Cliff Reid Profile picture
Sep 29 19 tweets 5 min read Read on X
Early 40s male with chest pain and collapse, looks horrible, SBP 80, lactate 7.
Previous large PE with pulmonary hypertension on echo 2 months ago, discharged on apixaban
POCUS on arrival shows:



The POCUS findings are consistent with cor pulmonale but in view of his previous echo, how do we know this is the acute cause of his shock? Should we thrombolyse?
His ECG shows right axis deviation and T wave inversion. This was NEW compared with the ECGs on record from his previous admission Image
Extending the POCUS down his IVC to his legs, his right common femoral vein was non-collapsible and contained echogenic material consistent with thrombus.

These data combined were enough for us to consider thrombolysis for acute massive PE
While alteplase was being prepared he had a CTPA (CT scanner within ED), confirming large bilateral pulmonary emboli
Image
Image
The CT also confirms right heart strain by the relative size of right and left ventricles Image
Another interesting CT finding was possible pulmonary infarcts
Image
Image
He was returned to Resus and consented for thrombolysis and advised of potential risk of haemorrhage including intracranial and pulmonary (because of the infarcts)
As the alteplase was begun he felt worse and dropped his BP Image
He was started on peripheral noradrenaline/norepinephrine but continued to deteriorate. He was given nebulised (iv) GTN 5mg then nebulised (iv) milrinone 5mg according to our non-official, not-publicly-endorsed evidence-sparse crashing PE quick reference guide Image
A femoral arterial line was placed under US guidance
He was placed on high flow nasal cannula oxygen FiO2 1.0, 30 l/min, not because his SpO2 was low, but because oxygen is a pulmonary vasodilator

The noradrenaline was increased
His BP, conscious level, and lactate improved. He was transferred to the ICU on 0.08 mcg/kg/min iv noradrenaline with a SBP of 105, MAP>65
The alteplase was still running (2 hr front loaded protocol)
Mindful that he'd gone to ICU before we'd started unfractionated heparin, I sent a text message to the intensivist to let her know he hadn't had heparin

This was her reply Image
The team did a great job saving this patient's life. It illustrates a few important learning points:
1. Cardiac POCUS is essential in the immediate assessment of patients with undifferentiated hypotension
2. Massive PE causes RV failure not just from mechanical obstruction due to clot, but from additional pulmonary vasoconstriction in non-occluded pulmonary arteries

A resuscitation strategy for acute RV failure includes ways to reduce RV afterload including pulmonary artery vasodilators
3. Our hospital does not have access to inhaled nitric oxide and is not an ECPR centre. We had to think creatively about how we can look after a crashing RV with what we have. We've used our crashing PE quick reference guide a few times now but I stress it's not validated or offically approved by any serious body
If you want to read more about the RV and inhaled GTN & milrinone, read this fantastic post by @PulmCrit emcrit.org/ibcc/pulmvaso/
Thanks for reading this resus case!

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More from @cliffreid

Jul 19
Here’s how I think we often fail our patients when treating ’sepsis’

a 🧵

1/11
In my capacity as both an emergency medicine and intensive care specialist I’ve observed that we sometimes:

- 1. Inappropriately diagnose other shock states as sepsis

2/11
- 2. Fail to use System 2 thinking when faced with hyperlactatemia

- 3. Fail to examine septic patients mindfully with a thorough ‘sepsis secondary survey’

3/11
Read 11 tweets
Nov 23, 2023
WTF is a ‘difficult airway’?

A 🧵

1/14
I avoid the term ‘difficult airway’ altogether

How we describe a situation can have a psychological framing effect that can affect our performance

2/
Mindset, confidence, and therefore performance are likely to be worse if you expect the airway to be ‘difficult’ rather than prepare for it to be ‘potentially challenging’

3/
Read 14 tweets
Nov 20, 2023
Let's review an intubation together - a 🧵
A previously well patient in her 60's presents with a first seizure & post-ictal coma
A nasopharyngeal airway has been placed for airway patency
She weighs 100kg
She receives 70mg propofol /100mg rocuronium after checklist completion, pre-ox & application of nasal cannula O2
This video shows what a nasopharygeal airway looks like, and how far it can go down

It was removed during laryngoscopy- not sure why. Consider leaving it in in case you need it to support facemask ventilation if laryngoscopy is unsuccessful
Read 11 tweets
Sep 15, 2023
Stopping someone from bleeding to death requires many keys steps

Our team uses this cognitive aid

Page 1 covers general measures to guide vascular access, haemostatic resuscitation, reversal of anticoagulation, and optimising of clotting

1/10 Image
Page 2 gives specific guidance on managing the location of haemorrhage, eg. epistaxis, haematemesis, etc

2/10 Image
We use this to ensure things aren't forgotten, such as maintaining normocalcaemia and normothermia, and that doses are at our fingertips, eg. for prothrombin complex concentrate or terlipressin

3/10 Image
Read 10 tweets
Jul 21, 2023
Very short🧵on AF in hospital 1/5

Atrial fibrillation in hospital often starts from interplay between underlying risk factors (substrate) & acute triggers Image
The 3 A's of acute management are

1. Acute trigger identification & management

2. AF rate/rhythm control

3. Anticoagulation - BUT:...

2/5 Image
...the risk/benefit assessment for anticoagulation must take into account the acute presentation

The approach that's used in chronic AF does not necessarily apply

For example, AF in common in critically ill patients, such as those with sepsis

3/5
Read 5 tweets
Dec 1, 2022
The iGel is a great supraglottic airway device

But like other supraglottic airway devices (SAD) it's not foolproof

Here's how to maximise your success with the iGel - a thread 🧵
Adequately positioned SADs produce a good seal and no leak
Ideally the iGel cuff should sit snugly over the larynx
Read 22 tweets

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