syncope in children , vasovagal syncope , fainting in children , causes of syncope in children , how to manage syncope in children , cardiac syncope , differnetial diagnosis of syncope , approach to syncope

1. SYNCOPE IN CHILDREN AND
ADOLESCENTS
Professor dr. Sayed Ismail
Al-Azhar school of
medicine

2. DEFINITION
The definition of syncope involves three components:
1.Loss of consciousness
2.Loss of postural tone
3.Recovery and return to baseline quickly
This third part of the definition is important. Simple neurocardiogenic syncope will have a return to
baseline usually within about 30 seconds. However if there is altered consciousness for more than about 5
minutes, then seizure or other neurological cause needs to be considered.

3. Causes :
1. Autonomic = Neurocardiogenic Syncope
a) Vasovagal syncope is the most common
b) Orthostatic
2. Neurologic etiologies, (10%):
a) Seizure
b) Migraine headaches,
c) psychological causes
3. Cardiac arrhythmia, (2 % of children)

4. Vasovagal syncope
• Vasovagal syncope is the most common cause of syncope in childhood.
• Mechanism : increases vagal stimulation a slowed heart rate, peripheral
vasodilatation hypotension decreased cerebral perfusion pressure
• S/S include dizziness, nausea, warmth, pallor, diaphoresis, visual changes
(including tunnel vision and visual blackout), and muffled hearing
• Mediated by trigger — fear, pain, phobias (blood, injections, etc.), being in a warm/crowded
environment , orthostatic stress, such as prolonged standing, lack of oral intake

5. Above is a great example of syncope. A child at a spelling bee, loses
consciousness, collapses to the ground and then very rapidly makes a
recovery to baseline and continues spelling the word given.

6. Orthostatic hypotension
• Defined as a fall of systolic BP at least 20
mmHg Or diastolic BP of at least 10 mmHg
within 3 minutes of standing when
compared to sitting position
• Common in young
• Causes : incomplete autonomic nervous
system compensation for stressors
• Treatment : stop medications , prevent
dehydration
Tilt Test
The heart rate and blood pressure will be
measured and recorded while you are in
positions including lying down, sitting and
standing.

7. Cardiac Causes of Syncope
• Those with Cardiac structural abnormalities
• Valvular defects
• Previous cardiac surgery
• Outflow Obstruction: left or right
• Arrhythmias
• Bradycardias: These can include complete heart block and
are usually due to:
• Rheumatic Fever
• Myocarditis
• Endocarditis
• Ventricular Tachycardia: This can be due to congenital
defects, electrolyte disturbances, drugs or myocarditis.
• Congenital long QT syndrome ( limit of 450 ms in males and 460
ms in females.)
• Brugada Syndrome
Hypertrophic Cardiomyopathy
Note the excessive precordial voltage, deep T-wave
inversions, and lateral deep Q waves

8. Brugada Syndrome
Note the “coved” or “shark-fin” ST
elevation in V1, ST elevation in V2, and T-
wave inversions in both leads
Brugada syndrome occurs secondary to mutations in
cardiac sodium channels that predispose the patient to
ventricular fibrillation and sudden cardiac death.
Structurally, the heart will be normal.
This is inherited in an autosomal dominant fashion and tends
to have a higher incidence in males and patients of Asian
descent.
Syncope in these patients is a concerning sign and is a risk
factor for sudden cardiac death

9. Red Flags for Cardiac Syncope
• Syncope occurs DURING exertion(rather than after exertion)
• There may have been chest pain or palpitations
• The patient has a murmur
• There may be congenital heart disease
• There may be a familial History of
• long QT Syndrome (read the case on the 9 yo with syncope)
• Sudden death
• Cardiomyopathy

10. Neurological Causes of
Syncope
• Consider Neurological causes of syncope if there is a post-ictal component.
• Patients that have a simple syncopal episode secondary to vasovagal causes, usually
recover very quickly. Patients that are confused for more than 5 minutes need to be
considered as having had a seizure.
• Patients that have a non-neurological cause of syncope usually collapse and then have
abnormal movements, that are usually anoxia-related and may be mistaken for
seizures. Those patients that have true seizures, usually seize and then drop. There
are some exceptions to this, which include atonic seizures, which usually have no
prodrome

11. Other neurological events
• Vertigo : vertiginous drop attacks mediated by the vestibulospinal reflex in
Meniere and other disorders of the vestibular system.
• Basilar and vestibular migraine symptoms including dizziness, imbalance,
and muffled hearing may overlap with syncope. Generally, time course, accompanying
headache, and personal and family history of migraine can differentiate migraine
mimics from syncope

12. Red Flags for Neurological Causes
• Neurological symptoms
• Post ictal state
• Injuries to Lip/Tongue
• Urinary Incontinence

13. Psychological causes of loss of consciousness
• Specific disorders that can be associated with loss of consciousness
include
• Conversion disorder,
• Malingering,
• Munchausen syndrome,
• Anxiety, depression, and
• Panic attacks.

14. An Approach
• History
• A good history will give the diagnosis in most cases.
• Seek the red flags of cardiac or neurological syncope.
• Is there a psychiatric history, or is there a suspected psychiatric cause for the syncope?
• Ask specific questions about cardiac family history. A family history of cardiomyopathy,
arrhythmia (including congenital long QT syndrome, placement of a pacemaker or
defibrillator, sudden cardiac death, or death from unknown cause may suggest a
cardiac cause for syncope.

15. Event history
• Typically, patients with vasovagal syncope can recall symptoms preceding the event.
• Specific triggers ; positional changes, illness, an emotional or painful stimulus, or a hot environment.
• Chest pain or palpitations immediately before or during syncope are red flags for more serious cardiac
etiologies .
• Neurological : position changes that provide a mechanism for CSF flow obstruction, such as bending forward
at the waist with head lowered.
• Prolonged bilateral jerking particularly if accompanied by fecal or urinary incontinence or lateral tongue
biting.
• One of the most critical features distinguishing seizures from vasovagal syncope is a post-ictal state of
confusion lasting many minutes to hours.
• Any focal neurological sign such as head or eye deviation before collapse..
• Psychological history, especially in patients presenting with frequently recurring loss of consciousness.
• Multiple syncopal events throughout the day without any triggers or presyncope should raise concern for a
psychological origin

16. Clinical Features Differentiating Syncope from Seizures
Clinical Feature Syncope Seizures
Provocation stimulus Frequent Rare
Duration of loss of
consciousness
Seconds to 1-2 minutes Greater than 1-2 minutes
Involuntary movements
Last < 15 seconds, not
synchronized
Last minutes, rhythmic,
synchronized
Timing of movements After loss of tone Before loss of tone
Tongue biting Rare Common
Incontinence Rare Common
Postictal confusion and
recovery period
Not present, recovery occurs
in seconds to a min
Present, recovery takes
many minutes to hours

17. Physical examination
• A complete physical examination, including cardiac and neurological examination, should be
performed.
• Heart rate and any heart rhythm irregularities.
• Auscultation for any new or loud murmurs or gallops.
• Palpation of the precordium for left or right ventricular heave.
• Obtaining orthostatic vital signs may also be helpful in confirming the diagnosis. With the patient in the
supine position a blood pressure and heart rate are recorded. The patient is then asked to stand for 3
minutes and the measurements are repeated. A drop in systolic blood pressure of greater than
20mmHg or a rise in heart rate of more than 30 beats per minute when standing is consistent with the
diagnosis of Orthostatic hypotension that may result in NMS.

18. there is some evidence that individuals with neurally mediated hypotension have a higher prevalence than
the general population of low iron storage and serum ferritin this is the case even in the presence of a normal
blood count or only mild anemia.
Given this association, obtaining a complete blood count as well as iron and ferritin
levels can be helpful in identifying patients with NMS without classic clinical history.
Neurological evaluation
• Detailed cranial nerve examination, funduscopic examination to rule out signs of
increased intracranial pressure, and testing of the vestibular system are sufficient to
exclude serious intracranial pathology.
• Brain imaging and electroencephalogram is not necessary, unless there is history or
examination evidence for underlying neurological pathology

19. Investigations
1. Certainly the ECG is the most important investigation. 12-lead electrocardiography, a
good screening tool in pediatrics for underlying cardiac abnormalities
2. An echocardiogram may be ordered if abnormalities are noted on the EKG or
cardiovascular examination.
3. Ambulatory monitor: You will wear a monitor that uses electrodes to record
information about your heart’s rate and rhythm.
4. Laboratory : a full blood count , iron status , blood glucose level
There is some evidence that individuals with neurally mediated hypotension have a higher prevalence than the general
population of low iron storage and serum ferritin

20. Vasovagal Cardiac Neurological Psychogenic
1-History • Syncope with position
changes, prolonged
standing, heat;
presyncope
(light-headed,
dizzy, nausea, warmth,
pallor, diaphoresis, visual
and hearing changes)
• Proceeded by growth
spurts, menses, rapid
weight loss
Syncope during
exercise
Palpitations, chest
pain
before or during
syncope
• Rapid, forceful loss of tone
• Headache before syncope
• Sudden, severe tiredness before
syncope
• single/ clustered, arrhythmic jerks
of one or more extremities
• Behavioral slowing/ arrest
followed by loss of muscle tone
• Prolonged post-ictal period
• Inability to describe anything
during the ictal phase
• Incontinence or lateral tongue
biting with prolonged low-
frequency, high-
amplitude,rhythmic bilateral
jerking
• Definitive head/eye deviation
before collapse
• Focal neurological signs after
syncope
Prolonged syncope
(minutes to hours)
Often unwitnessed
syncope
Strong history of
physical complaints
over several years
Hyperventilation
before syncope
Syncope while supine
with no concerning
neurological
Associations
DIFFERNTIAL DIAGNOSIS OF SYNCOPE

21. ` Vasovagal Cardiac Neurology Psychologic
2-Family
history
Similar NMS Cardiomyopathy
• Pacemaker/ICD
• Channelopathy: e.g., long
• QT, syndrome
• Sudden unexplained
death
• Seizures
• Migraines
• Neurocutaneous disorders
• Sleep disorders
• Vestibular disorders
Anxiety/depression
3-Vital signs Positive orthostatic
vital signs
Normal Normal Normal
Examination Normal Cardiac murmurs
Evidence of heart failure
on examination
Focal neurological abnormality
May be normal
Normal
ECG Normal Ventricular hypertrophy
Ventricularpre-excitation
Long QT interval
Abnormal t-waves
Heart block
May be normal
Normal Normal
Other tests echo EEG

22. Vasovagal syndrome

23. Syncope Mimics
•Seizures
•Metabolic disorders — hypoglycemia, hypoxia, hypocapnia due to hyperventilation
•Intoxication with drugs and/or alcohol
•Vertebrobasilar transient ischemic attacks
•Traumatic head injuries
•Psychiatric disorders – panic attacks, pseudosyncope
•Breath-holding spells
•Migraines
•Cataplexy

24. Patient management
• The first-line treatments for pediatric patients with vasovagal syncope include:
• Reassurance is paramount because patients and families are often concerned thata
serious or life-threatening medical problem may have caused the syncopal event.
• Adequate fluid and salt intake
• Regular exercise.
• Avoiding or changing the situations or “triggers” that cause a syncope episode.
• Medical treatment

25. • In patients who have failed lifestyle changes our approach has been to start with fludrocortisone in
patients with refractory NMS, and then to add midodrine in cases where the fludrocortisone is
ineffective.
• When using fludrocortisone it is important to monitor for hypokalemia, initial dosing for a typical patient
would be fludrocortisone 0.2 mg every morning.
• Fludrocortisone acts on the distal tubules of the kidney to improve the reabsorption of sodium ions into the
plasma increasing intravascular volume and blood pressure.
• If fludrocortisone fails to improve symptoms after another month despite titration, Midodrine is added at a
dose of 5 mg three times daily.
• Midodrine is an adrenergic alpha agonist and a vasoconstrictor. This medication may be titrated to 10 mg
three times daily if symptoms fail to improve after another month.
• Midodrine can cause supine hypertension so should not be given within 4 hours of sleep.