pop goes the wheezer)

O2 via BVM, slow:

Ventilate the patient slowly with a bag-valve-mask.  Look at the chest movements, listen to the breath sounds.

Is only one side of the chest moving?  Is it a bronchial intubation (check tube depth, see below), a mucus plug (suction the tube, see below) or a pneumothorax (usually unlikely, we’ll check for this later, see below, but if it’s a trauma patient ultrasound and/or perform a finger thoracostomy now)?

Squeezing the bag lets us get a feel for what is going on: is the patient easy or hard to ventilate.  If the bag collapses easily but the chest doesn’t move the tube probably isn’t in the trachea or is disconnected from the bag.  If it is hard to squeeze the bag: it might be a problem with the tube or the patient.  In the above X-Ray the patient has a R main bronchus intubation with R lung hyperinflation and L lung collapse (which happens amazingly rapidly).

Tubes:

Is it in the ETT in right place, is it blocked, is there a big leak (tube too small or has the cuff deflated)?  Check the capnography trace:  Is there a good wave form?  Is the tube at the right depth (around 22cm at the teeth for an adult or ~ 3 times tube diameter (actually 30 times), or black mark on ETT just through the cords in kids)?

Suction the tube.  If the suction catheter goes right down, the tube is patent.   You may suck out a big mucus plug or piece of broccoli.

Tubes is also for a nasogastric or orogastric tube.  If you haven’t got one in get someone to put one in while you continue to trouble shoot, otherwise make sure that is working (aspirate stomach contents, or insufflate air and listen to it gurgle in the stomach.

In the above X-Ray the ETT is down the R main stem bronchus (it was at 19cm at the teeth in a 3 year old) and the NG tube is curled up in the upper airway and has not decompressed the stomach.  Kids especially can be difficult to ventilate, be hypoxic or hypotensive due to gastric distension increasing intrathoracic pressure

Tweak the vent:

Do you need to reduce the tidal volume or respiratory rate if the patient has stiff lungs?  We usually start with a tidal volume of 6ml/kg ideal body weight.

If the patient is ventilating OK but is still hypoxic you probably need to increase the PEEP.

Sonogram:

Ultrasound to look for pneumothorax.  This is last because it is relatively rare.

Get a chest X-Ray as well, but hopefully you will have fixed the problem using the above mnemonic before the radiographer arrives.

 

If the above hasn’t worked (it will sort the problem 99% of the time) get senior help! (if you haven’t already)

Next steps will depend on whether it appears to be a ventilation problem (hypoxia, difficult to ventilate) or a circulatory problem (easy to ventilate but hypotensive).  eg see http://lifeinthefastlane.com/pulmonary-puzzle-013/

 

The above patient apparently tolerated the misplaced tubes very well and the only clue was an end tidal CO2 in the hundreds.  With repositioning of tubes the patient quickly improved.

Audio:

 

 

Reference:

http://emcrit.org/wp-content/uploads/2013/08/The-crashing-ventilated-patient_EMCrit-Conference.pdf

Music (on podcast)

Nga Hau e Wha by Hui-a  https://itunes.apple.com/nz/album/got-to-live-ep/id318363878 www.jeromekavanagh.com

 

LBBB and Sgarbossa

 

Left bundle branch blocks cause a lot of confusion.

People often mistake the normal anterior ST elevation of LBBB as an MI

Less frequently people miss significant concordant ST segment changes which may be a STEMI (by Sgarbossa Criteria)

The Law of Discordance or the Law of Appropriate Discordance

In a normal LBBB the ST segments should be isoelectric or go be in the opposite (discordant) direction from the dominant part of the QRS

LBBB

So typically in V1 the QRS is mainly negative and the ST segment in elevated.  This is normal for LBBB

In V6 the QRS is mainly positive and the ST segment is down.  This is normal for LBBB

Modified Sgarbossa Criteria for diagnosing STEMI in the presence of a LBBB

If there is concordant ST changes (ST segments in the same direction as the dominant part of the QRS) or a discordant ST elevation of greater than 1/4 of the amplitude of the S wave.

A: Concordant STE ≥ 1mm (in any lead) = Most specific for MI


B: Concordant STD ≥ 1mm in V1, V2, or V3 = Specific for MI


C: Discordant STE > 0.25 R or S wave

So, for example the ECG below shows a concordant ST depression in V3 (circled).  This only needs to be in a single lead. Therefore this meets Sgarbossa criteria for diagnosing a STEMI.

Sgarbossa

 

All of this applies to patients who have ventricular pacing as well (which usually causes a LBBB pattern on ECG)

This patient was not diagnosed as a STEMI, did not receive reperfusion therapy and died 9 hours later (but to keep this in perspective, in that hospital the patient would have had to be thrombolysed and there is only around a 1 in 43 chance that thrombolysis would save the average patients life even if given within 6 hours).

 

This ECG shows Sgarbossa +ve concordant changes in I, aVL and V3 (so Sgarbossa A + B)

Sgarbossa from Mattu

 

Here are some examples of Modified Sgarbossa C +ve complexes:

 

Modified Sgarbossa c from mattu

Most of us regard Sgarbossa as an indication for revascularisation (PCI or thrombolysis) because it has greater specificity for MI than standard STEMI criteria, but it is not in black and white as a criteria in the latest definition of MI.

If in Doubt

… get a second opinion.  If you don’t have senior support (eg smaller hospitals overnight) email (or take a photo on your phone and text or email, or fax) the ECG to the relevant specialist then phone them to get their interpretation.

Documentation

Time ECG read

Your interpretation

When repeat ECGs are needed (if they are)

Your name (get a stamp)

 

Slides

Audio only

 

References

Sgarbossa Criteria.  Life in the Fast Lane http://lifeinthefastlane.com/ecg-library/basics/sgarbossa/
Thrombolytics given for Major Heart Attack (STEMI).  The NNT. http://www.thennt.com/nnt/thrombolytics-for-major-heart-attack/

 

 

The future funding of FOAM

Free Open Access Medical Education or FOAM has been free to users and producers largely due to the generosity of this man

Cadogan1-280x200

the Godfather of FOAM, Mike Cadogan.

When I last spoke to him over a year ago, he was pouring over $75,000 a year of his own money to pay for technical support, Word Press fees and bandwidth to make FOAM happen.

A lot of us, me included (probably one of the narcissists he refers to), have taken this philanthropy for granted.

I have recently looked to getting funding from my employer to start another FOAM project, thus not putting more financial burden on Mike, but was quite happy to let him keep funding this website, leaving me only paying US$ 20/month for the audio hosting.

In the last few days we have had a wake up call from Mike in his post 5 Lessons Learned  This post is partly about self-care, valuing real life family and friends over a virtual life, and saying no, but it is also about the financial cost of FOAM.

We the FOAM producers need to find alternative, sustainable funding streams for FOAM.  I’m sure many already are eg EMCRIT’s CME option. Others of us need to obtain funding.  5 years from creation, FOAM has proved itself as one of, if not the of the best forms of medical education and practice improvement.  Now we need to get our employers and institutions to recognise this and fund FOAM.

We each need to go to our employers and say FOAM is the best thing in Continuous Quality Improvement (or what ever the latest buzz word is) since sliced bread and they need to contribute to it.

I have asked The Frontier Group, who provides a lot of the technical support for FOAM, for the true monetary cost of EM Tutorials (and for my next FOAM project), and I have started negotiations with my employer to get it to pay those costs.

In New Zealand each District Health Board gets tens of thousands of dollars a year per junior doctor of government funding for training.  This money largely just disappears into the hospitals’ coffers.  We need to claim some or all of that money and actually use it for education.  I’ve started negotiations at my hospital to have at least a good chunk of this money ring-fenced for education, managed by an education committee, and some of that will go to funding this website and podcast.

I suggest other FOAM producers start similar negotiations with their employers so that there is Learning and Development money  being used to ensure the amazing educational resource, that Mike has largely created and funded himself, is sustainable without draining his pocket anymore.

Peace

Out

 

 

 

Trauma: Lessons from the Military. Wing Commander Dr Paul Nealis


 

 

Key points

Stop bleeding!

Tourniquets are great.

Pack bleeding wounds firmly.  A roll of gauze works well. “Haemostatic dressings” eg quik clot, don’t seem to make much difference.  It appears the pack needs to be absorbent probably because they absorb water out of the blood in the wound thereby increasing the concentration of clotting factors.http://emtutorials.com/wp-admin/post-new.php

Don’t get hung up on big IV lines.  The difference in flow rate between a 18 and 16 gauge is not that great.  If the patient is bleeding out that fast they aint going to make it, and sometimes 18s are just easier to get in especially in a shocked patient.

Permissive hypotension: aim for a systolic of 80 (90 if head injury).  Don’t rely on mental status (BP 60 systolic but compensating and still conscious… 60 and compensating  still conscious …. 60 and still conscious … dead).

For massive haemorrhage transfuse and give tranexamic acid early.  For us this may mean sending an “unknown patient” label down to get some O-negative blood from the lab before the patient arrives.  Get FFP thawing ASAP. Get platelets ASAP.

Use ketamine rather than fentanyl in major trauma -> lives saved,  presumably by avoiding the sympatholytic effects of fentanyl

Ketamine appears to reduce the incidence of Post Traumatic Stress Disorder by 60%!  This may be by reducing the patients’ experience of pain and mutilation.

ED teams (in the military ED docs and nurses and military medics) resuscitate the patient, others behind the red line.  When the external bleeding has been stopped and the patient resuscitated, then the anaesthetist and surgeon are invited to take the patient to theatre/operating room

Some of the slides:

Audio only: