Category: Medical

Atrial Fibrillation/Flutter (AF)

Before you start 

  • Whats the cause? – treating the precipitant often sorts the AF (adding B-Blockers to Sepsis can make things worse)
  • Stable or Unstable?  – Electricity vs. Drugs
  • CHADS-VASC vs. ORBIT– Anticoagulation (previously HAS-BLED)
  • Rhythm vs. Rate control??
  • NEW Symptomatic Arrhythmia Clinic – referral form attached tho the PDF

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Nitrous Oxide Induced Neurotoxicity

Nitrous Oxide  has been used clinically and recreationally since its discovery in 1772. Since then Nitrous Oxide induced neurotoxicity have been reported, and has been shown to be dose depaendant. With infrequent users unlikely to be at risk of neurotoxicity, while heavier and habitual used at risk of serious neurological conserquences.

With the increase in recreation use of “Whippits” we need to remember to take a detailed recreation drug history when seeing patients presenting to ED with neurological symptoms. As Nitrous Oxide induced neurotoxicity is treatable.


Nitrous Oxide induced neurotoxicity can present as either spinal cord demyelination , peripheral neuropathy or a a combination of the two.

  • Demyelination of the dorsal columns of spinal cord 
    • Typically onset is subacute  (i.e. weeks), but acute onset has been reported in the literature
    • Typically symmetrical but can be unilateral
    • Signs
      • Pyramidal weakness – weak upper limb extensors, and lower limb flexors
      • Dorsal Column Sensory loss – Vibration, Proprioception, Fine touch
      • Sensory Ataxia – Incoordination due to loss of proprioception and weakness
    • Level – Most frequently cervical 4-6 levels, but can affect any.
  • Peripheral Neuropathy
    • Typically Symmetrical (but not always)
    • Sensory loss (often painful)
    • Distal Weakness
  • Optic Neuropathy  – has been reported and may present with visual disturbance.


Nitrous Oxide usage can render vitamin B12 inactive, which in-turn disrupts myelination, causing the demyelination of nerves.


  • Deficiencies: B12, Folate, copper, zinc
  • Inflammatory: Guillian-Barre syndrome, MS, Neurosarcoidosis
  • Infection: HIV, Syphilis
  • Cancer
  • Vascular: Spinal cord ischaemia, vasculitis


  • Vitamin B12 level (often in normal range)
  • Homocysteine and Methylmalonic Acid Level (not available in ED)
  • MRI – contrast enhanced


Start before Tests are back (i.e. on clinical suspicion)

  • IM Vitamine B12 1mg OD
  • PO Folic Acid 5mg OD


  • Discuss admission with Medical team as potential for SDEC management
  • Treat until clinical improvement(King’s Team noted the following)
    • Sometimes treat for 5-7days only
    • Often switch to alternate days IM Bit B12
    • Can teach to self administer
  • Further Testing
    • Homocysteine and Methylmalonic Acid levels – often improve quickly
    • MRI often lags clinical improvement endnote necessary to repeat
  • Majority Improve clinically – but futureabstinence is often challenging



ACS Pathway 2022

When is the ACS pathway used? 

The ACS pathway is for patients where coronary ischemia is in your differential. It is not a blanket pathway for chest pain of unknown cause. 

Patients presenting >8hrs post chest pain 

If an initial trop is taken >8 hours post chest pain, and patients have no new ECG ischaemia, and no history of unstable angina, there is no compulsion to repeat a second troponin. 

ACS Treatment (Not STEMI going for PPCI)

  • Aspirin 300mg stat
  • Ticagrelor 180mg stat
  • Fondaparinux 2.5mg sc stat. 

Anticoagulated with a NOAC, or with Warfarin (with a therapeutic INR),

  • Aspirin 300mg stat
  • Clopidogrel 300mg stat

Treatment STEMI going for PPCI

  • Aspirin 300mg stat
  • Plus Either:
    • Ticagrelor 180mg stat (Hx of CVA)
    • Prasugrel 60mg stat (NO Hx of CVA)

Direct admissions to CCU 

Patients with ST Elevation (if not accepted for primary PCI) or those with CP + new ST Depression should be discussed with a local Cardiologist and come directly to CCU. 

As it is difficult to be prescriptive for every other circumstance, a discussion with a senior / cardiologist may be worthwhile in order to best place your patient within the hospital. Factors that should make you think about a senior discussion are included on the pathway. 

Patients where MI is excluded 

If patients do exit the pathway (no new symptoms, no new ECG ischemia and troponins that meet the exit criteria to exclude an MI), two other important possibilities still require consideration: 

  1.  Is the history in keeping with unstable angina? (This is still an ACS). If so the patient will require an acute inpatient admission with telemetry and IP cardiology review. 
  2.  Is the chest pain due to a significant alternative diagnosis? If so this still needs to be actively considered/ investigated/ treated. 

NB: 2nd Trop should be done >8hr after chest pain (this may be <6hrs from the initial Trop)

Patients on Warfarin/DOAC : Use Asprin and Clopidogrel

PDF: Full Guidance


  • highSTEACS pathway developed in scotland. 
  • When do we take the blood samples? – The initial troponin must be taken at least 2hrs after chest pain, a second trop may be required 6hrs after the 1st  (AAU/CDU)
  • Do we need to do a HEART score? – No, evidence shows the use of risk stratification in these pathways doesn’t increase safety but only increases admissions
  • Can we rule out ACS after the first trop? [Symptoms of Unstable Angina require admission]
    • Troponin <5ng and the ecg is normal we can rule out ACS.
    • Troponin <39ng(female)/58ng(male) and >8hrs from onset of chest pain [this is a pragmatic decision agreed locally by EM/AM?cardiology]
  • Why does it have different cut offs for male/female? – It is known women have significantly lower troponin to men, ESC recommends using the different cut offs 
  • How should we treat transgender/intersex patients – There is no good evidence I can find (I would suggest using the female cut off – as patients who have transitioned to male are probably not going to have as high a troponin, and those who have transitioned to females may have reduced their baseline troponin with hormone therapy) – Be aware the lab can only report against the one registered sex for the patient.
  • Doesn’t highSTEACS have a 3hr Trop too? – Yes it does and in time we will be aiming to utilise this too. However, this relies on using Delta’s (i.e. the change in troponin), and it is felt that it is worth delaying introduction of this until we have got used to the new pathway.
  • Why are the numbers on the official highSTEACS pathway different? – This is because it uses the Abbott test.  the highSTEACS pathway has been also validated on the Siemens assay we will be using. As to why the Abbot and Siemens cut-offs are so different, this is due to the way the assays amplify the troponin present (its not as simple as a U&E that just measures what is there).


Emergency PEG/PEJ/RIG replacement

When a patients with a PEG/PEJ/RIG that has come out attends the ED its important that we can either replace it or insert an EN-Plug OR NG tube into the tract to maintain patentcy while being admitted (how to guide is below)

NG/Foley catheters must not be used to administer fluid or feed nor should the patient be sent home with it in-situ.

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Acute Cystitis and Pyelonephritis Pathway

A joint Medical-Urology pathway has been agreed for Pyelonephritis

Study Running  – Send Urine Sample prior to Antibiotics

(if this does not interfere with treatment of Red-Flag Sepsis)


Imaging in ED is only required if ED suspects:

  • Ureteric Obstruction – Renal colic symptoms/Hx of stone
  • Acute Surgical Abdomen
  • Emphysematous pyelonephritis – Rare necrotising infection of the renal tract, presenting with flank pain and fever, 90% in uncontrolled diabetes mellitus (but immunocompromise and stones also increase chances)
  • Renal Abscess – Presents with flank pain and fever, risk factors include; diabetes mellitus, Renal stones, obstruction

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