SYNCOPEA systematic and evidence based approach

Anne-Marie de Vries

Case76 Years old ♂

Sudden LOC, without prodromal symptoms

On his way from the couch to the fridge with a glass in his hand

Hit the floor with his right side of the head , bruises and lacerations rightsided, pieces of glass in skin on the right side. Bruised right shoulder

Wife, situated in next room suddenly heard a big “clatter”

No complaints, no palipitations, nil chest pain, no PTA

Physical ExaminationHR 130 irreg, BP 140/80 mmHg, GCS 15, RR 20, JVPNE

Palpitation of the skull; no crepitations, right sided lesions

C-Spine, nil tenderness midline & paravertebral

Chest; dual HS, nil murmurs, irreg, normal air entry on both lungs

Abdomen ; soft Pelvis stable

Nil fractures of extremities

Past Medical History• 2010 Anterior STEMI (LAD lesion), stented BMS.

• AF, on warfarin

• HTN

• Diverticulosis

MedicationWarfarin, Ramipril, Atenolol, Simvastatin, Panadol-osteo

ECG

Approach ?

CME Lecture Syncope1. Introduction

2. Guidelines (EB medicine.net)

3. Other existing guidelines; ESC, ACEP, UptoDate, Library SCGH-ED, LITFL

4. Take Home Message

What is Syncope ?Transient loss of consciousness and posture with spontaneous return to baseline neurologic function without resuscitative efforts (due to global cerebral hypoperfusion)

Characterized by: rapid onset, short duration, spontaneous complete recovery

Definition

Syncope is a symptom with a wide range of underlying conditions

Pre-Syncope

Almost losing consciousness

Emergency Medicine PracticeEBMEDICINE.NET

Syncope: Risk stratification and Clinical Decision making

S.Y.G Peeters, MD

A.E Hoek MD Rotterdam & The Hague The Netherlands

S.M. Mollink M.D

J.S.Huff MD, Professor EM and Neurology Virginia, USA

April 2014, Volume 16-4

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Guideline Ebmedicine.netCAT Critical Appraisal of Literature

Piramid of Evidence

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CAT• National Guideline Clearinghouse

• ACEP/ESC/NICE/CCS

• Primary Literature search: Ovid Medline/Embase/Cochrane; search terms;

1310 English articles

• Excluded; in hospital syncope

• Excluded: Case reports, expert opinion, letters, editorials

Literature consists mainly of prospective and retrospective cohort studies with small sample sizes

Geography

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Syncope-Numbers• 1-3% of all ED visits* (SCGH: 65.000 visits per year; 1950)

• Incidence increases with age (increase > 70 years)

• Patients presenting to the ED have a higher pretest probabilty of significant pathology compared to the general population**

• Use of algorithms* results in a reduction of undiagnosed cases from 70-50% to 25-17%***

• All cause mortality rate after ED visit for syncope is 1.4% at 30 days to 4.3% at 6 months and 7.6% after one year !

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3 Major Categories

1.Neurally mediated (=reflex-mediated)

2.Orthostatic-Hypotension

3.Cardiovascular-mediated

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Neurally-mediated SyncopeReflexes that control circulatory homeostatis become dysfunctional

1.Vasodepressor type: loss of upright vasoconstrictor tone

2.Cardio-inhibitory type: bradycardia

3.Mixed-type

Most frequent diagnosis in all age groups (60.2%)

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Neurally-mediated Syncope• Precipitated by trigger event: or orthostatic stress; fear, severe pain,

strong emotion, instrumentation (venapuncture) or vasovagal

• Situational syncope; coughing, micturation, defeacation, vomiting or swallowing

• Carotid sinus stimulation

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Orthostatic-mediated SyncopeAbnormal fall in SBP > 20 mmHg or increase of 20 in heart rate * resulting in a global cerebral hypoperfusion and symptoms

Common causes

1. Volume depletion; diarroeah, vomiting, hemorrhage

2. Autonomic nerve dysfunction

-Primary dysfynction; Parkinson’s - Secondary; DM,

- Drugs: Alcohol, diuretics, vasodilators

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Cardiovascular-mediated Syncope• Dysrhythmias most frequent cause:

intrinsic (SSS, pre-excitation, Brugada, LQTS) extrinsic (drugs; QT increasing drugs or beta blocking drugs, ischemia)

• Structural cardiovascular disease: Valves, pericardial, myocardial

• Obstruction; Massive PE (20%), Aortic dissection

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Subclavian Steel Syndrome• Rare syndrome caused by proximal narrowing of the subclavian artery.

Movement of the ipsilateral arm causes shunting from the vertebrobasilar system (into the arm musculature) due to reverse flow in the vertebral arteries resulting in cerebral hypoperfusion

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Differential Diagnosis-TLOCWithout global cerebral hypoperfusion

Without characteristics ; sudden onset, short duration, spontenous recovery

Causes of Transient Loss of Consiousness (TLOC): -Stroke, TIA (vertebrobasilar) -Subarachnoidal/subdural/epidural hemorrhage -Seizure -Metabolic -Toxins

Disorders that may mimic Syncope (no TLOC):

Cataplexy

Drop attacks

Psychogenic

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Approach• 1 Identify life-threatening causes

• 2 Systematic evaluation for etiology

• 3 Risk stratification for Adverse Events if etiology remains unclear

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History Highlights1. Consider syncope a life threatening event until proven otherwise

2. Start with a broad differential

3. Collateral history

4. Family history of cardiac sudden death

5. Review patient medication list (β-blockers, QT)

6. Be very wary with patients with inserted cardiac devices; pacemaker malfunction !

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Important historical facts• Prior to the Onset (activity, prodromal, circumstances)

• At the Onset of the episode (Associated symptoms, timing of symptoms)

• Witness information (Fall, injury, duration of loss of consciousness, movements, associated symptoms)

• After the episode (Mental status, associated symptoms)

• Past Medical family history, cardiovascular history, neurological, medications, previous events)

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Physical Examination• Abnormal vital signs

• Neck veins (distended)

• Capillary refill time*, mucosa

• Orthostatic hypotension*

• Murmurs, peripheral pulsus, cyanosis, edema

• Abdomen; palpable masses, PR examination

• Systematic neurological examination

• Trauma ? Head/C-Spine injuries ? Injuries ?

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ECGA normal ECG has a high predictive negative value

Focus on

1. Ischemia

2. Conduction disturbances

3. Pre-excitation pattern (delta wave, short PR-interval)

4. Prolonged QT (QTc)

5. Brugada sign

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Brugada• First described by brothers Brugada in 1992

• Mutation myocardial sodium channel deficit*

• Diagnosis= Brugada sign AND clinical criteria**

• Type 1 Brugada is diagnostic in ECG***

• 30% of Brugada’s present with Syncope as a first episode

• Therapy=ICD

• Screening ?

• Brugada is one of 4 type channelopathies

Additional investigations• CXR; low diagnostic yield

• CT Head and C-Spine: unless clear radiologic abnormalities or trauma

• Laboratory testing: β HCG in ♀♀

• Biomarkers ?

• Pacemaker interrogation in patients with a cardiac device

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Carotid Sinus Syndrome• Carotid Sinus Hypersensitivity after massage at Carotid Sinus

bifurcation

• CSH if CSM results in a ventricular pause > 3 secs and or fall SBP > 50 mmHg

• If these combine with syncope the diagnosis CSS is made

• CSH is more often in elderly male individuals

• CSH is unusual < 40 jaar

• Complications of CSM are neurological; do not perform in patients with a TIA, stroke < 3 months or carotid bruits (only if Duplex is negative)

Tilt table test

Confirm Dx of NMS in suspected patients (but not already proved by clinical history)Differentiation in patients with cardiovascular disease or heavy jerky movementsPrognosis relevant (eg pilots, truck drivers)

Different protocols with different subsequent sensitivity and specifityMain used protocols with isoprenaline or GTN

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Prolonged cardiac monitoring• Highest diagnostic yield in patients with cardiac history and abnormal

ECG

• Monitor high risk patients 24-72 hours (especially elderly patients with heart-failure)

EchocardiographyUsefull in patients with unexplained syncope with a cardiac history or abnormal ECG (yield 27%)

Patients with CAD/previous MI and syncope and reduced LVEF have an increased risk of sudden death ! (ACC & AHA class I and II recommendations for ICD therapy)

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30),

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Implantable Loop recorders ? (ILR) Advantage:

36 months loop ECG recording

activated by patient or predefined arrhythmia detection

If Diagnostic in unexplained syncope proven to be cost-effective

Disadvantage:

minor surgical procedure

high initial costs

difficulty distinguishing SVT/VT

farfield sensing fills up the memory loop

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Picture Study• Prospective multicenter observatory study 2006-2009 in 10 European

countries & Israel

• Indication: recurrent unexplained syncope or pre-syncope

• FUP: 1 year or up to event; leading to diagnosis

• In course of study; pts were evaluated by 3 different specialists, had a median of 13 tests (9-21) and 36% of patients experienced significant trauma with syncope

• 218 events were detected by ILR, in n=170 (78) of which 128 (75%) were of cardiac origin

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The Kaplan–Meier estimates of time to syncopal episode (green line) and time to syncopal episode where Reveal played a role in the diagnosis (red line).

Edvardsson N et al. Europace 2011;13:262-269

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2010. For permissions please email: journals.permissions@oxfordjournals.org

ISS

UE

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Issue classification of ECG recording Classification Suggested

mechanism

Type 1 Asystolie RR int > 3 sec 1A Sinusarrest1B Sinusbrady+AVblock1C Sudden onset AV block

ReflexReflex

Intrinsic

Type 2 Brady HR decrease > 30% or < 40/min for > 10 sec

Reflex

Type 3 No slight variation in HR

Uncertain

Type 4 Tachy HR > 120 or increase > 30%

1 Sinustachy2 AF3 SVT4 VT

UncertainArrhythmiaArrhythmiaArrhythmia

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Risk factors*• 1 Cardiovascular findings

Structural heart disease

Cardiovascular disease

Congestive heart failure

Abnormal ECG

Inserted cardiac devices

• 2 Evidence of bleeding

AAAA

Gastro-intestinal

Ectopic Pregnancy

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Short term high risk ECG criteria*ECG

Mobitz II

Bifascicular block

QRS > 0.12 s

Non sustained VT

Long and Short QT interval

Saddleback V1-V3

Negative T s in right precordial leads, epsilon waves & ventricular late potential

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Risk Stratification Decision Rules• No single rule is sufficiently sensitive or specific to be used in the ED

setting

• Adverse events are rare so syncope studies must recruit large numbers to be sufficently powered

• Variation in inclusion criteria and definitions add to complexity of interpretation

• Most external validation studies do not reproduce the same sensitivity and specifity HOWEVER they do correlate with ADVERSE outcomes

sour

ce: A

LIE

M

Risk Stratification Decision Rules

SFSR• C = History of Congestive Heart Failure

• H= Hemotocrit < 30%

• E = Abnormal ECG

• S = Shortness of breath

• S = at Triage: SBP < 90 mmHg

OESIL points collected

• Age > 65 years1

• History of cardiovascular disease 1

• Syncope without prodromes1

• Abnormal ECG1

• > 2 points increased risk for cardiac death

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Clinical Pathway for syncope (page 12)

1 Identify life-threatening causes2 Systematic evaluation for etiology3 Risk stratification for Adverse Events if etiology remains unclear

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Disposition at risk groups• High risk patients

• Low Risk patients

• Intermediate risk patients

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High Risk

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Low Risk

Clear benign cause and patients with unclear cause but without risk factors < 40 years+ normal physical examination+ normal ECG

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Intermediate Risk• Most difficult approach, their mamangement remains unclear

• Management relies on risk stratification application of the (EM) doctor

• Observation unit ?

• Non cardiovascular-mediated consider tilt table testing*

Elderly• Mostly due to OH (medication), reflex (CSH) and cardiac arrhythmia

• OH: not always reproducible at ED

• Gait, balance and slower protective reflexes contribute to higher incidence of falls. Cognitive impairment may alter the mechanism or amount of falls. Witness or collateral info is important !

• CSM, 24 hrs BP measurement, MMSE, ILR ?

• Tilt table testing is safe

Children• Mostly reflex syncope*

• Life threatening triggers in history: minority of children !

-Family history of SCD < 30 years

-Triggered by load noise, freight, extreme emotional stress

-Known or suspected cardiac disease

-Syncope while exercising (including swimming)

-Syncope while lying supine or sleeping, preceeded by chest pain or palpitations

Most syncope in children are benign and therapy should mostly be avoided

LIF

TL

Sep

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Discharge criteria• They do not have significant clinical risk factors, including:

abnormal ECG CVS risk factors Initial hypotension Initial history of shortness of breath

• Witnessed seizure activity or a history of seizures, especially when the event is unwitnessed

• Observations and clinical findings are normal

• Medications reviewed

• Safe home environment (especially the elderly)

• If uncertain then observe for 24 hours

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Driving ?• Restrictions to driving in patient with clearly benign cause is not

indicated

• Two studies reported a 10% patients experiencing syncope while driving (37% neurally mediated, 12% cardiac dysrhythmias) syncope recurrence rate was < 1%

• Consider the professional drivers & divers as a separate group; Truck drivers, bus drivers, pilots

Summary• 3 step Approach

• 1 Life threatening condition present ?

• 2 Determine the underlying etiology

• 3 In unclear etiology; perform risk stratification

Take home message

History, physical examination and ECG will unreveal most life threatening causes

Back to the case• Risk stratification ?

Age

Cardiovascular disease (STEMI)

Non sinus rhythm

No prodromal symptoms

General Medicine discharged patient from the ED with the suggestion to repeat an Echocardiography in out patient clinic (if not recently made)

Questions ?

Literature• EBmedicinenet, Syncope, risk stratification and clinical decision making,

S.Y.G.Peeters et al, Vol 16-4, April 2014

• ESC guidelines on Syncope, EHJ, 2009 (30) 2631-2671

• UptoDate; D McDermott, MD et al, last update 2014

• Local guidelines: J.Jeffers, Mainly based on EMP 2004 (edited 2009)

• Syncope, LIFTL

• Brugada: LITFL, ECG Library,

• ESC congres; Channelopathies, wich way to go ?

• ACC/AHA guidelines for defibrillator therapy

• PICTURE study (Reveal ICM guidelines, Edvardsson, Europace, February 2011;13 (2):262-269)