Download Investigation of syncope

Journal of the Accident and Medical Practitioners Association (JAMPA) 2009; Vol. 6 (No. 1)
 Accident and Medical Practitioners Association, New Zealand
___________________________________________________________________________
Review Article:
Investigation of Syncope and Proposed Case Audit
Stephen Adams, MBChB, DipAnaes (UK), FAMPA
Goodfellow Unit, University of Auckland School of Medicine, Auckland
About the author:
Dr Stephen Adams, MBChB, DipAnaes (UK), FAMPA, is Senior Lecturer in Community
Emergency Medicine at the Goodfellow Unit, University of Auckland School of Medicine,
Auckland. He is also a member of the Editorial Board of the Journal of the Accident and
Medical Practitioners Association (JAMPA).
Correspondence: Dr Stephen Adams, MBChB, DipAnaes (UK), FAMPA, Goodfellow Unit,
University of Auckland School of Medicine, Private Bag 92019, Auckland.
E-mail: [email protected]
Issues this article will address

Causes, diagnosis and differential diagnosis of syncope

Classification of syncope based on the triggering event

Decision rules for syncope (to stratify the risk and reduce the number of patients
admitted for more detailed investigations)
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Salient Points

The immediate investigation of syncopal episodes should consist, firstly, of
excluding other possible diagnoses.

Individuals with a clear history should be assessed for a risk of serious underlying
pathology, which is mainly of a cardiovascular nature.

Rules for stratifying that risk have been created to reduce the load of mainly
inpatient investigation, but as yet have poor specificity.
Key words: Syncope  Presyncope  Collapse  Convulsion  Diagnosis  Classification 
Risk stratification
Introduction
The presentation of a patient who has “passed out” or “has had a turn” is common in acute
medicine but includes a myriad of possible diagnoses, with prognoses ranging from the very
benign to life-threatening. Likewise, possible investigations include most of the diagnostic
modalities known to medicine, so an approach is required that is both economical but able to
rule out common serious illnesses and identify the group in need of hospital work-up. This
article reviews current thinking on the subject and outlines a possible audit process for
learning purposes.
As there are a number of categories of collapse, it is useful to review medical and popular
terminology:
 Collapse
(Popular): fall to ground without external input; cease to function due to a
sudden breakdown
(Physiological): abrupt loss of postural tone[1]
 Faint
(Popular): collapse with loss of consciousness and no convulsion.
Synonym: “pass out”
 Syncope
(Physiological): loss of tone and consciousness due to brain hypoperfusion
or global cerebral nutrition
(Clinical): a sudden and brief loss of consciousness associated with a loss
of postural tone, from which recovery is spontaneous[2,3]
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 Presyncope Lightheadedness, altered subjective state without loss of consciousness
and attributed to a syncopal mechanism.
Differential Diagnoses
There are a number of differential diagnoses. The main categories are listed below along
with the clinical assessment most likely to contribute to the diagnosis:
Differential diagnosis
Clinical assessment
Convulsion
Eyewitness account
Narcolepsy
History
Psychiatric disorder
History
Cataplexy
History
Trauma ‘KO’d’
Eyewitness account
Cerebrovascular accident
Neurological examination
Toxicity
History, investigations
Breath-holding
History.
Convulsion
The most important differential diagnosis is convulsion and for this, a history from an
eyewitness is crucial. A number of studies have assessed points of difference in the history
that are suggestive of a convulsion. Features sensitive for convulsions include:

Aura: déjà / jamais vu (not lightheadedness)

Post-episode confusion >2 minutes[4]

Post-episode headache

Tonic-clonic movements (prolonged)

Bite to lateral tongue[4.5]

Urinary incontinence

Flushed or blue appearance.
A scoring system to distinguish between convulsion and syncope, based on the history only,
has been developed by Sheldon et al:[6]
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Point scores for the diagnosis of seizures:[6]
Criteria
Regression coefficient (SE)
p-Value
Score
Loss of consciousness (LOC) with stress
4.73 (1.43)
0.001
2
Head turning to one side during LOC
4.56 (1.84)
0.013
2
Number of spells >30
3.60 (1.02)
0.001
1
Unresponsiveness during LOC
3.89 (1.09)
0.001
1
Diaphoresis before LOC
2.72 (1.25)
0.029
1
Any presyncope
4.90 (1.30)
0.001
2
LOC with prolonged standing or sitting
7.36 (2.11)
0.001
3
Score 1: Seizure
Score <1: Syncope
Narcolepsy
The sleep disorders nacolepsy and catalepsy may occasionally be mistaken for syncope.
They have a high degree of overlap and almost 50% of sufferers will also have an
identifiable psychiatric diagnosis.[7] The principal distinguishing features are the very
stereotyped triggers in narcolepsy that are not typical for syncope, and the absence of loss
of consciousness in catalepsy.
Psychiatric Disorders[8]
It should be borne in mind that patients with psychiatric disorders are strongly represented in
recurrent syncope of most aetiologies, and the presence of one of the following conditions
does not exclude syncope of organic cause:

Somatisation

Depression

Panic attacks

Generalised anxiety.
Breath-holding[9]
This occurs almost exclusively in early childhood and occurs as two distinct variants, both of
which may progress to a convulsion:
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1. Pallid breath-holding (full inspiration): this leads to a reflex vagal cardiac depression and
often occurs after a sudden minor injury, especially to the head.
2. Cyanotic breath-holding (expiratory): this is the hypoxic “hold breath until blue” type and
is frequently associated with anger or psychological upset.
Cerebrovascular Accident
A neurological evaluation should reveal any deficit, although in the case of a transient
ischaemic attack (TIA) this may have reverted to normal. TIA with loss of consciousness
may be considered a form of syncope under the physiological definition, but has a risk of
subsequent cerebrovascular accident.
Toxicity
The history is most likely to provide a diagnosis of toxicity, although very occasionally there
may be an occult poisoning. In particular, moderate carbon monoxide poisoning can lead to
loss of consciousness with spontaneous return on withdrawal of the source.
Traumatic Brain Injury
This should be evident from history but occasionally retrograde amnesia may conceal it.
Local skull or neck tenderness may be found but may reflect secondary injury from the
collapse.
Classification of Syncope
The classification of syncope is based on the trigger for a particular episode, although there
may be more than one pathological process involved. For example, in an elderly diabetic
person, hypoglycaemia may be the triggering event but there is also likely to be a
contribution from autonomic dysfunction and reduced cardiac output. The following
classification is largely based on that proposed by Hadjikoutisa et al:[10]
1. Cardiac syncope: two major mechanisms be responsible, either electrical (arrhythmia)
or contractile/mechanical causing a reduced cardiac output by ischaemia, aneurysm or
obstruction. These tend to occur suddenly without any prodrome and during exertion,
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rather than afterwards or at rest. There is frequently a rapid recovery. Palpitations are
frequently not reported.
2. Orthostatic syncope: this occurs with an absolute or regional deficiency in intravascular
volume as a result of volume depletion or loss of vasopressor reflexes, respectively. This
may be due to disease of the autonomic system such as Parkinson’s disease or to
drugs. The hallmark of orthostatic hypotension is a reproducible, measured fall in blood
pressure with standing.
3. Reflex syncope: abnormal vasomotor reflex activity may result in sudden loss of
vascular tone. The best-defined example is the carotid sinus syndrome where an
abnormal sensitivity of the carotid sinus to mechanical stretching when the head is
turned may cause sudden hypotension. In vasovagal syncope, the triggers are external
stimuli which are usually noxious (venipuncture, etc.) but may be quite specific to the
individual. A prodromal period is most common in vasovagal syncope and is one of its
hallmarks but one that has to be distinguished from a convulsive aura.
4. Metabolic syncope: most metabolic problems, apart from hypoglycaemia, are likely to
exhibit preceding symptoms. Hypokalemia may result in cardiac arrhythmias and
hypocalcaemia may produce depression of cardiac contractility. Hyponatraemia may
result in collapse and convulsion, but mental symptoms usually precede collapse.
Diagnosis of Syncope
There are numerous guidelines for assessment of syncopal collapse.[3,11] Assessment should
be guided by the history, preferably from both the patient and an eyewitness to the event,
but the following are commonly thought to constitute a minimum:
1. Examination: the Glasgow Coma Scale (GCS) score and especially any confusion or
somnolence should be noted. A screening neurological examination for any deficit
should be p. Temperature should be measured, as well as heart rate and blood
pressure. Blood pressure and heart rate should be recorded at the earliest opportunity
and repeated later supine then standing for 5 minutes. A systolic fall of 20 mm Hg is
diagnostic.[10] Lesser falls with symptom recurrence are suggestive.
The heart should be auscultated for murmurs suggestive of aortic stenosis, mitral
stenosis and hypertrophic obstructive cardiomyopathy. The chest should be examined
for any signs of heart failure or pulmonary embolism, although these may not always be
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present, and the abdomen examined for any source of haemorrhage, including a rectal
examination for gastrointestinal bleeding.
2. Office tests: a glucose dehydrogenase test will accurately exclude hypoglycaemia and
should be routine. A urinary hCG test should also be performed as pregnancy is not an
infrequent cause of new syncope in females, and routine urinary hCG testing avoids
unnecessary further investigation. However, an actively haemorrhaging ectopic
pregnancy may occasionally be painless.
3. Laboratory testing: there is some disagreement on the value of further blood tests in
patients with a nonsuggestive history and a normal examination. A full blood count
looking for anaemia or evidence of blood loss is the most commonly suggested test.
Some authors suggest that measurement of serum calcium is also useful as a routine
test.
4. Electrocardiogram: a 12-lead electrocardiogram should be performed at the earliest
opportunity. It should be examined for signs of arrhythmias, in particular sick sinus
syndrome, ventricular tachycardia, supraventricular tachycardia, heart block (other than
first degree) or pacemaker malfunction. In addition, there are a number of conditions with
a high risk of syncope and/or cardiac arrest that should be specifically looked for:
a) Long QT syndrome ‒ an electrophysiological abnormality that predisposes to
torsades de pointes, a specific variety of ventricular tachycardia. The QT interval
should be measured and corrected for rate in the form QTc = QT/√RR. Normal is
<440 msec.[12]
b) The Brugada syndrome ‒ an ECG pattern associated with syncope and sudden
death from ventricular tachycardia that degenerates into ventricular fibrillation. The
hallmarks are a partial right bundle branch block and ST segment elevation in leads
V1-V3.[13] The heart is structurally normal but there appears to be an overlap with:
c) Arrhythmogenic R ventricular cardiomyopathy ‒ which is also a possible and
potentially fatal cause of syncope. Its distinctive ECG features are QRS duration
>111 msec and T-wave depression in V1-V3.[12]
d) Patients with a dilated cardiomyopathy are at risk for arrhythmias, as are those with:
e) Obstructive cardiomyopathy. The characteristic ECG changes in this condition are
those of increased left ventricular QRS voltages, T-wave changes, and deep Qwaves in the lateral leads.
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f) Wolff-Parkinson-White syndrome ‒ which produces supraventricular tachycardias and
is characterised by a short PR interval, delta waves, a widened QRS interval, and Twave inversion.[12]
g) Signs of cardiac ischaemia should be sought including Q-waves, ST elevation or
depression, and T-wave abnormalities.
h) Pulmonary embolism may be associated with some nonspecific ECG changes,[14]
including tachycardia, R-axis deviation, and nonspecific ST- and T-wave changes.
The classic ‘S1Q3T3’ sign is neither specific nor sensitive, but should be noted.
Decision Rules for Syncope
There have been several attempts to develop a scoring system for syncope to reduce the
number of patients admitted for more detailed investigation.
The San Francisco Syncope Rule[15]
This rule was developed with the objective of reducing admissions from emergency
departments for investigation. It divides patients into low-risk and high-risk (requiring
inpatient assessment).
Yes
Abnormal ECG?
High-risk
No
Shortness of breath?
Yes
High-risk
No
Systolic BP <90 mm Hg?
Yes
High-risk
No
Haematocrit <0.3?
Yes
High-risk
No
Congestive heart failure?
No
Low-risk
Yes
High-risk
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Recent studies attempting to validate the San Francisco Syncope Rule have found it to have
low sensitivity in the elderly.[16] An Australian study found that Emergency Department
specialists’ clinical impression was superior.[17]
The OESIL Syncope Score[18,19]
This scoring system was derived by cardiologists in Northern Italy, along with an algorithm
that is more appropriate to inpatient investigation. One point is given for each of four criteria:
1.
Age greater than 65 years
2.
History of syncope without prodrome
3.
A history of cardiovascular disease, defined as:
a) Previous clinical or laboratory diagnosis of any form of structural heart disease,
including ischaemic heart disease, valvular dysfunction, and primary myocardial
disease
b) Previous diagnosis or clinical evidence of congestive heart failure
c) Previous diagnosis or clinical evidence of peripheral arterial disease
d) Previous diagnosis of stroke or transient ischaemic attack which was defined as
syncope without prodrome and an abnormal ECG
4.
An ECG where the tracing was considered abnormal if any of the following were
present:
a) Rhythm abnormalities (atrial fibrillation or flutter, supraventricular tachycardia,
multifocal atrial tachycardia, frequent or repetitive premature supraventricular or
ventricular complexes, sustained or nonsustained ventricular tachycardia, paced
rhythms)
b) Atrioventricular or intraventricular conduction disorders (complete atrioventricular
block, Mobitz I or Mobitz II atrioventricular block, bundle branch block, or
intraventricular conduction delay)
c) Left or right ventricular hypertrophy
d) Left axis deviation
e) Old myocardial infarction
f) ST segment and T-wave abnormalities consistent with or possibly related to
myocardial ischemia.
When evaluated versus mortality, higher OESIL scores are associated with an increased 12month mortality, as shown below:
10
OESIL score
12-Month mortality
0
0%
1
0.6-0.8%
2
14.0-19.6%
3
29.0-34.7%
4
52.9-57.1%
References
1.
Fitzpatrick AP, Cooper,P. Diagnosis and management of patients with blackouts. Heart
2006;92:559-68.
2.
Kapoor, WN. Syncope. N Engl J Med 2000;343(25):1856-62.
3.
The Task Force on Syncope, European Society of Cardiology. Guidelines on
management (diagnosis and treatment) of syncope ‒ update 2004. Europace
2004;6:467-537.
4.
McCorry D, McCorry A, Collapse with loss of awareness. BMJ 2007;334:153.
5.
Petkar S, Cooper, Fitzpatrick AP. How to avoid a misdiagnosis in patients presenting
with transient loss of consciousness. Postgrad Med J 2006;82:630-41.
6.
Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from
seizures. J Am Coll Cardiol 2002;40:142-8.
7.
Benca RM. Narcolepsy and excessive daytime sleepiness: diagnostic considerations,
epidemiology and comorbidities. J Clin Psychiatry 2007;68 Suppl 13:5-8.
8.
Ventura R, Maas R, Rüppel R, Stuhr U, Schuchert A, Meinertz T, Nienaber CA.
Psychiatric conditions in patients with recurrent unexplained syncope. Europace
2001;3(4):311-6.
9.
Breningstall GN. Breath-holding spells. Pediatr Neurol 1996;14:91-7.
10. Hadjikoutisa S, O’Callaghan P, Smith P. The investigation of syncope. Seizure
2004;13:537-48.
11. American College of Emergency Physicians. Clinical policy: critical issues in the
evaluation and Management of patients presenting with syncope. Ann Emerg Med
2001;37:771-6.
12.
Dovgalyuka J, Holstege D, Mattu A, Brady WJ. The electrocardiogram in the patient
with syncope. Am J Emerg Med 2007;25:688-701.
13.
Marcus FI. Electrocardiographic features of inherited diseases that predispose to the
development of cardiac arrhythmias, long QT syndrome, arrhythmogenic right
11
ventricular cardiomyopathy/dysplasia, and Brugagda syndrome. J Electrocardiol
2000;33 Suppl:1-11.
14.
Langan CJ, Weingart S. New diagnostic and treatment modalities for pulmonary
embolism: one path through the blood tests. Mt Sinai J Med 2006;73(2):528-41.
15.
Quinn JV, Stiell IG, McDermott DA, Sellers KL, Kohn MA, Wells GA. Derivation of the
San Francisco Syncope Rule to predict patients with short-term serious outcomes. Ann
Emerg Med 2004;43(2):224-32.
16.
Birnbaum A, Esses D, Bijur P, Wollowitz A, Gallagher EJ. Failure to validate the San
Francisco Syncope Rule in an independent emergency department population. Ann
Emerg Med 2008;52(2):151-9.
17.
Cosgriff TM, Kelly AM, Kerr D. External validation of the San Francisco Syncope Rule
in the Australian context. CJEM 2007;9(3):157-61.
18.
Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M. Development and
prospective validation of a risk stratification system for patients with syncope in the
emergency department: the OESIL risk score. Eur Heart J 2003;24(9):811-9.
19.
Ammirati F, Colivicchi F, Santini M. Diagnosing syncope in clinical practice.
Implementation of a simplified diagnostic algorithm in a multicentre prospective trial ‒
the OESIL 2 Study. Eur Heart J 2000;21(11):935-40.
Further Reading
American College of Emergency Physicians. Clinical policy: critical issues in the evaluation
and management of patients presenting with syncope. Ann Emerg Med 2001;37:771-6.
Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M. Development and
prospective validation of a risk stratification system for patients with syncope in the
emergency department: the OESIL risk score. Eur Heart J 2003;24(9):811-9.
Heaven, DJ Sutton R. Syncope. Crit Care Med 2000;28(11 Suppl):N116-20.
McCorry D, McCorry A. Collapse with loss of awareness. BMJ 2007:334:153.
Murtagh J. Fits, faints and funny turns. A general diagnostic approach. Aust Fam Physician
2003;32(4):203-6.
Petkar S, Cooper P, Fitzpatrick AP. How to avoid a misdiagnosis in patients presenting with
transient loss of consciousness. Postgrad Med J 2006;82:630-41.
12
SYNCOPE AUDIT
The following proposed audit will analyse consultation records for the presence of
information considered essential to the assessment of syncope.
Rationale
This audit is designed to audit clinical practice where a patient presents with a collapse
involving loss or near loss of consciousness (LOC), no significant epileptiform activity, and
an early full return of function with normal neurology.

Patient history:
a) Pre-event
b) Immediately post-event

Eyewitness account, especially the duration of LOC

Drug history

Basic neurological assessment – GCS (Glasgow Coma Scale) or AVPU (Alert, Voice,
Pain, Unresponsive) score

Pulse

Blood pressure, lying and standing

Heart sounds

Chest auscultation

Capillary glucose

Electrocardiogram

(Female) pregnancy test
Optional investigations which might be done at the A+M level:

Full blood count

Creatinine

Electrolytes

D-dimer.
Ten consecutive patients with this history or diagnosis (collapse, faint, syncope or
synonyms) and meeting this criterion should have their notes checked for completeness of
assessment.
The Excel Spreadsheet should be completed.