Syncope in children , Diagnosis and Management

waad80212 58 views 40 slides Jul 28, 2024
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About This Presentation

Syncope in children


Slide Content

Understand the term syncope.
Differentiate the serious causes of syncope
from those that are benign.
Know the appropriate testing needed in the
evaluation of syncope based upon the
presenting history.

Palpitations-sensation of strong, rapid, or
irregular heart beats.
Syncope–transient loss of consciousness and
postural tone due to generalized cerebral
ischemia with rapid and spontaneous
recovery.
Presyncope-no complete loss of
consciousness occurs.

Disorders without impairment of
consciousness:
Drop attacks.
Cataplexy.
Psychogenic pseudo-syncope.
Transient ischemic attacks.
Disorders with loss of consciousness:
Metabolic disorders.
Epilepsy.
Intoxications.
Vertebrobasilartransient ischemic attacks.

Affects 15% of children between 8-18 Y
Uncommon under age 7 Y therefore think
about:
Seizure disorders.
Breath holding.
Primary cardiac dysrhythmias.
Cardiovascular causes unusual but life-
threatening
Congenital malformations.
Valvulardisease.
Electrical abnormalities.

Observation Seizure Inadequate
Perfusion
Onset Sudden More gradual
Duration Minutes Seconds
Jerks Frequent Rare
Headache Frequent (after)Occasional (before)
Confusion afterFrequent Rare
IncontinenceFrequent Rare
Eye deviationHorizontal Vertical (or none)
Tongue bitingFrequent Rare
Prodrome Aura Dizziness
EEG Often abnormal Usually normal

Orthostatic
Cardiac
Arrhythmia
Structural
Cardio-
Pulmonary
1
•Vasovagal
•Carotid Sinus
•Situational
Cough
Post-
Micturition
2
•Drug-Induced
• Autonomic
Nervous
System
Failure
Primary
Secondary
3
•Brady
SN
Dysfunction
AV Block
•Tachy
VT
SVT
•Long QT
Syndrome
4
•Acute
Myocardial
Ischemia
•Aortic
Stenosis
•HCM
•Pulmonary
Hypertension
•Aortic
Dissection
Neurally-
Mediated
UnexplainedCauses = Approximately 1/3

Vasovagal.
Situational.
Psychiatric.
Long QT.
WPW syndrome.
RV dysplasia.
Hypertrophic cardiomyopathy.
Catecholaminergic VT.
Other genetic syndromes.

Vasovagal Events:
30% to 50% of cases.
Decreased PVR.
Decreased venous return.
Decreased cardiac output.
Hypotension.
Bradycardia.
In teens –think about pregnancy and drug
abuse.

Is the loss of consciousness attributable to
syncope or not?
Is heart disease present or absent?
Are there important clinical features in the
history that suggest the diagnosis?

Questions about circumstances just prior to attack
Position (supine, sitting , standing)
Activity (rest, change in posture, during or immediately
after exercise, during or immediately after urination,
defecation or swallowing)
Predisposing factors (crowded or warm place, prolonged
standing post-prandial period) and of precipitating events
(fear, intense pain, neck movements)
Questions about onset of the attack
Nausea, vomiting, feeling cold, sweating, pain in chest

Questions about attack (eye witness):
Skin color (pallor, cyanotic).
Duration of loss of consciousness.
Movements ( tonic-clonic, etc.).
Tongue biting.
Questions about the end of the attack:
Nausea, vomiting, diaphoresis, feeling cold,
muscle aches, confusion, skin color, wounds.

Questions about background:
Number and duration of syncope spells.
Family history of arrhythmic disease or
sudden death.
Presence of cardiac disease.
Neurological disease.
Medications (Hypotensive, negative.
chronotropic and antidepressant agents).

Neurally-Mediated Syncope:
Absence of cardiac disease.
Long history of syncope.
After sudden unexpected, unpleasant
sensation.
Prolonged standing in crowded, hot
places.
Nausea vomiting associated with syncope
During or after a meal.
With head rotation or pressure on carotid
sinus.
After exertion.

Syncope due to orthostatic hypotension:
After standing up.
Temporal relationship to taking a medication
that can cause hypotension.
Prolonged standing.
Presence of autonomic neuropathy.
After exertion.

Cardiac Syncope:
Presence of structural heart disease.
With exertion or supine.
Preceded by palpitations.
Family history of sudden death.

Vital signs:
Heart rate.
Orthostatic blood pressure change.
Cardiovascular exam: Is heart disease present?
ECG: Long QT, pre-excitation, conduction system
disease.
Echo: LV function, valve status, HCM.
Neurological exam.

Classically, abnormal if systolic BP decreases
by more than 20 points and/or pulse.
increases in pulse rate of more than 20 beats
per minute after a change from supine to
standing.
If there is only a pulse increase but no drop
in blood pressure, the test is less significant.

Distinguish true syncope from syncope mimics.
Determine presence of heart disease and risk for
sudden death.
Establish the cause of syncope with
sufficient certainty to:
Assess prognosis confidently.
Initiate effective preventive treatment.

Survival with and
without syncope
(adults and children).
6-month mortality rate
of greater than 10%.
Cardiac syncope
doubled the risk
of death.
Includes cardiac
arrhythmias.
No Syncope
Vasovagal/other
Cardiac Cause
0 5 10 15
Follow-Up (yr)
Probability of
Survival
1.0
0.8
0.6
0.4
0.2
0.0
Soteriades ES, et al. N Engl J Med.2002;347:878.

Yield for specific diagnosis low (5%).
Risk free and relatively inexpensive.
Abnormalities (BBB, previous MI,
nonsustained VT) guide further evaluation.
Recommended in almost all patients.

Routine use not recommended
May be glucose?
Should be done only if specifically suggested
by H&P.

EEG -not useful unless seizures.
Brain imaging -not useful unless focality.
Neurovascular studies.
No studies.
May be useful if bruits, or hx suggests
vertebrobasilar insufficiency.

History is key!!!!
Orthostatics:
take the time to do them correctly.
Cardiac vs Non-cardiac:
If you are not confident that it is NOT cardiac 
REFER.
ECG
Use it if you got ‘em!

11-year-old girl passed out during
reading; awoke after 3 min.
She was stiff with eyes rolled back ~
approx. 3 min.
Now awake and alert; no retractions;
skin color is normal.

Normal appearance, normal breathing, normal
circulation.
Vital signs: HR 70; RR 20; BP 90/60; T 37.7C Wt 39
kg; O
2sat 99%.
Three similar episodes; Preceded by palpitations
,one of them associated with “exercise.”
PMH and FH: Negative.

What is your general impression of this
patient?

Loss of consciousness.
Lasted only a few minutes.
Minimal or no postictal state.
No stigmata of seizure: Urinary incontinence,
bitten tongue, witnessed tonic-clonic activity.

Is the loss of consciousness attributable to
syncope or not?
Is heart disease present or absent?
Are there important clinical features in the
history that suggest the diagnosis?

Stable
Patient with syncope.
In no distress; normal exam.
Concerning/ominous history.
What are your initial management
priorities?

Laboratory is often normal but may include:
Electrolytes / Ca
++
, Mg
++
, PO
4.
CBC with differential.

cardiac enzyme.
Radiology:
CXR offers little.
CT or MRI of the brain and neck may be
indicated if considering seizures or injury

ECG/Holter.
Echocardiography
Cardiac MRI
Continuous cardiac monitoring
EEG
Genetic testing
Stress ECG

Differntial diagnosis :
Structural heart defect :
•Known Congenital heart disease (Ebstein’s
anomaly,LTGA,ASD)
•Hypertrophic cardiomyopathy
•Anomalous origin of the LCA
•Myocarditis
•Arrhythmogenic RV dysplasia
•Coronary artery disease
•Primary or secondary pulmonary hypertension.

Normal heart structure.
WPW syndrome.
Long or short QT syndrome.
Brugada syndrome.
CPVT.

QT (corrected)
QTc= QT (msec)
√R-R (sec)
= 640/ 1.05
= 610 msec
> 450 m sec is long
Long QT syndrome (Jervell-Nielson-Lange)

Inherited genetic disorder that puts the child at
risk for paroxysmalventriculartachcardia
/ventricular fibrillation and sudden death.
May also result from electrolyte imbalance,
malnutrition (anorexia and bulimia), myocarditis
and CNS trauma
Speculation that it may be associated with SIDS
(unproven)
No warning; results in death.

Long QT syndrome:
Congenital long QT associated with hypertrophic
cardiomyopathy.
Long QT defined as corrected QT longer than 0.44 s
T wave alternans sometimes present.
Can have normal ECG in the department.
Two clinical syndromes not associated with structural
heart disease: Romano-Ward and Jervell-Lange-
Nielsen.
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