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I have completed bits of my EM training from India. Currently I am boarded with credentials from Christian Medical College, Vellore and also from the prestigious Royal College of Emergency Medicine, UK.  I am currently working in London as an A&E doctor, trying to appreciate the differences in the practise and culture of Emergency Medicine across different healthcare systems. I have always been an avid FOAMed supporter because FOAMed played an indispensable role during the days of my initial training. Through this blog, I aspire to disseminate knowledge and stay up to date with the EM literature. 

Monday, April 17, 2017

Transient Global Amnesia

Recently, I was taking care of an elderly female who presented to the ED with isolated amnesia. I thought of some rare stroke syndrome until she was seen by a Neurology attending who called it "Transient Global Amnesia". I was not even aware of this diagnostic entity. 

What is Transient Global Amnesia (TGA)?
Transient global amnesia (TGA) is syndrome characterised by the acute onset of anterograde or retrograde amnesia that can last up to 24 hours in the absence
 of other neurologic deficits. TGA exhibits isolated loss of new memory formation limited to facts and events and patients retain motor tasks and coordination. The classic TGA patient asks the same questions repeatedly in the absence of other signs or symptoms. However, symptoms resolve gradually and spontaneously within 24 hours without the need for medical intervention. The definitive diagnosis of TGA cannot be made until symptoms have resolved. 




How does TGA present?
The classic TGA patient asks the same questions repeatedly in the absence of other signs or symptoms. They exhibit anterograde memory loss. For instance, a patient might repeatedly ask "Have we met before" despite several introductions. Other common concurrent symptoms seen with TGA are headache, nausea, and vomiting. 

What are they key points to cover while examining a suspected TGA?
Do a full neurological exam (Cranial Nerves, Sensory-Motor, Cerebellum, Reflexes). Memory function forms a crucial part of the examination as patients with TGA experience explicit memory loss i.e only the loss of memory pertaining to new facts and events (mainly stored by the hippocampus). By contrast, implicit memories (stored in the cerebellum and the basal ganglia) should not be compromised. For example, a TGA patient retains the ability to operate a car or the ability to open a door with a key. Patients also retain all other cognitive functions. 


1. Test immediate versus delayed recall. Immediate recall remains intact in TGA patients, while delayed recall (after 5 minutes) is impaired.
2. Assess attention span. Executive function abilities such as “serial 7s” or spelling the word “world” backwards remains intact during TGA.
3. Test procedural memory. TGA patients retain task memory (eg, making a paper airplane).
4. MMSE


What is the diagnostic criterion for TGA?
  1. Witnessed at onset and during attack
  2. Must have anterograde amnesia

  3. No focal neurological symptoms or signs during or after

  4. No epileptic features
  5. No clouding of consciousness, no loss of personal identity, and no cognitive impairment other than amnesia

  6. No head injury in the past 72 hours

  7. No seizures in the last 2 years, and not on medication for epilepsy
  8. Must resolve in 24 hours

Differentials for TGA
  • Seizure/transient epileptic amnesia 
(lasts < 1 hour)
  • Stroke (rarely presents as isolated amnesia) 

  • Atypical migraine 

  • Head injury/occult trauma/concussion syndrome 
(Manage as Head Injury)
  • Medication and recreational drug side effect 

  • Herpetic encephalitis 
(fails to resolve in <24hrs)
  • Early neurosyphilis 

  • HIV dementia 

  • Alcohol psychosis 
  • Alcohol blackout 



TGA cannot be definitely diagnosed unless and until all symptoms have resolved in under 24 hours. 

What are the risk factors for TGA?

  • Past history of TGA
  • Advanced Age
  • Migraneous Headaches

Diagnostic Tests
The yield of extensive diagnostic testing in search of occult etiologies is low if history is not concerning and examination is normal. However, certain high-risk patients require extensive workup. Imaging is warranted only if examination is concerning  and when the duration of symptoms approaching 24 hours without resolution of symptoms. MRI is preferred over CT whenever possible to rule out an unusual neurological syndromes. If there is any suspicion of an acute ischemic stroke, immediate computed tomography (CT) should be obtained. EEG can be done to rule in seizures.
Any patient with suspects TGA that does not resolve in 24 hours requires a broader investigation (MRI/CT, LP, EEG), admission, and neurologic consultation.

Who needs a extensive work up?
  • Absence of witness at onset
  • Patients aged < 50 years warrant special consideration, as TGA is rare in young individuals
  • High risk - Immunocompromised, Age<50, drugs/alcohol use, Abnormal Vital Signs

Treatment
  • Administer Thiamine if there is h/o chronic alcoholism
  • Hold medications that may explain amnestic symptoms (BZDs)
  • Admit in ED Observation unit or as an in-patient for 1-2 days and watch until resolution of symptoms
  • Mainstay of Rx is serial neuro examinations until the patient returns to baseline
  • Neurology Consultation 
Most TGA syndromes resolve in < 10 hours. Patients should be observed until symptoms clear. Patients with presumed TGA do not have decisional capacity and therefore must not be permitted to be discharged against medical advice while symptoms are present.



Take Home:

  • TGA is characterised by the acute onset of amnesia that can last up to 24 hours in the absence
 of other neurologic deficits. Symptoms resolve gradually and spontaneously within 24 hours without the need for medical intervention. 
  • The definitive diagnosis of TGA cannot be made until symptoms have resolved. 
  • For a classic case, do minimum tests but pay special attention  to high-risk individuals as well as any patient with abnormal vital signs or unusual symptoms.

References:

  1. Faust JS, Nemes A. Transient Global Amnesia: Emergency Department Evaluation And Management. Emergency medicine practice. 2016 Aug;18(6):1.
  2. Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classi cation. A study of 153 cases. J Neurol Neu- rosurg Psychiatry. 1990;53(10):834-843.
  3. Hodges JR, Ward CD. Observations during transient global amnesia. A behavioural and neuropsychological study of ve cases. Brain. 1989;112 (Pt 3):595-620.
  4. Brown J. ED evaluation of transient global amnesia. Ann Emerg Med. 1997;30(4):522-526. 
  5. Quinette P, Guillery-Girard B, Dayan J, et al. What does transient global amnesia really mean? Review of the litera- ture and thorough study of 142 cases. Brain. 2006;129(Pt 7):1640-1658.
  6. The transient global amnesia syndrome. JAMA. 1966;198(7):778-779. 


Posted by:


              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic

Monday, April 10, 2017

Atrial Fibrillation - ED Management

Pathophysiology
AF is a supraventricular tachycardia that arises from disorganized atrial depolarisation. Electrical remodelling results in multiple reentry circuits or rapidly ring atrial foci and shortening of atrial refractoriness and action potential contributing to the maintenance of AF. Patients with a fast ventricular rate need rate-control medications that slow down the conduction through AV node. 





EKG Findings in AF
  • Presence of low-amplitude brillatory waves on ECG without de ned P-waves
  • Irregularly irregular ventricular rhythm
  • Fibrillatory waves typically have a rate of > 300 beats per minute
  • Ventricular rate is typically between 100 and 160 beats per minute





Why should we treat AF with rapid ventricular rate in a stable/asymptomatic patient?
A persistently elevated ventricular rate during AF (usually > 120 beats/min) for prolonged time periods may result in mitral regurgitation, eventually leading to a dilated ventricular cardiomyopathy (tachycardia-induced cardiomyopathy).



Causes of AF
  • HTN
  • Thyrotoxicosis
  • Acute alcohol intoxication
  • ASD
  • IHD
  • Pericarditis
  • Myocardial Contusion
  • Valvular Heart Disease
  • Pulmonary Embolism
  • Pneumonia
  • Sepsis
  • Digoxin Toxicity
  • Obesity
  • Hypothermia
  • Pre-excitation Syndromes (WPW)


ED Management
The goals of AF management revolve around achieving hemodynamic stability, symptomatic treatment for fast ventricular rate, and the prevention of thromboembolic complications. This post is limited to attaining symptomatic treatment and hemodynamic stability. Use of clinical decision rules regarding the need for oral anticoagulation is not addressed here. 


Who needs immediate Electrical Cardioversion?

Anyone in AF with RVR (Rapid Ventricular Rate) who is unstable needs electrical cardioversion. These are the four signs/symptoms of instability: 

  1. Altered mental status
  2. Ischemic chest discomfort
  3. Acute heart failure
  4. Hypotension
In addition, these two sub-groups are also considered for electrical cardioversion:
  1. AF with rates b/w 250-300 and bizarre QRS morphology (suggesting WPW syndrome)
  2. When medications fail in stable patients


Caveat:  Patients who look well with a BP around 80-90 systolic may be treated with medications to control the rate/rhythm. If they look unwell with the same numbers, then do Synchronised Cardioversion. Don't stick to that arbitrary cut off of 90/60 for everyone. Decision to electrically cardiovert is based on symptoms and clinical appearance. 

Electrical cardioversion is the quickest way to rate control in AF because it converts the patient back to sinus rhythm. Patients with chronic AF will eventually go back to an irregular rhthym. Thus ED management is primarily based on rate control unless they are unstable. 

Procedural sedation and carries a risk of embolic events and cardiac arrhythmias. Analgosedation (Not just sedation) is recommended during electrical cardioversion. Give them some sedation with propofol/etomidate/BZD and add fentanyl/morphine for pain relief. Propofol/etomidate/BZD do not provide any pain relief. 



When doing Synchronised DC Cardioversion, 
  • Start with higher energy gives a better success rate
  • Consider anterior-posterior pad placement for biphasic defibrillators
  • Time with patient’s respiratory cycle, shock during full expiration  

Rate Control v/s Rhythm Control
Multiple studies have shown no difference in all cause/cardiovascular mortality or stroke rate among patients treated with rate or rhythm control. 50% of new AF spontaneously convert to Sinus Rhythm within 48 hours. Pro- longed outpatient attempts to establish or maintain a sinus rhythm in patients with recurrent atrial fibrillation do not offer a clear benefit compared with rate control. AF can present in these 6 ways:
  

1. AF with WPW (Rates more than 200 with bizarre QRS complexes)
Synchronised electrical cardioversion is the primary treatment for unstable patients with an accessory pathway or those who present with a very rapid heart rate, even if stable. Stable patients can be treated with Sync. Cardioversion/Procainamide. Unstable patients certainly need immediate Sync. Cardioversion. 





2. Acute (New-onset) Hemodynamically Stable AF - It is reasonable to start with rate control to relieve symptoms. A good history is needed to figure out the cause (Sepsis, PE, Thyrotoxicosis) and start specific treatment. Almost 50% convert to Sinus Rhythm spontaneously within 48 hours. 

Pharmacological Cardioversion with (Amiodarone/Procainamide/Ibutilide) is also an acceptable option. Before pharmacological cardioversion, ensure that QTc and serum electrolytes are within normal ranges as rhythm control medication prolong QTc and increase the risk of Torsades. 

Patients may not be able to correctly identify the time of onset of AF based on their symptoms and the use of TEE has shown that a clot may be present in the atrium up to 13% of the time in patients with AF < 72 hours duration. Therefore, it is recommended to give unfractioned heparin concurrently (unless contraindicated) by an initial IV bolus injection followed by a continuous infusion. Thereafter, oral anticoagulation (INR 2.0-3.0) should be provided for at least 4 weeks.

Bottomline - Any unstable patient needs immediate electrical cardioversion regardless of acute or chronic AF. If acute, give heparin and do synchronised electrical cardioversion. Very often Chronic AFs are already on oral anti-coagulation obviating the need for concurrent heparin. 

3. Acute Hemodynamically Unstable AF - Treat with Synchronised electrical cardioversion. Always make your best attempts to provide some analgesia and sedation prior to delivering shock. 

There is a another school of thought that assumes that hypotension (unstable) in Rapid AF is due to the rapid ventricular rate. Thus giving rate/rhythm control medications will slow down the heart allowing adequate ventricular filling which will improve the CO/blood pressure. Therefore, it sounds reasonable to try medications but be prepared for cardioversion if medications fail. 

Other causes of hypotension should be investigated before concluding that the rate is causing the hemodynamic deterioration.

4. Chronic Hemodynamically Stable AF -R his is the most common subgroup that presents to the ED with fast ventricular rates. Rate control with CCB/BB/Digoxin/Mg. Amiodarone is falling out of favour due to significant side effects. Check out what Amal Mattu thinks about Amiodarone. 




5. Chronic Hemodynamically Unstable AF - Treat with electrical cardioversion. Check if they are on oral anti-coagulation. If not on oral anticoagulants, give concurrent heparin. The risk of thromboembolism is high as this is long standing AF and thus this subgroup is often treated with rate-control medications to avoid Sync. Cardioversion and subsequent risk of thrombo-embolism. Again, those who support rate-control with drugs use for unstable patients argue that rate control with medication will revert the signs of instability. 


6. Unstable AF who fails Electrical Cardioversion
This is a grey area. One way to reduce hypotension includes pretreatment with push-dose phenylephrine (50-200 mcg every 1-2 minutes) to a goal diastolic blood pressure > 60 mm Hg. IV Calcium (5-10 mL of calcium gluconate) may reduce  hypotensive effects of verapamil without compromising the rate controlling property. Following pretreatment with Phenylephrine and Calcium, slow them down with verapamil (2.5 mg/min continuous drip until heart rate < 100 beats/min (or 50-mg total dose) or amiodarone (150-mg bolus).

Phenylephrine/Calcium premedication prior to Verapamil can be considered for any unstable patient. 


Another way is to treat with antiarrhythmic agent such as amiodarone, ecainide, ibutilide, propafenone, or stall and re-attempt  electrical cardioversion. 

Choosing a Rate-Controlling Agent: With rate-controlling medications We try to prolong the atrioventricular refractory periods, thus slowing atrioventricular nodal conduction.


  • BB: Often the first line medication to treat AF in the absence of pre-excitation syndromes. Beta blockers should be the first drug of choice in patients with congestive heart failure or left ventricular dysfunction, post-operative AF, hypertension, thyrotoxicosis, and acute coronary syndromes. Use BB with caution in patients with hypotension or acutely decompensated heart failure.
  • CCB: CCBs are another first-line medications for the treatment of acute AF. CCB are preferred over BB on COPDs. Diltiazem tends to be more popular than verapamil for acute rate control, as verapamil has more potent negative inotropic and vasodilator effects that may lead to hypotension. 
  • Digoxin: Digoxin has both negative chronotropic and positive inotropic effects, which is particularly useful in patients with congestive heart failure, but the onset of action may take few hours. It is especially useful in hypotensive patients. Digoxin has a synergistic effect with BB/CCB. Verapamil may increase the concentration of digoxin.
  • Mg: Magnesium decreases conduction through the AV node but Mg use is most often recommended only as an adjunctive therapy. Magnesium may also promote conversion to sinus rhythm, with some studies showing 50% to 60% of patients converted to sinus rhythm.



Choosing a Rhythm Control Agent

Options include: Procainamide, Amiodarone, Flecainide, Ibutilide. 


Flecainide and propafenone are reserved for patients without significant structural heart disease, hypertension, ischemia, or heart failure. 

For Preexcitation syndromes such as Wolff-Parkinson White syndrome, the use of AV nodal blocking agents such as beta blockers, calcium channel blockers, and digoxin may induce ventricular brillation and are contraindicated.

Procainamide slows conduction through the accessory pathway and prolong the refractory period in the bypass tract, and they can be safely used in patients in rapid AF with Wolff-Parkinson-White syndrome. Procainamide is safer than Amiodarone in WPW Syndrome. 


Summary:
Management of AF is quite variable and largely dependent on local protocols and physician preferences. From ED management standpoint, rate control remains our priority and sync electrical Cardioversion is reserved for unstable patients, stable patients who do not show improvement with medications alone and for stable patients with an ECG suggestive of an accessory pathway. 

Whenever you try medications for unstable patients, be prepared for electrical cardioversion as these medications have the potential to worsen hypotension. 


  1. AF with WPW - Sync Cardioversion for stable/unstable, Procainamide for stable
  2. Acute Stable AF - Rate Control with BB/CCB/Dig/Mg and wait for spontaneous cardioversion or Rhythm control with Procainamide/Amio
  3. Acute Unstable AF - Sync Cardioversion with concurrent heparin, May try rate control first
  4. Chronic Stable AF - Rate control with BB/CCB/Digoxin/ Mg
  5. Chronic Unstable AF - Sync. Electrical Cardioversion with heparin (if not on oral anti-coags), or rate control with BB/CCB/Mg/Digoxin, Consider phenylephrine/Calcium to premedicate and administer verapamil/amiodarone drip.  
  6. AF Refractory to Cardioversion - After failed shocks, try medications and then shock again or Use phenylephrine/Calcium to premedicate and administer verapamil/amiodarone drip. 

Posted by:


              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic