Syncope assessement
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Transcript of Syncope assessement
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)
ES
C G
uide
lines
on
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J 20
09 (
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
The
Pic
tury
stu
dy: E
dvar
dsso
n et
al:
Use
of
an i
mpl
anta
ble
loop
rec
orde
r to
incr
ease
the
diag
nost
ic y
ield
in u
nexp
lain
ed s
ynco
pe; P
ictu
re r
egis
try
; Eur
opac
e; F
eb 2
011;
13
92):
262
-269
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
The
Pic
ture
Stu
dy: N
.Eva
rdss
on e
t al,
Eur
opac
e 2
009
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: [email protected]
ISS
UE
; Int
erna
tiona
l Stu
dy o
n S
ynco
pe o
f un
kno
wn
etio
logy
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
ES
C g
uide
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200
9
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
tem
ber
2014
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)