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EMERGENCY MEDICINE
Liverpool Hospital
The Weekly Probe
1st October 2013
Volume 16 Issue 27
Trauma Calling Criteria- starting yesterday the calling criteria for the Trauma team have
changed. Look for the posters around the department. However if in doubt re whether to call, discuss
with the SS on duty early.
Stroke Calls - Stroke Code Flow chart pathways have been revised and updated to include activation
via ambulance, the new flow charts can be viewed on our intranet.
Congrats – a belated congratulations to Frances who successfully completed her primary exams,
jumping that first and most painful big hurdle and is now an advanced trainee. Well done Frances!
Measles Alert- I think after the 3rd warning in the last 4 months we should be permanently aware of
measles outbreaks in the community after another memo from the MoH this week. Alert the public
health unit via switch and the advice is to perform :



Blood for serology (measles IgM and IgG)
Urine AND a nose and throat viral swab, or NPA [infants] for IFA/PCR.
Mark request as urgent.
THIS WEEK
Syncope
Next week’s case
Joke / Quote of the Week
The Week Ahead
.
Syncope
A 47yo lady presents after collapsing at home. She described a wave of ascending chest discomfort
preceding the event with nil other associated symptoms. After she fell to the flor she is noted to have
transient rigidity of all her limbs with transient, and “she went blue”. This all resolved spontaneously
and by the time she arrives she has normal vitals including a BSL , there is a normal examination and
ECG. What are you going to do?
Syncope is a common and at times challenging presentation, yet a topic we haven’t touched on for 5
years! After some recent cases it’s time for a review once again. It’s a meaty topic so a bit long but
worth “digesting”.
Syncope is a symptom complex that is composed of a brief loss of consciousness associated with
an inability to maintain postural tone that spontaneously and completely resolves without medical
intervention.
It is distinct from vertigo, seizures, coma, and states of altered consciousness. Syncope is a
symptom not a disease – it has a large differential diagnosis, is difficult to evaluate, and can be
disabling. Any process that transiently reduces cerebral perfusion may be the precipitant of
syncope. The mortality rate is generally low, but may be up to 33% at 1 yr in patients with a cardiac
origin.
The central issues in the evaluation of syncope are establishing the cause of syncope with a focus on
identifying or risk stratifying :
1. potentially life-threatening causes (eg arrhythmias, PEs, SAH, dissection, ACS)
2. those that may benefit from intervention (eg bradys or medication related hypotension)
and subsequently deciding whether the patient needs to be admitted, and treating the causes of
syncope effectively to reduce recurrences and potentially improve patient outcomes.
Below is a list of causes- note that despite intensive investigation, the cause of syncope is not
identified in up to 45% of cases.
Type or Cause of Syncope
Reflex mediated
Vasovagal
Situational (Cough / Micturation / Defecation)
Orthostatic hypotension
Medications
14% (8-37%)
3% (1-8%)
11% (4-13%)
3% (0-7%)
Cardiac
Organic heart disease
3% (1-8%)
Aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism, pulmonary HT’n, myxoma, myocardial infarction,
Arrhythmias
Editor: Peter Wyllie
14% (4-26%)
Bradyarrhythmias
Sinus node disease
Second- or third-degree heart block
Pacemaker malfunction
Drug induced
Tachyarrhythmias
Ventricular tachycardia
Torsade de pointes
Supraventricular tachycardia
Neurological
7% (3-32%)
Migraines (basilar artery)
Transient ischemic attacks (esp VBI)
Seizures (atonic, temporal lobe or unwitnessed grand mal)
Subclavian steal
Psychiatric
Other
5% (0-7%)
Including carotid sinus syncope, hypoglycemia, hyperventilation
Unknown
As in many other conditions, a good history, physical examination, and ECG form the cornerstone
of the initial evaluation of a patient with syncope.
After these are completed, ~45% of patients have a primary diagnosis made and a further 8% have a
presumptive diagnosis that can be confirmed by directed testing. Note the majority to not get a
diagnosis despite investigations.
Elderly patients are particularly difficult to evaluate, because they are susceptible to syncope as a
result of the interaction of multiple coexisting illnesses, medications, and physiologic impairments due
to aging. The initial approach to evaluating the “well” normal elderly patients should be to look for a
single cause of syncope, yet if this is not possible, pick off and prioritise the multiple abnormalities
before invasive or extensive diagnostic testing is considered.
History
The first key step is taking a thorough history. This will define an event as syncope and provides a
description of the event to help in the diagnosis or in the formulation of a differential diagnosis (use
the patient, bystanders, relatives) .
Relevant historical features include what the patient was doing before the episode, the precipitating
factors (e.g., pain and anxiety), postural or exertional symptoms, the situations in which episodes
occur (e.g., after urination), associated neurologic symptoms, a history of cardiac disease, a history of
psychiatric illness, and a family history of sudden death ((long QT syndrome, Brugada syndrome,
hypertrophic cardiomyopathy). The history should also include a thorough review of systems
(including GIT, neurological systems, cardiorespiratory systems).
A brief (< 5 seconds) or absent prodrome may be present with arrhythmias while neurocardiogenic or
vasovagal syncope typically has a longer prodrome with associated nausea and vomiting.
Focal neurologic or postictal symptoms suggest a neurologic cause. However be aware that seizures
(esp mild brief tonic-clonic activity – “convulsive syncope”) may be related to cerebral hypoperfusion
frequently accompany other causes of syncope; the classic story is the person with a vasovagal who
collapses in or is put into a chair in the upright position. Enquire about associated colour change
especially if the patient is pale and sweaty, which may be indicative of reduced peripheral blood flow ,
as compared to a cerebral electrical event. Witnesses may help to distinguish a seizure from
Editor: Peter Wyllie
cardiovascular loss of consciousness as patients with the latter the confusion afterwards is often
shorter than the post-ictal phase assoc with a seizure.
Medications, such as antihypertensive agents and antidepressants, may not only cause orthostatic
hypotension, particularly in the elderly, but also favour neurocardiogenic syncope. Antiarrhythmic
agents may cause proarrhythmia with loss of consciousness or even cardiac arrest. A variety of
medications can cause QT prolongation and torsades.
The presence of heart disease in patients with syncope has been identified as the most important
factor in prognosis and risk stratification. However studies have shown that the higher mortality is
largely due to underlying cardiovascular disease in patients with cardiac syncope. A study comparing
patients with and without syncope matched for cardiac disease and other important clinical variables
found that cardiac syncope was not a significant predictor of overall or cardiac 1-year survival. Rather,
underlying heart disease, especially congestive heart failure, was found to be the significant survival
predictor. Similarly, a study of hospitalised syncope patients found that the risk of dying was not
associated with cardiac cause but correlated with age and comorbidities, which included
cardiovascular diseases. However in regards to age there is no discrete cut-off but “older” patients
are at higher risk (PS old is not > 35yo!!) with a continuum of gradually increasing risk as you get
older. In a study of patients with advanced heart failure, poor left ventricular function was associated
with high risk of sudden death regardless of the cause of syncope.
When a patient presents with exertional syncope, consider structural lesions which produce a fixed
cardiac output such as HOCM & AS, conduction abnormalities (WPW, long QT), coronary artery
abnormalities and arrhythmogenic cellular dysplasias.
EXAMINATION
Physical examination should concentrate on orthostatic changes and cardiovascular or neurologic
signs. Cardiovascular examination may suggest an “obstructive” cause, such as aortic stenosis, mitral
stenosis,or HOCM. Persistent hypotension is concerning and suggestive of other pathologies eg
sepsis, bleeding, heart failure.
Signs of congestive heart failure suggest significant organic heart disease.
Orthostatic blood pressure should be measured 2-3 min after the patient stands up, following a
supine period of five minutes. However consider that:
- orthostatic hypotension is found in 40% of asymptomatic pts > 75yo
- many “high risk” patients will have also have orthostasis
- Recurrence of symptoms is more significant than any numeric changes in BP
- Therefore relying on this as the cause of the syncope should be symptom related
and a diagnosis of exclusion in otherwise low risk patients.
Tongue biting esp if lateral is very specific for convulsive seizures yet low sensitivity.
Look for abdominal pain or tenderness – consider PR when rectal bleeding is considered.
Neurological exam looking for focal deficits + neck stiffness.
INVESTIGATIONS
Since syncope is a symptom and not a disease, the diagnostic assessment should focus on
physiologic states that could plausibly cause a sudden loss of consciousness. There are a battery of
tests which may be considered in the investigation of syncope. Which “trigger you pull” depends on
the history and exam.
Blood tests rarely yield diagnostic info – done if suggested by Hx or physical exam – even in those
with seizures only 2-3 % had hypo Ca, low BSL, hypoNa, hypoCa or renal failure.
ECGs is the most important test to perform. The most common abnormalities (such as bundle-branch
block and old myocardial infarction) can be clues to possible causes of syncope, but a cause is only
rarely assigned on the basis of an ECG (in less than 5 percent of patients).
Our focus in the ECG is looking for evidence of life threats including:
- PE – SIQ3 or SIQ3T3 (rightward axis) / New RBBB or incomplete RBBB / SVTs / STsegment elevations or depressions or T-wave inversions, esp anteroseptal + inferior
leads
- Acute Coronary Syndrome
- Tachy / Bradycardias & AV-blocks
Editor: Peter Wyllie
-
-
WPW / Pre-excitation- short PR interval broad QRS- delta waves
Long / Short QT syndromes- QTc > 440msec may be a antecedent of Torsade
Hypertrophic cardiomyopathy- increased QRS voltage & widening and ST-segment/Twave changes consistent with ventricular hypertrophy- apical HOCM may have giant T
wave inversion. Deep narrow Q waves may be seen in the lateral (or inferior) leads
Brugada syndrome (in) complete RBBB pattern with coved or saddle shaped STs in v13- note these changes may fluctuate
Arrhythmogenic RV dysplasia- Results in paroxysmal episodes of VT with a LBBB
morphology – may see epsilon wave (small positive deflection between the end of the
QRS and the start of the T wave) / T wave inversions in V2-3 / may have prolonged Swave upstroke V1-3 - Localised QRS widening in V1-3 (without RBBB)- RV changes
also seen on echo
Cardiac monitoring is indicated when symptoms suggest arrhythmic syncope (brief loss of
consciousness, palpitations with syncope, absence of prodrome, and prompt recovery of clear
mentation), in the presence of structural heart disease / CCF or an abnormal electrocardiogram, and
in unexplained syncope. Take into consideration one study of syncope patients which showed the
predictors of arrhythmias were abnormal ECG (odds ratio [OR]: 8.1), a history of congestive heart
failure (OR 5.3), and age older than 65 (OR: 5.4). They found the risk of arrhythmias ranged from 02% in patients with no risk factors to 6-17% for patients with one risk factor, 35-41% for patients with
two risk factors, and 27-60% for those with three risk factors.
As an outpatient we may consider ambulatory (Holter) monitoring - symptoms are found to occur in
conjunction with arrhythmias in 4 percent of patients (leading to a diagnosis of arrhythmic syncope),
and symptoms occur without arrhythmias in 17 percent (potentially ruling out arrhythmic syncope). In
79 percent of patients, either brief arrhythmias or no arrhythmias are found. Note however arrhythmic
syncope cannot be excluded in these patients, because arrhythmias may be episodic. If there are
recurrent episodes not captured on a 24 hour holter, loop monitoring can be considered. This can be
external like a Holter but worn for up to 1 month, or implanted in the chest!
However increasing the duration of monitoring to periods as long as 72 hours has not been found to
increase the yield for symptomatic arrhythmias in one study.
Echocardiograms should be considered where there is evidence of structural heart disease,
suspected arrhythmic syncope, or an abnormal ECG. However they rarely reveal unsuspected
abnormalities of cardiac function (in 5 to 10 percent of patients), and the discovery of such
abnormalities does not necessarily lead to the diagnosis of a cause.
Exercise stress testing should be considered if ischemic heart disease is suspected or there is a
history of exertional syncope and echocardiography excludes an obstructive cardiac lesion or
hypertrophic cardiomyopathy. In unselected patients, the diagnostic yield of exercise stress testing is
very low.
Electrophysiologic (EPS) tests may be considered for diagnosis and/or management of WPW,
Brugada or other suspected tachyarrythmias.
Tilt table testing? This is talked about in the literature yet I’ve never seen a patient referred for this
test in the past. In the past this was done at RNSH – maybe a reader can let me know if this is still
used over there.
Consider carotid-sinus hypersensitivity in patients with spontaneous symptoms suggestive of carotidsinus syncope (e.g., syncope while shaving or while turning the head – such as our patient having her
hair done) and in elderly patients with recurrent syncope and a negative diagnostic evaluation. To
diagnose this try carotid sinus massage - The carotid sinus is massaged for 5-10 seconds - positive if
> 50mmHg drop in SBP or ventricular pause > 3 seconds.
Consider EEG if the patient has experienced symptoms suggestive of a seizure or a history of a
convulsive disorder.
CT scans of the head provide new diagnostic information in 4 % of cases. Almost all of these patients
have focal neurologic findings, history consistent with a seizure or new onset headaches. Transient
Editor: Peter Wyllie
ischemic attacks involving the carotid or vertebrobasilar arteries rarely result in syncope. Drop attack
is more often a symptom of vertebrobasilar ischemia. There are no studies demonstrating the
usefulness of transcranial or carotid Doppler studies in evaluating syncope. These tests are not
recommended unless the patient has focal neurologic symptoms or signs of transient ischemia.
B-HCG and FAST if a female presents with syncope and abdominal pain - ? ectopic ? haemorrhagic
ovarian cyst rupture
Just to reinforce a number of “red flag” associations when we tie syncope with other symptoms or
results:
Syncope + headache= SAH or intracranial bleed
Syncope + neuro deficit= stroke/TIA or intracranial bleed
Syncope + (prolonged) confusion= seizure
Syncope + chest pain= MI, PE, or aortic dissection
Syncope + back/abdominal pain in older patient= AAA
Syncope + positive HCG= ectopic pregnancy
Admission – there are a number of risk stratification tools including the San Francisco, EGSYS,
Oesil, Rose rules etc etc. However looking at each of these rules, there a number of common
elements which stratify those at risk.
You don’t need a mnemonic :
- Those at risk of arrhythmias – abnormal ECG / those with a Hx of ventricular
arrhythmias/ Hx or signs of CCF / syncope proceeded by palpitations, chest pain or
exertion
- Those with evidence of bleeding – hypotension on arrival or anaemia
However use your brain and also consider other medical problems, other symptoms and social
factors.
OVERALL
Putting this together
Initial evaluation (history, physical examination, orthostatic blood pressure, and ECG) helps divide
patients into 2 groups, those with a certain or suspected diagnosis and those with unexplained
syncope.
One suggested algorithm is shown below. Add on those aspects of history, exam and investigations
comments on earlier– note the history and exam + ECG is the main differentiating factor! (OHD =
organic heart disease)
Editor: Peter Wyllie
A)
Treatment
Treatment of patients with syncope focuses on the underlying cause of the symptom. Advise the
patients on how to prevent episodes by avoiding triggers such as prolonged standing, heat, large
meals, fasting, lack of sleep, alcohol, and dehydration. Vasodilators may be discontinued because
they may increase susceptibility to vasovagal syncope. Patients should also be instructed on
recognising presyncopal symptoms and manoeuvres that prevent loss of consciousness, to assume a
supine position on premonitory symptoms, and to avoid activities that may lead to serious injury.
There may be benefits with moderate graded exercise and progressive periods in an upright position.
The effectiveness of drug therapy in preventing recurrent neurally mediated syncope is open to
question. If the patient has symptomatic orthostatic hypotension consider volume replacement when
the patient has intravascular volume depletion and the discontinuation or reduction of the doses of
drugs that may be responsible for orthostasis eg duiretics. In cases of autonomic failure, increasing
the intake of salt and fluid and using support stockings may be beneficial. Fludrocortisone is the drug
of first choice for patients with autonomic failure.
Permanent pacing is indicated for patients with syncope and atrioventricular block or sinus node
dysfunction carotid sinus syndrome and in selected patients with disabling symptoms from vasovagal
syncope with a bradycardic component. Patients with syncope and bifascicular block who have
intermittent complete heart block or type II second degree A-V block should also be referred for
pacemaker implantation.
However most patients without heart disease can be effectively evaluated and managed as
outpatients. However in patients without a diagnosis, the patient should be closely followed up by
their LMO or specialist. Give them good education on when to return and where, and document this
advice.
Refs – Neurocardiogenic syncope - BMJ 2004; 329: 336-341 / Diagnosing Syncope Ann Intern Med
1997 Jun; 126 (12): 989-96 / Circulation 2002; 106: 1606-1609 / ecgpedia.com/ Huff et al , Clinical
Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the
Emergency Department with Syncope Ann Emerg Med. 2007;49:431-444
Editor: Peter Wyllie
NEXT WEEK
Next issue we’ll look at one of the most important topics we’ve ever discussed.
Occasionally our care is suboptimal due to errors of ignorance related to inadequate knowledge.
However in many cases it’s errors of implementation that occur during application of the knowledge
that get us and patients in trouble. What are these errors ? What can we do about this?
QUOTE OF THE WEEK
? Any quotes out there
Please forward any funny and litigious quotes you may hear on the floor (happy to publish names if
you want)
THE WEEK AHEAD
Tuesdays - 11.30-2.30 Intern teaching -Thomas & Rachel Moore
Wednesday
0800-0900 Critical Care Journal Club. ICU Conf Room / 12.30-1.30 Resident MO in
Thomas & Rachel Moore
Thursday 0730-0800 Trauma Audit. Education Centre / 0800-0830 MET Review Education centre /
1300-1400 Medical Grand Rounds. Auditorium.
Editor: Peter Wyllie