Syncope / Dizziness
Syncope is a transient loss of consciousness due to cerebral hypoperfusion, and dizziness is a sensation of unsteadiness or lightheadedness, which in children and adolescents most commonly results from vasovagal mechanisms, orthostatic intolerance, or benign paroxysmal vertigo of childhood.
Syncope / Dizziness in Paediatrics
Syncope derives from the Greek synkoptein — "syn" (together) + "koptein" (to cut off) — literally meaning "to cut off together," i.e., a sudden interruption of blood supply to the brain.
Syncope is defined as a sudden, transient loss of consciousness (TLOC) and postural tone with spontaneous and complete recovery, caused by transient global cerebral hypoperfusion [1][2].
The key physiological point: loss of consciousness occurs within ≤ 8–10 seconds of cessation of cerebral blood flow to the reticular activating system (RAS) in the brainstem/midbrain. This is true in adults and children alike, but the paediatric brain is somewhat more vulnerable to transient hypoperfusion because of its relatively higher metabolic rate [1].
Presyncope ("near-faint") is the subjective feeling that one is about to lose consciousness — lightheadedness, dimming of vision, warmth, nausea — but the child does not actually lose consciousness. Presyncope shares the same pathophysiology and differential diagnosis as syncope; it is just a milder form along the same spectrum.
Dizziness is a broader, less specific symptom that children (and parents) may describe. It is critical to unpack what "dizzy" means before jumping to conclusions. In paediatrics, especially in younger children who lack the vocabulary, the history is almost entirely from caregivers and observers [1][2].
Dizziness encompasses several distinct syndromes:
| Symptom | What the child/parent means | Underlying mechanism |
|---|---|---|
| Vertigo | "The room is spinning" or "I'm spinning" | Abnormal perception of movement — vestibular (peripheral or central) |
| Presyncope / syncope | "I feel faint," "everything goes black," "I nearly passed out" | Global cerebral hypoperfusion |
| Unsteadiness / disequilibrium | "I feel wobbly," "I can't walk straight" | Cerebellar ataxia, proprioceptive dysfunction, visual disturbance, joint disease |
| Non-specific lightheadedness | "I feel weird in my head," "spaced out" | Anxiety, hyperventilation, panic attacks, hypoglycaemia, psychogenic non-epileptic attacks |
It is essential to distinguish these categories because the differential diagnosis, workup, and management differ entirely [1][2].
Clinical Pearl — The First Question to Ask
When a child or adolescent presents with "dizziness," the single most important question is: "What exactly do you mean by dizzy?" Get them to describe it without using the word "dizzy." Are things spinning? Do you feel like you might faint? Do you feel off-balance? This one question redirects your entire diagnostic pathway.
2. Epidemiology
- Very common: syncope accounts for ~1% of paediatric emergency department visits [1].
- Lifetime prevalence: approximately 15–25% of children will experience at least one syncopal episode before adulthood; the peak incidence is in adolescence (ages 10–19 years), particularly around 15–19 years [3].
- Sex: slight female predominance in adolescence (F > M, approximately 2:1), partly because vasovagal syncope is more common in females, and partly because the hormonal and autonomic changes of puberty trigger more episodes in girls.
- Benign aetiology in the vast majority: > 60–80% of paediatric syncope is neurocardiogenic (vasovagal or reflex syncope) [1][2].
- Cardiac syncope is rare but life-threatening: accounts for only 2–6% of paediatric syncope but carries a significantly increased mortality risk (up to 30% if undiagnosed cardiac cause) [1][2].
- Breath-holding spells (a form of reflex syncope in young children) occur in ~5% of children aged 6 months to 5 years, with peak at 1–3 years [1].
- Less well-studied than in adults.
- Most common cause in young children: benign paroxysmal vertigo of childhood (a migraine equivalent, distinct from BPPV in adults).
- In adolescents: vasovagal presyncope and anxiety-related dizziness (hyperventilation) are the most common causes.
- True vestibular pathology is relatively rare in children.
- In HK's subtropical climate, hot and humid environments (especially during summer) are a common trigger for vasovagal syncope during school assemblies, sports, and public transport.
- Postural orthostatic tachycardia syndrome (POTS) is increasingly recognized in Hong Kong adolescents, particularly in the post-COVID era.
- Long QT syndrome (LQTS) — an important cause of cardiac syncope — is relevant in HK because specific LQTS-associated mutations (e.g., KCNQ1, KCNH2) are found in the Chinese population. Family screening is important [2].
- School-based screening ECGs are not routine in HK, so a high index of suspicion for cardiac syncope is essential.
3. Risk Factors
Risk factors can be divided into those predisposing to benign (reflex/neurocardiogenic) syncope vs. those raising suspicion for cardiac syncope:
- Adolescence, especially female sex
- Dehydration (poor fluid intake, hot weather, exercise without adequate hydration)
- Prolonged standing (school assemblies, bus queues)
- Hot, stuffy, crowded environments
- Emotional triggers: pain, fear, sight of blood, needles (very common in paediatrics — think vaccination clinics!)
- Sleep deprivation (extremely common in HK adolescents due to academic pressures)
- Skipping meals (common in HK secondary school students)
- Family history of fainting (genetic predisposition to vasovagal sensitivity)
- Family history of sudden cardiac death (especially < 40 years), LQTS, Brugada syndrome, hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC)
- Syncope during exertion (as opposed to after exertion)
- Syncope while supine or swimming
- Preceding palpitations or chest pain
- Known structural heart disease (e.g., repaired or unrepaired congenital heart disease)
- Abnormal ECG (prolonged QTc, pre-excitation/delta wave, Brugada pattern, pathological Q waves)
- Use of QT-prolonging medications
- History of seizures refractory to anti-seizure medications (may actually be cardiac syncope with anoxic convulsions misdiagnosed as epilepsy)
High Yield — Red Flags for Cardiac Syncope
Any child with syncope during exertion, syncope while supine or in water, family history of sudden death < 40 years, preceding palpitations, or abnormal ECG must be evaluated urgently for cardiac causes. Missing cardiac syncope can be fatal. The 30% mortality figure for undiagnosed cardiac syncope should keep you awake at night [1][2].
4. Relevant Anatomy and Physiology
- Consciousness depends on adequate perfusion of the reticular activating system (RAS) in the brainstem (midbrain/pons) and both cerebral hemispheres.
- The brain receives ~15% of cardiac output but accounts for ~20% of total body oxygen consumption — it has essentially no energy reserves and no capacity for anaerobic metabolism in the acute setting.
- In paediatric patients, the brain-to-body metabolic ratio is even higher, making children potentially more sensitive to transient hypoperfusion.
- LOC occurs within 8–10 seconds of cessation of cerebral blood flow (or a drop in mean arterial pressure [MAP] below the lower limit of autoregulation) [1].
Understanding syncope requires understanding how blood pressure is maintained:
Blood Pressure = Cardiac Output × Systemic Vascular Resistance (SVR)
Where: Cardiac Output = Stroke Volume × Heart Rate
Any mechanism that ↓CO or ↓SVR (or both) → ↓BP → ↓cerebral perfusion → syncope.
Normal BP Maintenance on Standing (Orthostatic Reflex):
- On standing, ~500–700 mL of blood pools in the lower extremities and splanchnic circulation due to gravity.
- This reduces venous return → ↓preload → ↓stroke volume → initial ↓BP (transient drop of ~10–20 mmHg systolic).
- Baroreceptors in the carotid sinus and aortic arch detect the ↓BP → signals via CN IX (glossopharyngeal) and CN X (vagus) to the nucleus tractus solitarius (NTS) in the medulla.
- The NTS orchestrates the response:
- ↑Sympathetic outflow: ↑HR (via β1 receptors on SA node), ↑contractility, ↑SVR (via α1 receptors on arterioles), venoconstriction (to ↑venous return)
- ↓Parasympathetic (vagal) outflow: removes the "brake" on heart rate
- Net result: BP is restored within seconds.
In children, this reflex arc is still maturing, which is one reason why adolescents are particularly prone to vasovagal syncope — their autonomic nervous system is "learning" to calibrate, and the overshoot or paradoxical vagal response is more common.
This is the key mechanism behind the most common type of paediatric syncope — vasovagal syncope:
- A trigger (e.g., prolonged standing, dehydration, emotional stress) causes venous pooling → ↓venous return → ↓preload.
- The heart compensates by beating more vigorously (↑sympathetic tone → ↑contractility with a relatively empty ventricle).
- Mechanoreceptors (C-fibres) in the left ventricular wall are paradoxically activated by the vigorous contraction of a near-empty ventricle.
- These C-fibres send afferents via the vagus nerve to the NTS, which misinterprets this as hypertension/hypercontractility.
- The NTS triggers an exaggerated vagal response:
- ↑Parasympathetic output → bradycardia (cardioinhibitory component)
- ↓Sympathetic output → vasodilation → ↓SVR (vasodepressor component)
- The combined effect: ↓↓BP and/or ↓↓HR → ↓cerebral perfusion → syncope.
This is why vasovagal syncope is also called neurocardiogenic syncope — the nervous system (neuro-) causes inappropriate cardiac (-cardiogenic) slowing/vasodilation.
| Feature | Implication for Syncope |
|---|---|
| Relatively higher vagal tone in children vs. adults | More susceptible to bradycardia-mediated syncope |
| Immature autonomic nervous system in adolescents | Exaggerated or paradoxical responses to orthostatic stress |
| Lower blood volume per kg in young children | More susceptible to dehydration-related syncope |
| Higher metabolic rate of the brain | Less tolerance for transient hypoperfusion |
| Growth spurts in adolescence | Rapid increase in body size may outpace cardiovascular adaptation → orthostatic intolerance |
| Age | Heart Rate (bpm) | Systolic BP (mmHg) | Diastolic BP (mmHg) |
|---|---|---|---|
| Neonate | 120–160 | 60–80 | 30–50 |
| Infant (1–12 months) | 100–150 | 70–90 | 40–60 |
| Toddler (1–3 years) | 80–130 | 80–100 | 50–70 |
| Pre-school (3–6 years) | 80–120 | 85–110 | 55–75 |
| School-age (6–12 years) | 70–110 | 90–120 | 60–80 |
| Adolescent (12–18 years) | 60–100 | 100–130 | 65–85 |
Remember: blood pressure norms in paediatrics are defined by age, sex, and height percentile. A systolic BP < 5th percentile for age = hypotension.
5. Aetiology (with Paediatric Focus, Relevant to Hong Kong)
The aetiological classification of syncope in children follows the same framework as adults but with very different proportions and some unique paediatric entities [1][2]:
| Category | Proportion | Mechanism |
|---|---|---|
| Neurocardiogenic (reflex) syncope | ~60–80% | Exaggerated autonomic reflex → ↓HR and/or ↓SVR → ↓BP → ↓cerebral perfusion |
| Orthostatic syncope | ~8–10% | Impaired vasoconstriction on standing → ↓BP |
| Cardiac syncope | ~2–6% | Arrhythmia or structural heart disease → ↓CO |
| Neurological causes | ~1–3% | Seizure (not true syncope but a key differential), basilar migraine, subclavian steal |
| Metabolic / other | ~2–5% | Hypoglycaemia, hyperventilation, anaemia, drugs |
| Psychogenic | ~3–5% | Psychogenic pseudosyncope (conversion disorder) |
| Unexplained | ~5–20% | No identifiable cause after workup |
5.2 Neurocardiogenic (Reflex) Syncope — The Most Common Cause in Children
"Reflex syncope" is the umbrella term. It encompasses several subtypes, all sharing the final common pathway of inappropriate vagal activation ± sympathetic withdrawal → ↓BP and/or ↓HR:
- The single most common cause of syncope in older children and adolescents [1][2].
- Trigger: prolonged standing, hot/crowded environments, emotional stress, pain, fear, blood/needle phobia.
- Mechanism: Bezold-Jarisch reflex (described above).
- Three subtypes based on the predominant efferent limb:
- Vasodepressor (most common in paediatrics): predominantly ↓SVR (vasodilation) → ↓BP
- Cardioinhibitory: predominantly ↓HR (bradycardia or asystole)
- Mixed: both components
- Usually when standing [1][2].
- A/w situational trigger [1][2].
- Usually brief (in minutes) [1][2].
- Pallor [1][2].
Pathophysiology in detail (vasodepressor type): Trigger → venous pooling → ↓venous return → vigorous contraction of underfilled LV → activation of LV mechanoreceptors → vagal afferents → NTS → paradoxical ↑vagal efferent + ↓sympathetic efferent → vasodilation + bradycardia → ↓cerebral perfusion → presyncope → syncope.
These are a form of reflex syncope unique to young children. They are NOT voluntary and the name "breath-holding" is misleading — the child does not choose to hold their breath [1].
Two types:
(a) Expiratory apnoea syncope ("cyanotic" or "blue" breath-holding spells):
- Trigger: anger, frustration, crying [1]
- Feature: child holds breath in expiration → goes blue (cyanotic), becomes stiff then limp ± LOC; rapid recovery [1]
- Mechanism: Vigorous crying → prolonged forced expiration → ↑intrathoracic pressure (Valsalva-like effect) → ↓venous return → ↓CO → ↓cerebral perfusion → syncope. The cyanosis is from hypoxia during apnoea.
- Not dangerous, self-limiting. The child resumes breathing reflexively.
(b) Reflex asystolic (anoxic) syncope ("pallid" breath-holding spells):
- MoA: excess vagal stimulation → cardiac asystole [1]
- Trigger: sudden pain/discomfort, head trauma, cold food, fright, fever [1]
- Feature: stop breathing and go pale (pallid), become stiff ± brief GTCS; usually rapid recovery but occasionally ≥ 1 hour if severe [1]
- Mechanism: The trigger (e.g., a bump to the head) provokes an exaggerated vagal reflex → cardiac asystole (pause of several seconds) → ↓cerebral perfusion → LOC + pallor (no blood reaching the skin). If the asystole is prolonged enough, anoxic seizure (brief tonic-clonic movements) may occur — this is NOT epilepsy, it is a consequence of brain hypoperfusion.
- Often confused with epileptic seizures — important differential.
Anoxic Convulsion ≠ Epilepsy
A brief tonic-clonic movement following syncope (of any type) is an anoxic convulsion, not an epileptic seizure. It occurs because the hypoxic brain generates abnormal electrical discharges. It does NOT require anti-seizure medication. The key differentiator: the convulsion occurs AFTER LOC (not before), and the episode is preceded by a clear syncopal trigger/prodrome. The EEG between episodes is normal [1].
- Trigger-specific subtypes of reflex syncope:
- Micturition syncope: occurs during or after urination, typically in adolescent males. Mechanism: bladder emptying → ↓intra-abdominal pressure → vagal activation + ↓venous return.
- Defecation syncope: straining → Valsalva → ↓venous return.
- Cough syncope: severe coughing bout → ↑intrathoracic pressure → ↓venous return. More relevant in children with pertussis or severe asthma.
- Swallow syncope: cold drink or bolus → vagal reflex via oesophageal afferents.
- Hair-grooming syncope: hair brushing/combing → CN V stimulation → vagal response (described in adolescent girls).
- Rare in children (primarily a disease of elderly adults).
- Mechanism: hypersensitivity of carotid sinus baroreceptors → exaggerated vagal response to minimal carotid stimulation (e.g., tight collar, head turning).
- Mentioned for completeness; not a significant paediatric entity.
5.3 Orthostatic Syncope
- Defined as a drop in systolic BP ≥ 20 mmHg or diastolic BP ≥ 10 mmHg within 3 minutes of standing (same definition applies to paediatrics, though less studied in children) [2].
- Causes in paediatrics:
- Dehydration (most common in children — gastroenteritis, poor fluid intake, hot weather)
- Acute blood loss / haemorrhage (e.g., trauma, GI bleed)
- Medications: antihypertensives (rare in children), antipsychotics, TCAs, diuretics
- Autonomic neuropathy: rare in children; seen in diabetes (uncommon in paediatric DM), Guillain-Barré syndrome, familial dysautonomia (Riley-Day syndrome)
- Adrenal insufficiency: Addison's disease, congenital adrenal hyperplasia → ↓cortisol and/or ↓aldosterone → inability to maintain vascular tone/volume
- Increasingly recognized in paediatric/adolescent population, especially post-COVID-19.
- Defined as: sustained ↑HR ≥ 40 bpm (or HR > 120 bpm) within 10 minutes of standing in adolescents (≥ 30 bpm in adults), WITHOUT orthostatic hypotension, AND with symptoms present for ≥ 3 months [3].
- Symptoms: lightheadedness, presyncope (frank syncope is uncommon in pure POTS), palpitations, tremulousness, exercise intolerance, nausea, fatigue, brain fog.
- Pathophysiology: likely heterogeneous; proposed mechanisms include:
- Peripheral autonomic neuropathy (neuropathic POTS): impaired lower extremity vasoconstriction → excessive venous pooling → compensatory tachycardia
- Hyperadrenergic POTS: excessive sympathetic drive
- Hypovolaemic POTS: low blood volume → compensatory tachycardia
- HK relevance: increasingly diagnosed post-COVID in HK adolescents. Important to recognize because it significantly affects school attendance and quality of life.
5.4 Cardiac Syncope — Rare but Dangerous
Cardiac syncope accounts for only 2–6% of paediatric syncope but is the most dangerous category [1][2].
These produce syncope via ↓CO from either too slow (↓diastolic filling is not the issue here — it's ↓HR × SV → ↓CO) or too fast (↓diastolic filling time → ↓SV → ↓CO) a heart rate.
| Arrhythmia | Mechanism | Key Features |
|---|---|---|
| Long QT Syndrome (LQTS) | Delayed repolarization → torsades de pointes (polymorphic VT) → ↓CO | Family Hx of sudden death, syncope during exertion/emotion/swimming (LQTS1), auditory stimuli (LQTS2), or sleep (LQTS3). QTc > 470 ms in males, > 480 ms in females |
| Brugada Syndrome | Sodium channelopathy → VT/VF | Coved ST elevation in V1–V3, typically presents in adolescence/young adulthood, more common in SE Asian males |
| Wolff-Parkinson-White (WPW) | Accessory pathway → re-entrant SVT or AF with rapid ventricular response | Delta wave on ECG, palpitations preceding syncope |
| Catecholaminergic polymorphic VT (CPVT) | Abnormal calcium handling in cardiomyocytes → exercise- or emotion-triggered bidirectional/polymorphic VT | Syncope or cardiac arrest during exercise or emotional stress; resting ECG often normal |
| Complete heart block (3° AV block) | No conduction from atria to ventricles → bradycardia | Can be congenital (associated with maternal anti-Ro/La antibodies in neonatal lupus) or acquired (post-cardiac surgery, myocarditis) |
| Condition | Mechanism | Clinical Clues |
|---|---|---|
| Hypertrophic cardiomyopathy (HCM) | LVOT obstruction → inability to ↑CO during exertion + vasodilation → ↓cerebral perfusion | Syncope/presyncope during exertion, family Hx of HCM or sudden death, systolic murmur that ↑ with Valsalva [2] |
| Severe aortic stenosis (AS) | Fixed outflow obstruction → inability to ↑CO during exertion | Ejection systolic murmur radiating to carotids |
| Anomalous origin of coronary artery | Extrinsic compression during exertion → myocardial ischaemia → arrhythmia or ↓CO | Exertional syncope in an otherwise well young person; often a cause of sudden death in young athletes |
| Pulmonary hypertension | ↑RV afterload → inability to ↑CO → exertional syncope | Exertional dyspnoea, loud P2, RV heave |
| Cardiac tumours (e.g., atrial myxoma, rhabdomyoma) | Obstruction of blood flow, especially position-dependent | Rare; rhabdomyoma in infancy a/w tuberous sclerosis |
| Acute myocarditis / dilated cardiomyopathy | ↓systolic function → ↓CO | Preceding viral illness, signs of heart failure |
Exertional Syncope = Cardiac Until Proven Otherwise
In paediatrics, syncope occurring DURING exercise (not after, not at rest) must be assumed cardiac until proven otherwise. The most common causes are LQTS, HCM, CPVT, and anomalous coronary artery origin. These children need urgent cardiology referral, ECG, and echocardiography [2].
| Condition | Mechanism | Distinguishing Features |
|---|---|---|
| Epileptic seizure | Abnormal electrical activities in the brain [1][2] | Preceded by aura (déjà vu, olfactory hallucinations), LOC typically > 1 min, a/w incontinence, tongue-biting, uprolling eyeball, slow recovery with prolonged confusion [1][2] |
| Migraine with brainstem aura (basilar migraine) | Transient brainstem ischaemia → vertigo, ataxia, visual changes, LOC | Vertigo + headache, visual aura, family Hx migraine |
| Benign paroxysmal vertigo of childhood | Migraine equivalent; ?transient vestibular dysfunction | Episodic vertigo lasting minutes, no LOC, age 2–6 years, normal between episodes, often evolves into migraine later |
| Subclavian steal syndrome | Proximal subclavian stenosis → arm exercise "steals" blood from vertebrobasilar circulation | Extremely rare in children; possible in repaired coarctation of aorta |
| Cause | Mechanism |
|---|---|
| Hypoglycaemia | ↓glucose supply to brain → neuroglycopenia → confusion, LOC. More relevant in diabetic children on insulin, adrenal insufficiency, ketotic hypoglycaemia of childhood |
| Anaemia (severe) | ↓O₂-carrying capacity → ↓O₂ delivery to brain. Must be severe or acute (e.g., acute haemorrhage, splenic sequestration in sickle cell disease) |
| Hyperventilation / panic attacks | ↓PaCO₂ → cerebral vasoconstriction → ↓cerebral blood flow. Also causes perioral and distal tingling. Common in anxious adolescents |
| Drug-related | QT-prolonging drugs (macrolides, antipsychotics, ondansetron), β-blockers (bradycardia), vasodilators |
| Pregnancy (in older adolescents) | ↓SVR + mechanical IVC compression → orthostatic hypotension |
| Toxins / poisoning | Carbon monoxide, organophosphates — always consider in HK context (e.g., charcoal burning for self-harm, gas heaters) |
- Not true syncope: no cerebral hypoperfusion.
- Mechanism: conversion disorder / functional neurological symptom disorder.
- Clues: episodes last longer than typical syncope (minutes to hours), eyes often closed (in true syncope eyes are usually open), no pallor, no injury, normal HR and BP during episodes, often in the context of underlying psychiatric comorbidity.
- Important: this is a diagnosis of exclusion. Do not label a child "psychogenic" without ruling out dangerous causes.
The European Society of Cardiology (ESC) classification (adapted for paediatrics) is the most widely used framework [3]:
| Category | Common Paediatric Causes |
|---|---|
| Vertigo (peripheral vestibular) | Benign paroxysmal vertigo of childhood, vestibular neuritis, labyrinthitis, otitis media with effusion, post-traumatic |
| Vertigo (central) | Migraine with brainstem aura, posterior fossa tumour, demyelination (rare), Chiari malformation |
| Presyncope / syncope | All causes above |
| Disequilibrium | Cerebellar ataxia (acute: post-infectious cerebellitis; chronic: posterior fossa tumour, Friedreich's ataxia), peripheral neuropathy |
| Non-specific lightheadedness | Anxiety, hyperventilation, panic disorder, depression, somatization |
8. Clinical Features — Symptoms and Signs
8.1 Symptoms
The clinical history is by far the most important diagnostic tool in evaluating syncope and dizziness. In paediatrics, you must obtain the history from both the child and the witnesses (parents, teachers, bystanders) [1][2].
| Symptom | Pathophysiological Basis | Suggests |
|---|---|---|
| Nausea | Vagal activation → ↑GI motility | Neurocardiogenic syncope [1][2] |
| Lightheadedness | ↓Cerebral perfusion (early, before LOC) | Neurocardiogenic syncope [1][2] |
| Sweating (diaphoresis) | Sympathetic activation (early phase before vagal takeover) + vagal cholinergic stimulation of sweat glands | Neurocardiogenic syncope [1][2] |
| Visual dimming / "greying out" / "tunnel vision" | ↓perfusion to retina → retinal ischaemia (retinal ganglion cells are exquisitely sensitive to hypoperfusion) | Presyncope of any cause |
| Tinnitus / ringing in ears | ↓perfusion to cochlea | Presyncope |
| Warmth / flushing | Vasodilation in the cutaneous circulation (paradoxical vasodilation before collapse) | Vasovagal |
| Palpitations / chest pain | ↑HR (sympathetic compensation) or arrhythmia | If prominent and preceding syncope → think cardiac cause [2] |
| Aura: déjà vu, olfactory hallucinations, peculiar taste, anxiety, abdominal pain | Focal cortical electrical discharge | Epileptic seizure [1][2] |
| No prodrome | Sudden ↓CO without time for compensatory symptoms | Cardiac syncope (often none — usually sudden) [1][2] |
| Feature | Pathophysiological Basis | Suggests |
|---|---|---|
| Extreme "death-like" pallor | ↓CO + reflex vasoconstriction of cutaneous vessels (sympathetic vasoconstriction diverting blood to vital organs) | Cardiac syncope [1][2] |
| Pallor | Vasodilation + ↓CO | Vasovagal syncope [1][2] |
| Cyanosis (blue spells) | Apnoea during expiration → hypoxia | Cyanotic breath-holding spell [1] |
| Sudden onset, in any position ± a/w exertion | Arrhythmia or outflow obstruction not dependent on posture | Cardiac syncope [1][2] |
| Usually brief (< 1 min) | Self-terminating arrhythmia or transient obstruction | Cardiac syncope [1][2] |
| Duration typically seconds to minutes | Once supine, cerebral perfusion restores quickly | Vasovagal |
| LOC > 1 min, a/w incontinence, tongue-biting, uprolling eyes | Sustained abnormal cortical electrical activity | Epileptic seizure [1][2] |
| Tonic-clonic movements AFTER LOC (brief, < 15 seconds) | Anoxic brain → transient cortical discharge secondary to hypoperfusion (NOT epilepsy) | Anoxic convulsion in syncope — this is a common exam trap! |
| Eyes open and rolled up | Brainstem reflex during LOC | Can be seen in both syncope and seizures |
| Eyes closed, resisting eye-opening | Voluntary | Psychogenic pseudosyncope |
| Feature | Pathophysiological Basis | Suggests |
|---|---|---|
| Recovery quick and without confusion | Cerebral perfusion restores immediately once supine; no neuronal injury | Vasovagal or cardiac syncope [1][2] |
| Recovery slow with prolonged confusion, headache, focal neurological signs | Post-ictal state: neuronal exhaustion and metabolic debt after sustained abnormal electrical activity | Epileptic seizure [1][2] |
| Fatigue / emotional upset after event | Normal post-syncopal or post-breath-holding response | Reflex syncope / breath-holding spells |
| Todd's paralysis (transient focal weakness) | Focal cortical exhaustion post-seizure | Seizure |
8.2 Signs (On Examination)
In most children with syncope, the examination is normal between episodes. The purpose of examination is to:
- Assess haemodynamic status (is the child still compromised?)
- Look for clues to an underlying cause
- Exclude structural heart disease
| Sign | Pathophysiological Basis | Significance |
|---|---|---|
| Pallor (conjunctivae, palms) | ↓Hb → ↓O₂ delivery; or vasospasm/vasoconstriction | Anaemia as cause or consequence; recent haemorrhage |
| Tachycardia at rest | Compensatory ↑HR for ↓SV or ↓volume | Dehydration, anaemia, ongoing blood loss, heart failure |
| Orthostatic BP changes (lying → standing) | ↓venous return → ↓SV → ↓BP on standing | Orthostatic hypotension (drop ≥ 20 mmHg systolic or ≥ 10 mmHg diastolic within 3 min of standing) |
| Postural tachycardia (HR ↑ ≥ 40 bpm on standing without BP drop) | Excessive sympathetic compensation for poor venous return | POTS |
| Dehydration signs (dry mucous membranes, sunken eyes, ↓skin turgor, ↓UO) | Inadequate fluid intake or excessive losses | Hypovolaemic predisposition to syncope |
| Sign | Pathophysiological Basis | Significance |
|---|---|---|
| Murmur: ejection systolic at LLSE ↑ with Valsalva | Dynamic LVOT obstruction (HCM) — Valsalva ↓preload → ↓LV cavity size → more obstruction → louder murmur | HCM |
| Murmur: ejection systolic at RUSE radiating to carotids | Fixed LVOT obstruction (aortic stenosis) — turbulent flow across narrowed valve | Severe AS |
| Murmur: widely fixed split S2 | ASD → equalization of filling times | Congenital heart disease |
| Loud P2 | Pulmonary hypertension → forceful closure of pulmonary valve | Pulmonary HTN |
| Displaced apex, gallop rhythm (S3) | Dilated cardiomyopathy, myocarditis | ↓CO as cause |
| Irregular pulse | Arrhythmia | Arrhythmic syncope |
| Sign | Significance |
|---|---|
| Focal neurological deficit | NOT expected in syncope — suggests stroke, space-occupying lesion, or post-ictal Todd's paralysis |
| Papilloedema | ↑ICP (tumour, IIH) — important to check fundoscopy |
| Nystagmus | Peripheral or central vestibular pathology (for dizziness presentations) |
| Ataxia | Cerebellar or proprioceptive pathology |
| Sign | Significance |
|---|---|
| Skin stigmata: café-au-lait spots, ash-leaf macules | NF1 (associated with phaeochromocytoma), tuberous sclerosis (associated with cardiac rhabdomyoma) |
| Marfanoid habitus (tall, arachnodactyly, pectus) | Marfan syndrome → mitral valve prolapse, aortic root dilation |
| Hearing impairment | Jervell and Lange-Nielsen syndrome (autosomal recessive LQTS with sensorineural deafness) |
| Iron deficiency features (koilonychia, angular stomatitis) | Anaemia contributing to syncope |
This section explicitly links "why" to "what you see":
-
Why does prolonged standing cause vasovagal syncope? Because gravity causes venous pooling in the legs → ↓venous return → ↓preload → vigorous contraction of underfilled LV → paradoxical vagal activation (Bezold-Jarisch reflex) → ↓HR + vasodilation → ↓cerebral perfusion.
-
Why do children with cyanotic breath-holding spells turn blue? Because the child holds breath in expiration → no gas exchange → ↓PaO₂ → desaturation → visible cyanosis. The ↑intrathoracic pressure also ↓venous return → ↓CO → eventual LOC.
-
Why do children with pallid breath-holding spells turn white (not blue)? Because the primary mechanism is vagal-mediated cardiac asystole, not apnoea. The heart stops briefly → no blood being pumped → skin becomes pale/white due to lack of perfusion. The anoxia is from ↓CO, not from ↓oxygenation.
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Why can syncope cause brief convulsive movements? Because after ~10–15 seconds of cerebral hypoperfusion, cortical neurons discharge aberrantly due to hypoxia → brief tonic or tonic-clonic movements. This is an anoxic seizure, not epilepsy. The EEG shows diffuse slowing (not epileptiform discharges).
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Why is syncope during exertion a red flag for cardiac disease? Because during exercise, normal physiology demands ↑CO. If there is a fixed obstruction (HCM, AS) or an exercise-triggered arrhythmia (LQTS, CPVT), the heart cannot meet demand → ↓cerebral perfusion → syncope. In contrast, vasovagal syncope typically occurs AFTER exercise (during the recovery phase when peripheral vasodilation persists but CO drops).
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Why does cardiac syncope occur without a prodrome? Because arrhythmias (e.g., VT, VF, complete heart block) cause an abrupt ↓CO. There is no time for the gradual sympathetic → vagal shift seen in vasovagal syncope. The child drops without warning.
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Why is the recovery from syncope quick but from seizures slow? In syncope, once the child falls flat, gravity restores venous return → CO ↑ → cerebral perfusion restores → rapid recovery. In seizures, the brain has been in a state of sustained electrical hyperactivity → post-ictal neuronal exhaustion and metabolic debt → slow recovery with confusion.
The history is the single most important diagnostic tool — it determines the cause in up to 60–80% of cases without any investigations [2].
10.1 Key History Elements
Before the event:
- What was the child doing? (Standing, sitting, lying, exercising, swimming)
- Was there a trigger? (Pain, blood, needle, emotion, hot room, dehydration)
- Any prodromal symptoms? (Nausea, lightheadedness, visual changes, palpitations)
- Any preceding illness? (Viral illness → myocarditis; gastroenteritis → dehydration)
During the event:
- Who witnessed it? (Get their account)
- Duration of LOC?
- Colour change? (Pale, blue, flushed)
- Movements? (Tonic-clonic — and if so, did they start before or after LOC?)
- Incontinence? Tongue-biting?
- Position of eyes?
After the event:
- How quickly did the child recover?
- Post-ictal confusion?
- Any focal weakness?
- Nausea, fatigue?
Background:
- Previous similar episodes?
- Past medical history (especially cardiac history, epilepsy)
- Family history of sudden cardiac death < 40 years, LQTS, HCM, deafness, drowning [2]
- Drug history (QT-prolonging medications)
- Exercise history
- Psychosocial history (stress, anxiety, school problems — especially in HK adolescents)
- Menstrual history (in adolescent females — pregnancy, anaemia)
| Feature | Paediatric | Adult |
|---|---|---|
| Most common cause | Vasovagal (~70%) | Vasovagal (~60%) |
| Unique paediatric entities | Breath-holding spells (6 mo – 5 yr) | Not applicable |
| Cardiac syncope proportion | 2–6% | ~15% |
| Common cardiac causes | LQTS, HCM, CPVT, anomalous coronary, WPW | AF, VT, AS, MI |
| POTS | Increasingly recognized (esp post-COVID) | Well-recognized |
| Orthostatic hypotension | Usually dehydration, rarely autonomic | Often medications, autonomic neuropathy |
| Psychogenic pseudosyncope | Consider in adolescents | More common |
High Yield Summary
Definition:
- Syncope = transient LOC + loss of postural tone + spontaneous recovery, due to ↓global cerebral perfusion (LOC within 8–10 sec of hypoperfusion to the RAS).
- Dizziness = broad term — must differentiate vertigo vs. presyncope vs. disequilibrium vs. non-specific lightheadedness.
Epidemiology:
- Lifetime prevalence ~15–25% in children; peak in adolescence; F > M.
-
60–80% neurocardiogenic; cardiac syncope only 2–6% but potentially fatal.
Most Common Causes:
- Vasovagal syncope is the #1 cause overall.
- Breath-holding spells (cyanotic and pallid) are the key paediatric-specific entities (age 6 mo – 5 yr).
- Cardiac syncope (LQTS, HCM, CPVT, anomalous coronary) = rare but life-threatening.
Red Flags for Cardiac Syncope:
- Syncope during exertion
- Syncope while supine or in water
- Family Hx of sudden death < 40 years
- Preceding palpitations / chest pain
- Abnormal ECG
- No prodrome (sudden collapse)
Pathophysiology:
- Vasovagal: venous pooling → ↓VR → vigorous LV contraction → Bezold-Jarisch reflex → paradoxical vagal activation → ↓HR + ↓SVR → ↓BP → syncope.
- Breath-holding (cyanotic): crying → forced expiration → ↑intrathoracic pressure + apnoea → ↓VR + hypoxia → syncope.
- Breath-holding (pallid): trigger → excess vagal stimulation → cardiac asystole → ↓cerebral perfusion → pallor → syncope.
- Cardiac: arrhythmia/obstruction → abrupt ↓CO → syncope without warning.
Anoxic Seizure ≠ Epilepsy: Brief tonic-clonic movements after LOC in syncope = anoxic convulsion from brain hypoperfusion, NOT epilepsy.
Clinical Differentiators:
- Vasovagal: prodrome (nausea, lightheadedness, sweating), standing, trigger, pallor, brief, rapid recovery.
- Cardiac: no prodrome, sudden, any position, exertional, death-like pallor, brief, rapid recovery BUT risk of death.
- Seizure: aura, LOC > 1 min, tonic-clonic movements from onset, incontinence, tongue-biting, slow recovery with post-ictal confusion.
Active Recall - Syncope / Dizziness in Paediatrics
[1] Senior notes: Adrian Lui Pediatrics.pdf (p117 — Paroxysmal disorders, breath-holding spells, vasovagal syncope, cardiac syncope) [2] Senior notes: Ryan Ho Fundamentals.pdf (p208–210 — Syncope section: mechanisms, cardiogenic vs neurocardiogenic vs seizure table, arrhythmic and structural causes) [3] Senior notes: Ryan Ho Cardiology.pdf (p63 — Syncope: mechanisms, epidemiology, differential table)
Differential Diagnosis of Syncope / Dizziness in Children
The differential diagnosis of a child presenting with "syncope" or "dizziness" is one of the broadest in paediatric medicine. The critical first step — as covered in the earlier section — is to unpack what the child and caregiver mean by their complaint. A structured approach prevents you from chasing the wrong diagnoses entirely.
Think of it this way: a child who says "I feel dizzy" could have anything from benign positional vertigo to a cardiac channelopathy. Your job is to systematically narrow the field using the history, age, context, and examination.
The differentials split into two broad presentations — each then branches by mechanism:
The Number One Exam Mistake
Students often jump straight to cardiac causes of syncope because they are dramatic and memorable. But > 60–80% of paediatric syncope is neurocardiogenic (reflex) [1][3]. The differentials must be ranked by probability AND danger. You need to exclude the dangerous (cardiac, metabolic) quickly, but the most likely answer in any exam stem about an otherwise well adolescent who fainted is vasovagal syncope.
A. Differential Diagnosis of TRUE SYNCOPE (Transient Loss of Consciousness)
This is the child who actually lost consciousness transiently with spontaneous recovery. The key differentials are between causes of syncope (cerebral hypoperfusion), seizure (electrical brain dysfunction), and pseudosyncope (psychogenic).
All subtypes share the final common pathway: an exaggerated autonomic reflex causes inappropriate vagal activation ± sympathetic withdrawal → ↓HR and/or ↓SVR → ↓BP → ↓cerebral perfusion → TLOC [1][3][4].
| Diagnosis | Age Group | Key Differentiating Features | Why This Mechanism? |
|---|---|---|---|
| Vasovagal syncope | Older children, adolescents (peak 15–19 yr) | Usually when standing; a/w situational trigger (hot/crowded environment, prolonged standing, fear, pain); prodrome of nausea, lightheadedness, sweating, pallor; LOC < 1 min; rapid recovery without confusion [1][3][4] | Bezold-Jarisch reflex: venous pooling → ↓VR → vigorous contraction of underfilled LV → vagal afferent activation → paradoxical ↑vagal + ↓sympathetic → ↓HR + vasodilation |
| Expiratory apnoea syncope ("blue/cyanotic breath-holding spell") | 6 months – 5 years | Trigger: anger, crying; hold breath in expiration → go blue, stiff then limp ± LOC; rapid recovery [1] | Prolonged forced expiration → ↑intrathoracic pressure (Valsalva) + apnoea → ↓VR → ↓CO + hypoxia → cyanosis + LOC |
| Reflex asystolic syncope ("pallid breath-holding spell") | 6 months – 5 years | Trigger: sudden pain/discomfort, head trauma, cold food, fright, fever; stop breathing → go pale (not blue), stiff ± brief GTCS; usually rapid recovery but occasionally ≥ 1 hour if severe [1] | Excess vagal stimulation → cardiac asystole → ↓cerebral perfusion → pallor (no blood flow to skin) → LOC ± anoxic convulsion |
| Situational syncope | Any age (more common in adolescence) | Syncope during/after specific triggers: micturition, defecation, coughing, swallowing cold food, hair-grooming | Each trigger has a specific vagal afferent pathway (e.g., bladder distension → pelvic parasympathetics; oesophageal cold stimulus → vagal reflex; cough → ↑intrathoracic pressure → ↓VR) |
How to differentiate vasovagal from cardiac syncope on history alone:
- Vasovagal: prodrome present (nausea, lightheadedness, sweating) [3][4], positional (standing), identifiable trigger, pallor, rapid recovery
- Cardiac: often no prodrome ("usually sudden") [3][4], can occur in any position including supine, ± preceded by palpitation, chest pain [3][4], extreme "death-like" pallor, may occur during exertion
Mechanism: impaired compensatory vasoconstriction or volume depletion on assuming the upright position → ↓BP → ↓cerebral perfusion.
| Diagnosis | Key Differentiating Features | Why? |
|---|---|---|
| Dehydration / hypovolaemia | History of GI losses (vomiting, diarrhoea), poor intake, hot weather, exercise; signs of dehydration; postural BP drop ≥ 20 mmHg systolic | ↓Intravascular volume → ↓VR → ↓SV → exaggerated postural ↓BP |
| Hypovolaemic syncope (e.g., haemorrhage, dehydration, anaphylaxis) [1] | Acute pallor, tachycardia, hypotension; look for source of bleeding or anaphylactic features (urticaria, wheeze, angioedema) | Severe volume loss → ↓CO → ↓cerebral perfusion. In anaphylaxis: vasodilation + capillary leak compound the hypovolaemia |
| Postural orthostatic tachycardia syndrome (POTS) | Adolescent (esp. female), chronic symptoms (≥ 3 months), HR ↑ ≥ 40 bpm on standing WITHOUT BP drop; presyncope, fatigue, palpitations, brain fog; increasingly recognised post-COVID | Impaired peripheral vasoconstriction → excessive venous pooling → compensatory ↑HR; frank syncope is uncommon in pure POTS |
| Drug-induced orthostatic hypotension | Recent medication change (antihypertensives — rare in children; antipsychotics, TCAs, α-blockers) | Drug-mediated vasodilation or volume depletion → inadequate reflex compensation |
| Adrenal insufficiency | Fatigue, weight loss, hyperpigmentation (primary), hypoglycaemia, hypoNa, hyperK; may present as adrenal crisis with shock [5] | ↓Cortisol → ↓vascular tone + ↓ability to retain Na/H₂O → hypovolaemia + vasodilation → orthostatic hypotension |
| Autonomic neuropathy (rare in children) | Guillain-Barré syndrome, familial dysautonomia (Riley-Day — Ashkenazi Jewish children); absent sweating, fixed HR | Damage to autonomic nerves → failure of vasoconstriction + HR response on standing |
A3. Cardiac Syncope — ~2–6% (but Potentially Fatal)
Mechanism: arrhythmia or structural cardiac disease → sudden ↓CO → ↓cerebral perfusion. The key distinguishing feature: often none (usually sudden); ± preceded by palpitation, chest pain [3][4].
| Diagnosis | Age | Key Differentiating Features | Why? |
|---|---|---|---|
| Long QT syndrome (LQTS) [1] | Any age; present in childhood | Family Hx of sudden death, syncope triggered by exertion (LQTS1), auditory stimuli (LQTS2), or sleep (LQTS3); prolonged QTc on ECG ( > 470 ms M, > 480 ms F); torsades de pointes | Delayed cardiac repolarisation (K⁺ or Na⁺ channel mutations) → early after-depolarisations → polymorphic VT (TdP) → ↓CO → LOC |
| Catecholaminergic polymorphic VT (CPVT) | School-age and adolescent | Syncope/cardiac arrest during exercise or emotional stress; resting ECG often normal; diagnosis by exercise stress test showing bidirectional VT | Ryanodine receptor (RyR2) mutation → abnormal Ca²⁺ release during adrenergic stimulation → triggered activity → bidirectional or polymorphic VT |
| Wolff-Parkinson-White (WPW) | Any age (congenital accessory pathway) | Palpitations preceding syncope; delta wave on resting ECG; SVT or pre-excited AF → very rapid ventricular rate → ↓diastolic filling → ↓CO | Accessory pathway (Bundle of Kent) allows re-entrant circuit (SVT) or rapid conduction of AF directly to ventricles bypassing AV node delay |
| Brugada syndrome | Adolescent / young adult | Syncope or cardiac arrest at rest or during sleep; coved ST elevation V1–V3; more common in SE Asian males | Na⁺ channelopathy → transmural voltage gradient in RV → phase 2 re-entry → VT/VF |
| Complete heart block (3° AV block) | Neonatal–childhood | Congenital: neonatal lupus (maternal anti-Ro/La); acquired: post-cardiac surgery, myocarditis; low resting HR; may present as hydrops fetalis | No conduction atria → ventricles → ventricular escape rhythm at 30–50 bpm → inadequate CO during exertion → syncope |
| SVT / AF / VT | Any age | Preceding palpitations; rapid onset/offset; pallor; ECG during event diagnostic | Rapid rate → ↓diastolic filling time → ↓SV → ↓CO |
Causes of exercise-related syncope [3][4]:
- LVOT obstruction: AS, HCM
- RVOT obstruction: pulmonary HTN
- Cardiomyopathy: DCM, HCM, ARVC
- Coronary artery disease: atherosclerotic, anomalous origin of coronary arteries
- Arrhythmogenic: VT, SVT, WPW, LQTS
| Diagnosis | Key Differentiating Features | Why? |
|---|---|---|
| Hypertrophic cardiomyopathy (HCM) | Exertional syncope, family Hx of HCM or sudden death, systolic murmur at LLSE ↑ with Valsalva, abnormal ECG (LVH, deep Q waves), pathological hypertrophy on echo | Dynamic LVOT obstruction + diastolic dysfunction → inability to ↑CO during exertion → ↓cerebral perfusion; also substrate for VT/VF |
| Severe aortic stenosis | Exertional syncope/presyncope, ejection systolic murmur radiating to carotids; may be congenital bicuspid valve | Fixed LVOT obstruction → inability to ↑CO during exertion + exertional vasodilation → ↓cerebral perfusion |
| Anomalous origin of coronary artery | Exertional syncope or sudden death in an otherwise well young person; may have no murmur | Aberrant course (typically LCA from right sinus with interarterial course between aorta and PA) → extrinsic compression during exertion → myocardial ischaemia → VT/VF or ↓CO [3][4] |
| Pulmonary hypertension | Exertional syncope, exertional dyspnoea, loud P2, RV heave; may be primary or secondary (e.g., congenital heart disease with Eisenmenger) | ↑RV afterload → inability to ↑CO during exercise → exertional syncope |
| Cardiac tamponade / myocarditis / DCM | Signs of heart failure (tachycardia, hepatomegaly, gallop, poor perfusion); preceding viral illness (myocarditis); pulsus paradoxus (tamponade) | ↓Systolic function or ↓diastolic filling → ↓CO → ↓cerebral perfusion |
| Cardiac tumour (e.g., atrial myxoma, rhabdomyoma) | Positional syncope (may occur with specific body positions that cause tumour to obstruct valve orifice); rhabdomyoma in infancy a/w tuberous sclerosis | Mechanical obstruction of intracardiac blood flow |
These are not true syncope (mechanism is not cerebral hypoperfusion) but present with TLOC and are the most important differential to distinguish.
| Diagnosis | Key Differentiating Features | Why This is Different From Syncope |
|---|---|---|
| Epileptic seizure | Preceded by aura (déjà vu, olfactory hallucinations); LOC typically > 1 min; tonic-clonic movements BEGIN at onset of LOC (not after); a/w incontinence, tongue-biting, uprolling eyeballs; recovery slow with prolonged post-ictal confusion, headache, focal neurological signs [1][3][4] | Mechanism: abnormal electrical activities in the brain [3][4] — not hypoperfusion. Key: convulsions in epilepsy begin simultaneously with LOC; in syncopal anoxic convulsion, the movements come AFTER LOC from a clearly syncopal prodrome |
| Febrile seizure | Fever ≥ 38°C, age 6 months – 5 years; brief GTCS; absence of CNS infection, metabolic disturbance, Hx of afebrile seizure [1] | Not hypoperfusion; temperature-dependent lowering of seizure threshold in immature brain |
| Absence seizure | Brief staring spells (5–15 seconds) without falling; can be provoked by hyperventilation; 3 Hz spike-and-wave on EEG | Not true LOC in the sense of collapse — child "blanks out" but remains upright. Parents may describe as "dizzy" or "zoning out" |
| Migraine with brainstem aura | Vertigo, visual aura, ataxia, dysarthria ± LOC; followed by headache; family Hx of migraine | Transient brainstem dysfunction (possibly cortical spreading depression extending to brainstem) — not simple hypoperfusion |
| Raised ICP | Morning headache worsened by coughing/straining, vomiting, papilloedema, progressive neurological signs, personality change; posterior fossa tumour in children may present with ataxia and vertigo | Mass effect → compression of brainstem → impaired consciousness; or transient herniation during Valsalva |
Anoxic Convulsion vs Epileptic Seizure — The Exam Trap
A brief tonic-clonic movement AFTER the onset of syncope is an anoxic (syncopal) convulsion, NOT epilepsy [1]. The key differentiator: (1) timing — movements come AFTER LOC in syncope but FROM THE START in seizure; (2) duration — anoxic convulsions last < 15 seconds vs. seizures typically > 1 min; (3) recovery — rapid in syncope, slow with confusion in seizure; (4) EEG — normal interictally in anoxic convulsion. This is commonly tested because misdiagnosis leads to inappropriate anti-seizure medication.
| Diagnosis | Key Differentiating Features | Why? |
|---|---|---|
| Hypoglycaemia | Adrenergic symptoms (palpitation, sweating, anxiety, tremor, tachycardia) followed by neuroglycopenic symptoms (hunger, paraesthesia, seizures, focal weakness, ↓consciousness, drowsiness, coma) [5]; relevant in diabetic children on insulin, neonates, ketotic hypoglycaemia of childhood, adrenal insufficiency | ↓Glucose to brain → neuroglycopenia → CNS dysfunction; confirmed by Whipple's triad [5] |
| Severe anaemia (acute) | Pallor, tachycardia, postural dizziness, SOB; Hx of acute blood loss, haemolytic crisis (e.g., splenic sequestration in SCD), heavy menstrual loss in adolescent girls; SOB on exertion, palpitation, dizziness/syncope (may be postural) [6] | Severe or acute ↓Hb → ↓O₂-carrying capacity → ↓O₂ delivery to brain → presyncope/syncope |
| Hyperventilation | Anxious adolescent; perioral and distal tingling/numbness; feeling of SOB with normal SpO₂; carpopedal spasm | ↓PaCO₂ → cerebral vasoconstriction → ↓cerebral blood flow; also respiratory alkalosis → ↑Ca²⁺ binding to albumin → relative hypocalcaemia → paraesthesia |
| Carbon monoxide poisoning | Headache, nausea, confusion, LOC; exposure history (gas heater, closed car, charcoal burning — relevant in HK self-harm context); "cherry red" skin (late/unreliable); normal SpO₂ on pulse ox (CO mimics O₂ on standard pulse ox) | CO displaces O₂ from Hb (CO affinity 200–250× O₂) → ↓O₂ delivery → tissue hypoxia; also direct mitochondrial toxicity |
| Electrolyte disturbance | Hyponatraemia (seizures, confusion); hypokalaemia (weakness, arrhythmia); hypocalcaemia (tetany, seizures) | Various — hypoNa causes cerebral oedema → impaired neuronal function; hypoCa causes neuronal hyperexcitability |
| Drug / toxin ingestion | Adolescents: recreational drugs, intentional overdose; younger children: accidental ingestion | Mechanism varies by agent: sedatives → CNS depression; sympathomimetics → arrhythmia; anticholinergics → altered consciousness |
| Diagnosis | Key Differentiating Features | Why? |
|---|---|---|
| Psychogenic pseudosyncope / non-epileptic attacks | Episodes longer than typical syncope (minutes to hours); eyes often closed and actively resisting opening (in true syncope eyes are usually open); no pallor; normal HR and BP during episodes; no injury despite frequent "collapses"; underlying psychiatric comorbidity; adolescents under psychosocial stress | Mechanism: psychogenic [4] — no cerebral hypoperfusion, no abnormal electrical discharge. This is a conversion/functional neurological symptom disorder. Normal haemodynamics during the event differentiate it from true syncope |
Clinical Pearl — Eyes Open vs Closed
In true syncope, the eyes are typically open (sometimes rolled upward) because the brainstem's reticular activation system is suppressed — it takes active cortical effort to close the eyes. In psychogenic pseudosyncope, the eyes are typically closed and the patient may resist passive eye-opening. This is a quick bedside clue but not 100% reliable — always consider the overall clinical picture.
B. Differential Diagnosis of DIZZINESS (Without True TLOC)
For children who describe "dizziness" without actual LOC, the differentials pivot depending on which of the four subtypes of dizziness is present:
| Diagnosis | Age / Context | Key Differentiating Features | Why? |
|---|---|---|---|
| Benign paroxysmal vertigo of childhood (BPVC) | 2–6 years (migraine equivalent) | Episodic vertigo lasting seconds to minutes; pallor, nystagmus, ataxia during attack; NO LOC; completely normal between episodes; often family Hx of migraine; may evolve into migraine in later childhood | Thought to be a migraine equivalent affecting the vestibular system; mechanism likely similar to cortical spreading depression affecting vestibular nuclei |
| Vestibular neuritis / labyrinthitis | Any age (often post-viral) | Acute onset of sustained severe rotatory vertigo, nausea/vomiting; horizontal nystagmus (fast phase away from affected side); hearing loss if labyrinthitis (cochlea involved) | Inflammation of vestibular nerve (CN VIII) → asymmetric vestibular input → brain perceives rotation |
| Otitis media with effusion / middle ear disease | Young children | Dizziness/unsteadiness with concurrent ear symptoms (otalgia, hearing loss, otorrhoea); abnormal tympanic membrane | Middle ear inflammation/effusion → secondary labyrinthine irritation |
| Benign paroxysmal positional vertigo (BPPV) | Rare in children (adults/elderly); adolescents possible post-trauma | Brief (< 1 min) episodes provoked by specific head positions; positive Dix-Hallpike test with characteristic geotropic torsional nystagmus | Otoconia dislodged from utricle into semicircular canal (usually posterior) → endolymph displacement → inappropriate cupula stimulation |
| Post-traumatic vertigo | Post head injury | Vertigo following head trauma; may be BPPV-type or more prolonged (labyrinthine concussion) | Trauma → otolith displacement or labyrinthine damage |
| Posterior fossa tumour | Any age (peak 5–10 yr for medulloblastoma, ependymoma, cerebellar astrocytoma) | Progressive vertigo, ataxia, headache (especially morning, worsened by Valsalva), vomiting, papilloedema, cranial nerve palsies; signs of ↑ICP | Mass effect on cerebellum/brainstem → direct vestibular nuclear compression + ↑ICP from obstructive hydrocephalus (4th ventricle obstruction) |
| Migraine with brainstem aura (basilar migraine) | Adolescents | Vertigo, visual aura (scotoma, blurring), dysarthria, tinnitus ± LOC; followed by headache; family Hx | Cortical spreading depression affecting brainstem/vestibular structures |
| Diagnosis | Key Differentiating Features | Why? |
|---|---|---|
| Acute post-infectious cerebellitis | Acute ataxia 1–2 weeks after viral illness (varicella, EBV); unsteady wide-based gait; truncal ataxia; self-limiting | Immune-mediated inflammation of cerebellum → cerebellar dysfunction → impaired coordination and balance |
| Cerebellar tumour | Progressive ataxia, headache, vomiting, papilloedema | Mass effect on cerebellum → progressive loss of balance and coordination |
| Friedreich's ataxia | Adolescent; progressive ataxia + pes cavus + scoliosis + cardiomyopathy; AR inheritance | GAA trinucleotide repeat in frataxin gene → mitochondrial dysfunction in dorsal root ganglia + cerebellum + heart |
| Peripheral neuropathy | Glove-and-stocking sensory loss, ↓reflexes; Charcot-Marie-Tooth in children; GBS if acute | Loss of proprioceptive input → impaired balance (sensory ataxia) |
| Diagnosis | Key Differentiating Features | Why? |
|---|---|---|
| Anxiety / panic attacks | Adolescent; feelings of dizziness, unsteadiness, light-headedness, or faint [7]; associated palpitations, SOB, trembling, chest discomfort, paraesthesia, derealization; recurrent unexpected attacks (panic disorder) or situational (social anxiety, specific phobia, GAD) | Hyperventilation → ↓PaCO₂ → cerebral vasoconstriction → ↓cerebral blood flow; autonomic arousal mimics presyncope [7][8] |
| Somatisation / somatic symptom disorder | Non-specific: fatigue, syncope, dizziness [9]; chronic, causes distress/impairment; excessive health-related thoughts and behaviours; multiple somatic complaints without adequate medical explanation | Amplification of normal somatic sensations through excessive attention and anxiety; central sensitisation |
| Medication side effects | Temporal relationship with drug initiation/dose change; sedating antihistamines, anti-seizure medications, antipsychotics | Drug-specific mechanisms: sedation, vasodilation, vestibular suppression |
| Hypoglycaemia (mild) | Shakiness, hunger, irritability, difficulty concentrating, lightheadedness; resolves with food; timing related to meals or insulin | ↓Glucose → ↓substrate for neuronal function → non-specific CNS symptoms |
Because the differential in paediatrics varies dramatically with age, here is a practical age-stratified summary:
| Age Group | Most Likely Causes of Syncope | Most Likely Causes of Dizziness |
|---|---|---|
| Neonate – 6 months | Cardiac arrhythmia (congenital LQTS, complete heart block from neonatal lupus), cardiac structural disease, metabolic (hypoglycaemia, inborn errors), sepsis/shock | Rarely reported; consider seizure, metabolic |
| 6 months – 5 years | Breath-holding spells (cyanotic and pallid) [1], febrile seizures (differential), cardiac arrhythmia (rare), intussusception (pallor/lethargy can mimic syncope) | Benign paroxysmal vertigo of childhood, otitis media, acute cerebellitis |
| 5–12 years | Vasovagal syncope (becoming more common), orthostatic (dehydration), cardiac (HCM, LQTS, CPVT), epilepsy | BPVC, migraine, anxiety (emerging), posterior fossa tumour |
| 12–18 years (adolescence) | Vasovagal syncope (most common), POTS, orthostatic hypotension (dehydration, eating disorders), cardiac (LQTS, HCM, WPW, CPVT), anxiety/hyperventilation, psychogenic pseudosyncope, pregnancy | Migraine (with/without aura), anxiety/panic, vestibular neuritis, BPPV (post-trauma), hyperventilation, somatisation |
Don't Forget in Adolescents
Always ask about eating disorders (anorexia → dehydration, electrolyte disturbance, bradycardia, orthostatic hypotension), pregnancy (in any post-menarchal adolescent), substance use (recreational drugs, energy drinks → arrhythmias), and self-harm / intentional overdose (carbon monoxide, medication overdose) — particularly relevant in the Hong Kong context where these presentations are increasingly common.
| Feature | Vasovagal | Cardiac | Seizure | Breath-Holding (Cyanotic) | Breath-Holding (Pallid) | POTS | Psychogenic |
|---|---|---|---|---|---|---|---|
| Age | Adolescent | Any | Any | 6 mo–5 yr | 6 mo–5 yr | Adolescent | Adolescent |
| Prodrome | Nausea, lightheaded, sweating | Often none | Aura | Crying, anger | Pain, fright | Lightheaded, palpitations | Variable |
| Trigger | Standing, heat, pain, emotion | Exertion, swimming, sleep, loud noise | Often none / sleep deprivation | Temper tantrum | Sudden pain/head bump | Standing | Psychosocial stress |
| Colour | Pale | Death-like pallor | Normal → cyanotic (if prolonged) | Blue | Pale/white | Normal | Normal |
| Duration LOC | < 1 min | < 1 min | > 1 min | Seconds | Seconds | Rarely true LOC | Minutes–hours |
| Convulsive movements | Brief anoxic seizure possible (after LOC) | Brief anoxic seizure possible | From onset of LOC | ± brief GTCS after LOC | ± brief GTCS | No | Variable, non-stereotyped |
| Recovery | Rapid, no confusion | Rapid if self-terminating | Slow, prolonged confusion | Rapid | Rapid (may be prolonged if severe) | Rapid | Variable |
| ECG | Normal | Often abnormal | Normal (between episodes) | Normal | Normal | Normal (↑HR on standing) | Normal |
The history alone will give you the answer in 60–80% of cases [3]. Here is how to reason through it systematically:
Step 1: Was there true LOC?
- Yes → syncope vs seizure vs pseudosyncope
- No → vertigo vs disequilibrium vs lightheadedness
Step 2: If true LOC — what was the context?
- During exertion → cardiac until proven otherwise (HCM, LQTS, CPVT, anomalous coronary)
- After exertion → vasovagal (vasodilation persists, CO drops)
- Standing/hot room/emotional trigger → vasovagal
- Crying/temper tantrum (age < 5 yr) → cyanotic breath-holding
- Sudden pain/head bump (age < 5 yr) → pallid breath-holding
- Supine/sleeping → cardiac arrhythmia (LQTS type 3, Brugada)
- During swimming → LQTS type 1 (cold water + exertion)
Step 3: Was there a prodrome?
- Yes (nausea, lightheadedness, sweating) → neurocardiogenic
- Yes (aura: déjà vu, smell, taste) → seizure
- No prodrome (sudden drop) → cardiac
Step 4: What happened during the event?
- Convulsive movements FROM the start + LOC > 1 min + incontinence + tongue bite → seizure
- Brief twitch AFTER LOC → anoxic convulsion (not epilepsy)
- Blue coloration → cyanotic breath-holding OR prolonged seizure
- Pallor → pallid breath-holding, vasovagal, or cardiac
Step 5: How fast was recovery?
- Rapid, no confusion → syncope (any type) or breath-holding
- Slow with prolonged confusion, headache, focal neurological signs → seizure [3][4]
Step 6: Red flags for cardiac?
- Family Hx sudden death < 40 yr
- Syncope during exertion / swimming / auditory stimulus
- Preceding palpitations
- Known heart disease
- Abnormal ECG → If any present: urgent cardiology referral, ECG, echo
Step 7: Red flags for something sinister?
- Progressive neurological symptoms → tumour / ↑ICP
- Focal neurological signs → stroke (extremely rare in children unless SCD, cardiac, prothrombotic)
- Papilloedema → ↑ICP
High Yield Summary — Differential Diagnosis
- > 60–80% of paediatric syncope is neurocardiogenic (reflex) — vasovagal in adolescents, breath-holding spells in toddlers.
- Cardiac syncope is only 2–6% but potentially lethal — red flags: exertional, no prodrome, family Hx sudden death, palpitations, abnormal ECG.
- The key differential for syncope is seizure — differentiate by timing of convulsive movements (after LOC = anoxic convulsion of syncope; from onset = seizure), duration of LOC ( < 1 min syncope vs > 1 min seizure), and speed of recovery (rapid = syncope; slow with confusion = seizure).
- Breath-holding spells are paediatric-specific (6 mo–5 yr): cyanotic type = expiratory apnoea from crying; pallid type = vagal-mediated asystole from pain/fright.
- Dizziness without LOC: vertigo (vestibular — BPVC most common in young children, migraine in adolescents), disequilibrium (cerebellar), lightheadedness (anxiety/hyperventilation most common in adolescents).
- In adolescents, always consider: POTS, anxiety/panic, eating disorders, pregnancy, substance use, self-harm.
- Age-based approach is essential: the differential diagnosis changes dramatically from neonates (cardiac, metabolic) to toddlers (breath-holding, febrile seizures) to adolescents (vasovagal, POTS, anxiety, cardiac channelopathies).
Active Recall - Differential Diagnosis of Syncope/Dizziness in Paediatrics
References
[1] Senior notes: Adrian Lui Pediatrics.pdf (p117 — Paroxysmal disorders, breath-holding spells, vasovagal syncope, cardiac syncope, febrile seizures) [3] Senior notes: Ryan Ho Fundamentals.pdf (p208–210, p323 — Syncope mechanisms, cardiogenic vs neurocardiogenic vs seizure table, exercise-related syncope causes) [4] Senior notes: Ryan Ho Cardiology.pdf (p63–66 — Syncope mechanisms, neurocardiogenic pathogenesis, structural/arrhythmic causes, exercise-related syncope causes, tilt-table test) [5] Senior notes: Ryan Ho Endocrine.pdf (p71, p94 — Adrenal insufficiency, hypoglycaemia clinical features and Whipple's triad) [6] Senior notes: Ryan Ho Haemtology.pdf (p10 — Symptoms of anaemia including dizziness/syncope) [7] Senior notes: Ryan Ho Psychiatry.pdf (p173, p178–179 — Panic disorder clinical features, GAD somatic features including dizziness) [8] Senior notes: Ryan Ho Psychiatry.pdf (p75 — Delirium differential including non-convulsive status epilepticus) [9] Senior notes: Ryan Ho Psychiatry.pdf (p202 — Somatic symptom disorder including syncope and dizziness as non-specific presentations)
Diagnostic Criteria, Algorithm, and Investigations for Paediatric Syncope / Dizziness
Unlike conditions such as rheumatic fever or Kawasaki disease, syncope is a symptom, not a disease. There is no single set of "diagnostic criteria" for syncope itself. Instead, the diagnostic process aims to:
- Confirm that the event was true syncope (transient global cerebral hypoperfusion with LOC and spontaneous recovery)
- Identify the specific aetiology (reflex, orthostatic, cardiac, or other)
- Risk-stratify the child — is this benign, or does it carry a risk of sudden death?
The European Society of Cardiology (ESC) 2018 Guidelines (applicable to all ages, adapted for paediatrics) and the American Heart Association/American College of Cardiology (AHA/ACC) 2017 Guideline for the Evaluation and Management of Syncope provide the framework. For paediatrics specifically, the approach is informed by Paediatric Cardiology Society consensus statements and the ESC paediatric addendum [3][4][10].
The fundamental principle: the history is the single most powerful diagnostic tool — it determines the cause in up to 60–80% of cases [3][4].
The ESC 2018 defines syncope as requiring ALL of:
| Criterion | Explanation |
|---|---|
| Transient loss of consciousness (TLOC) | The child truly lost consciousness — not just "felt faint" (that is presyncope) |
| Loss of postural tone | The child fell or would have fallen if unsupported |
| Rapid onset | Sudden or near-sudden — not a gradual decline in consciousness |
| Short duration | Typically seconds to < 2 minutes |
| Spontaneous and complete recovery | No resuscitation required; full return to baseline. If a child requires intervention to regain consciousness, this is NOT simple syncope — think seizure, cardiac arrest, metabolic coma |
| Due to transient global cerebral hypoperfusion | This is what separates syncope from other causes of TLOC (seizure, concussion, psychogenic) |
Clinical Pearl — Not Every 'Blackout' is Syncope
If the child did not lose consciousness (presyncope), if recovery was slow with prolonged confusion (seizure), if there was no loss of postural tone (absence seizure), or if resuscitation was needed (cardiac arrest), it is NOT syncope by definition. Getting the definition right is the first diagnostic step.
3. Risk Stratification — Identifying the Dangerous Minority
The whole point of the diagnostic workup is to separate the ~95% of children with benign syncope from the ~2–6% with life-threatening cardiac causes. Multiple scoring systems exist for adults (San Francisco Syncope Rule, OESIL, EGSYS), but none are validated in the paediatric population. Therefore, in children we rely on clinical red flags [3][4][10].
| Red Flag | Why It Points to Cardiac | Action |
|---|---|---|
| Syncope during exertion | Exercise ↑cardiac demand → structural obstruction or arrhythmia unmasked | Urgent ECG + echo + cardiology referral |
| Syncope while supine or swimming | Posture-independent syncope not explained by reflex mechanism; cold water + exertion triggers LQTS1 | Urgent ECG + cardiology |
| No prodrome — sudden collapse | Abrupt ↓CO from arrhythmia — no time for autonomic warning symptoms [3][4] | Urgent ECG |
| Preceded by palpitations or chest pain | Suggests arrhythmia or coronary ischaemia preceding the syncope [4] | ECG + ambulatory monitoring |
| Family Hx of sudden cardiac death < 40 years, LQTS, HCM, drowning, SIDS | Inherited channelopathies and cardiomyopathies are familial | ECG on patient AND first-degree relatives |
| Abnormal cardiac examination (murmur, irregular rhythm, signs of HF) | Structural heart disease | Echo + ECG + cardiology |
| Abnormal ECG | Direct evidence of electrical substrate for arrhythmia | See ECG interpretation section below |
| Known congenital heart disease (repaired or unrepaired) | Substrate for arrhythmia or haemodynamic compromise | Specialist follow-up |
| Recurrent syncope refractory to treatment | May have been misdiagnosed as vasovagal | Extended monitoring |
- Classic prodrome (nausea, lightheadedness, sweating, visual dimming)
- Identifiable trigger (standing, heat, pain, blood/needle, emotion)
- Age-appropriate context (adolescent at school assembly)
- Normal cardiac examination
- Normal ECG
- Rapid and complete recovery
- Family history of fainting (not sudden death)
In a child with ALL low-risk features and a classic vasovagal history, minimal or no further investigation beyond history, examination, and ECG is required [10].
5. Investigation Modalities — Detailed
This bears repeating because it cannot be overemphasised: clear Hx most important [3][4]. In paediatrics, you must get the history from multiple sources — the child, the parent/caregiver, any witness (teacher, friend, coach).
Key history components covered in prior sections. The structured "5 Ws" approach is useful:
- Who: age, sex, background medical history, family history
- What: exactly what happened — description from the child AND witnesses
- When: timing relative to meals, sleep, menstrual cycle; time of day
- Where: school assembly (heat/standing), swimming pool, bed (supine)
- Why: identifiable trigger or provoking factor
Family History — Ask Specifically
Don't just ask "Is there any family history?" — be specific: "Has anyone in the family died suddenly before age 40? Has anyone had unexplained drowning, a single-vehicle car accident, seizures, fainting spells, or a pacemaker/defibrillator?"
| Component | What to Check | Why |
|---|---|---|
| Vitals: HR, BP (supine AND standing), RR, SpO₂, temp | Active standing test: check BP and HR supine, then at 1, 3, and 5 minutes of standing | To detect orthostatic hypotension (↓SBP ≥ 20 or ↓DBP ≥ 10 within 3 min) or POTS (↑HR ≥ 40 in adolescents) [4] |
| Cardiovascular exam | Murmurs (HCM: systolic at LLSE ↑ Valsalva; AS: ejection systolic RUSE → carotids), rhythm irregularity, S2 splitting, RV heave, apex displacement, gallop | To detect structural heart disease or arrhythmia |
| Hydration status | Mucous membranes, skin turgor, cap refill, JVP (older children) | To identify dehydration as contributor |
| Neurological exam | Tone, power, reflexes, coordination, cranial nerves, fundoscopy (papilloedema) | To exclude neurological cause (raised ICP, posterior fossa lesion) — focal signs are NOT expected in true syncope |
| Growth parameters | Height, weight, BMI plotted on growth charts | Poor growth → chronic disease; low BMI → eating disorder; tall with arachnodactyly → Marfan |
| Skin | Café-au-lait spots (NF1), ash-leaf macules (tuberous sclerosis), hyperpigmentation (Addison's) | Syndromic associations with cardiac/metabolic disease |
A 12-lead ECG should be performed in EVERY child presenting with syncope. This is the single most important investigation after the history and examination [3][4][10].
Why? Because an ECG can directly identify an arrhythmic substrate that would explain (or predict) cardiac syncope. It is cheap, non-invasive, widely available, and can be life-saving.
Interpretation — What to look for systematically:
| ECG Finding | What It Suggests | Pathophysiology |
|---|---|---|
| Prolonged QTc > 470 ms in males, > 460 ms in females [4] | Long QT syndrome (LQTS) | Delayed ventricular repolarisation → ↑vulnerability to triggered activity → torsades de pointes (TdP) |
| Biphasic/notched T waves [4] | LQTS (commonly found but insensitive) | Abnormal repolarisation morphology from channelopathy |
| Delta wave (short PR + slurred QRS upstroke) | Wolff-Parkinson-White (WPW) | Accessory pathway (Bundle of Kent) pre-excites the ventricle → short PR, delta wave |
| Coved ST elevation in V1–V3 | Brugada syndrome | Na⁺ channelopathy → transmural voltage gradient in RV epicardium → characteristic ST morphology |
| Deep Q waves in lateral/inferior leads + LVH pattern | Hypertrophic cardiomyopathy (HCM) | Septal hypertrophy → "dagger-like" Q waves from septal depolarisation; ↑voltage from thickened myocardium |
| Complete heart block (dissociated P waves and QRS) | 3° AV block | No conduction from atria to ventricles → risk of bradycardia-related syncope |
| Sinus bradycardia below normal range for age | Sick sinus syndrome, athletic heart, drug effect | ↓SA node automaticity → insufficient HR → ↓CO |
| Ventricular pre-excitation | WPW or other accessory pathway | Allows re-entrant tachycardia |
| ST-segment changes | Myocarditis, coronary anomaly (rare in children) | Myocardial ischaemia or inflammation |
| RV strain pattern (RAD, RVH, RBBB) | Pulmonary hypertension, PE (rare in children), ARVC | ↑RV pressure/volume overload |
| Epsilon waves (small potentials at terminal QRS in V1–V3) | Arrhythmogenic RV cardiomyopathy (ARVC) | Fibrofatty replacement of RV myocardium → delayed depolarisation |
| Normal ECG | Reassuring but does NOT exclude all cardiac causes (CPVT has normal resting ECG!) | CPVT only shows arrhythmia during adrenergic stimulation (exercise) |
Paediatric ECG norms differ from adults — key age-specific considerations:
- Neonates: right axis deviation and RV dominance are NORMAL (because of the high pulmonary vascular resistance in utero). Don't call this "RVH."
- QTc calculation: use Bazett's formula (QTc = QT / √RR). In neonates, QTc up to 460 ms can be normal in the first week, but persistent QTc > 470 ms warrants investigation.
- HR norms: resting HR decreases with age (neonate 120–160 bpm → adolescent 60–100 bpm). Sinus bradycardia below the age-appropriate range is concerning.
CPVT Trap
Catecholaminergic polymorphic VT (CPVT) has a normal resting ECG. If you suspect exercise-triggered cardiac syncope and the resting ECG is normal, you MUST proceed to exercise stress testing. A normal resting ECG does not exclude cardiac syncope.
Routine blood tests are not needed for classic vasovagal syncope but are indicated when the history suggests a non-reflex cause:
| Test | When to Order | Key Findings & Interpretation |
|---|---|---|
| Capillary/venous blood glucose | Suspicion of hypoglycaemia (diabetic on insulin, neonatal, prolonged fasting) | Low glucose concurrent with symptoms + resolution with correction = Whipple's triad [5] |
| CBC with differential | Pallor, menorrhagia, poor diet, suspected anaemia [6] | ↓Hb → anaemia contributing to presyncope; MCV guides type (microcytic → iron deficiency most common in paediatrics) |
| Electrolytes (Na, K, Ca, Mg) | Vomiting, diarrhoea, diuretic use, seizure features, recurrent syncope [4][11] | HypoK → arrhythmia; hypoNa → seizure; hypoCa → tetany/seizure; hypoMg → arrhythmia |
| TFT | Tachycardia, weight loss, tremor, goitre | Hyperthyroidism → ↑HR → tachyarrhythmia; hypothyroidism → bradycardia |
| Cortisol / ACTH (synacthen test) | Hypotension, hyperpigmentation, hypoNa, hyperK, hypoglycaemia | ↓Cortisol → adrenal insufficiency → inability to maintain vascular tone [5] |
| β-hCG (in post-menarchal adolescents) | ALL adolescent females with syncope or dizziness | Pregnancy → supine hypotension (IVC compression), ↓SVR, anaemia |
| Cardiac enzymes (troponin) | Chest pain, ECG changes, suspected myocarditis | ↑Troponin → myocardial injury |
| BNP / NT-proBNP | Suspected heart failure | ↑BNP → ventricular wall stress from volume/pressure overload |
| Drug levels / toxicology screen | Suspected ingestion, adolescent with unexplained LOC | Detection of causative agent |
| ABG + lactate | Shock, prolonged collapse, respiratory symptoms [11] | Metabolic acidosis with ↑lactate → poor tissue perfusion |
| Indication | What to Look For | Interpretation |
|---|---|---|
| Any clinical suspicion of structural heart disease (murmur, signs of HF, abnormal ECG) | Chamber dimensions, wall thickness, valve function, LVOT gradient, coronary origins, pericardial effusion | HCM: asymmetric septal hypertrophy ≥ 15 mm (or > 2 SD for body surface area in children), LVOT gradient ≥ 30 mmHg at rest |
| Exertional syncope [3][4] | As above + specifically assess for dynamic LVOT obstruction (HCM), fixed obstruction (AS), anomalous coronary origins, RV function (ARVC, pulmonary HTN) | Anomalous coronary: LCA from right sinus coursing between aorta and PA |
| Family Hx of HCM or sudden death | Screen for subclinical HCM | LV wall thickness, systolic anterior motion of mitral valve |
| Abnormal ECG | Assess for structural correlate | E.g., deep Q waves on ECG → check for septal hypertrophy |
Paediatric-specific point: In young children, echocardiography is the primary imaging modality (no radiation, widely available, excellent acoustic windows in children due to thinner chest walls). It can usually visualize coronary artery origins in children (harder in adults).
The gold standard for diagnosing arrhythmic syncope is demonstrating the arrhythmia at the time of symptoms — this is known as symptom-rhythm correlation [4].
| Modality | Duration | When to Use | How It Works |
|---|---|---|---|
| Holter monitoring | 24–72 hours (up to 7 days) | Daily or near-daily symptoms | Continuous recording with patient-activated event markers; child presses a button when symptomatic [3][4] |
| Event (loop) monitors | 2–4 weeks | Weekly or monthly symptoms | Continuous "loop" recording that overwrites itself; patient activates the device to save the rhythm strip when symptoms occur [3][4] |
| Patch recorder (e.g., Zio patch) | Up to 14 days | Intermediate frequency symptoms | Small adhesive patch on chest; continuous recording; sent for analysis after wearing period [3][4] |
| Implantable loop recorder (ILR) | Up to 3 years | Very infrequent (< 1/month) but recurrent, concerning symptoms | Subcutaneously implanted in prepectoral region; continuous monitoring; auto-detects arrhythmias and patient-activated events [3][4] |
Paediatric considerations:
- Holter monitors are well-tolerated even in young children. Use paediatric-sized electrodes.
- ILRs are increasingly used in children (e.g., Reveal LINQ™ — very small device). Requires brief general anaesthesia for implantation in young children.
- The key principle: the monitoring duration must match the symptom frequency. Putting a 24-hour Holter on a child who faints once every 3 months is almost guaranteed to yield nothing useful.
| Indication | What to Look For | Interpretation |
|---|---|---|
| Exertional syncope | Arrhythmia during/after exercise, BP response, exercise capacity | VT during exercise = CPVT or other exercise-triggered arrhythmia |
| Suspected CPVT (resting ECG normal, exertional syncope) | Bidirectional or polymorphic VT provoked by exercise | Diagnostic for CPVT |
| Suspected LQTS | QTc behaviour during exercise and recovery | Maladaptation of QT interval to changing HR [4] — QTc should shorten with ↑HR; failure to shorten or paradoxical prolongation suggests LQTS |
| Suspected exercise-related structural syncope (HCM, AS) | BP response, occurrence of arrhythmia, ST changes | Failure of SBP to rise ≥ 20 mmHg with exercise or a drop during exercise → ominous in HCM |
Paediatric considerations: Performed on age-appropriate equipment (bicycle ergometry more feasible in younger children). Must have resuscitation equipment immediately available. Contraindicated in acute myocarditis, severe AS with symptoms, or known unstable arrhythmia.
Workup: usually not required (dx by exclusion) but may be useful when atypical/recurrent [3][4].
| Aspect | Detail |
|---|---|
| Indication | Recurrent unexplained syncope when clinical features are atypical for vasovagal; differentiating convulsive syncope from epilepsy; diagnosing psychogenic pseudosyncope; confirming delayed orthostatic hypotension or POTS [3][4] |
| Procedure | Patient tilted from supine to 60–70° for 20–45 minutes ± pharmacological provocation (low-dose isoproterenol or sublingual nitrates) [3][4] |
| Positive result | ↓HR (cardioinhibitory type) and/or ↓BP (vasodepressor type) reproducing the patient's typical symptoms [3][4] |
| Negative result | No haemodynamic change and no symptoms during the entire test |
| Limitations | Findings are suggestive of tendency/predisposition to reflex syncope only [3][4] — it does not definitively prove that the presenting episode was vasovagal. Sensitivity ~60–70%, specificity ~85–90%. False negatives are common in children. |
| POTS diagnosis | During tilt: sustained HR ↑ ≥ 40 bpm in adolescents (or HR > 120 bpm absolute) within 10 minutes WITHOUT significant BP drop |
Pharmacological provocation:
- Isoproterenol may paradoxically trigger vasovagal syncope, presumably due to activation of central circulation mechanoreceptors [4] — this ↑sensitivity but ↓specificity.
- Nitroglycerin causes venodilation → ↓VR → ↓SV without impeding SN response of ↑HR and arterial vasoconstriction [4].
Paediatric considerations: Can be performed in children from about age 6–7 years. Younger children may not tolerate the prolonged standing period. In centres without tilt-table facilities, a supervised active standing test (standing motionless against a wall for up to 10 minutes with HR and BP monitoring) can serve as a simpler alternative.
| Indication | What to Look For | Interpretation |
|---|---|---|
| Suspicion of epileptic seizure (aura, LOC > 1 min, post-ictal confusion, tongue-biting, incontinence) | Epileptiform discharges (spikes, sharp waves, spike-wave complexes) | If present → supports epilepsy diagnosis; if normal → does NOT exclude epilepsy (only ~50% sensitivity on single routine EEG) |
| Differentiating convulsive syncope from epilepsy | Normal inter-ictal EEG → favours syncopal anoxic seizure, not epilepsy | Anoxic seizures show diffuse slowing during the event (if captured on simultaneous EEG/tilt), not epileptiform discharges |
| Video-EEG telemetry | Correlation of clinical event with EEG findings | Can definitively diagnose psychogenic non-epileptic events (normal EEG during clinical "seizure") |
An EEG should NOT be routinely ordered for syncope unless there are specific features suggesting seizure. An EEG is a test for epilepsy, not for syncope.
| Indication | Modality | What to Look For |
|---|---|---|
| Focal neurological signs on examination | CT brain (urgent) → MRI brain | Space-occupying lesion, haemorrhage, structural abnormality |
| Papilloedema | MRI brain with MRV | Posterior fossa tumour, hydrocephalus, cerebral venous sinus thrombosis |
| Progressive headache + ataxia + vomiting (raised ICP) | MRI brain | Posterior fossa tumour (medulloblastoma, ependymoma, pilocytic astrocytoma) |
| New focal seizure | MRI brain | Structural lesion |
Neuroimaging is NOT indicated for typical vasovagal syncope or breath-holding spells with normal examination. Ordering a CT brain for every fainting child is unnecessary and exposes them to radiation.
| Indication | What to Look For |
|---|---|
| Suspected ARVC | Fibrofatty replacement of RV myocardium, RV wall motion abnormalities, RV dilation |
| Equivocal echocardiography for HCM | Precise wall thickness measurement, fibrosis on late gadolinium enhancement (LGE) |
| Suspected myocarditis | Myocardial oedema (T2-weighted), LGE pattern (subepicardial/mid-wall) |
| Anomalous coronary artery assessment | Precise delineation of coronary origin and course |
Paediatric consideration: May require sedation or general anaesthesia in young children. CT coronary angiography is an alternative for coronary anatomy assessment (lower spatial resolution for myocardial tissue characterization but excellent for coronary origins).
Indication: suspected arrhythmic aetiology in cardiomyopathy, BBB, SVT, WPW; undiagnosed syncope with multiple recurrence [3][4].
NOT indicated if normal ECG, normal cardiac structure/function unless arrhythmic aetiology suspected [3][4].
Procedure:
- Multipolar catheters placed in different sites of heart
- Record intracardiac electrical signals
- Pace at different areas and look for abnormalities
- Induce arrhythmias by injection of pro-arrhythmic drugs → search for abnormal pathways [3][4]
Paediatric considerations: Performed under general anaesthesia in children. Risk–benefit must be carefully weighed. Usually reserved for cases where non-invasive testing has not been diagnostic and there is strong clinical suspicion.
| Indication | Genes Tested | When |
|---|---|---|
| Clinical or ECG diagnosis of LQTS | KCNQ1 (LQT1), KCNH2 (LQT2), SCN5A (LQT3), and others | After clinical/ECG diagnosis established; also cascade screening of first-degree relatives |
| Clinical suspicion of CPVT | RYR2, CASQ2 | After positive exercise stress test |
| Brugada syndrome | SCN5A (only ~20–30% yield) | After clinical/ECG diagnosis |
| HCM | MYH7, MYBPC3, and others | After echo diagnosis; cascade family screening |
| ARVC | PKP2, DSP, DSG2, DSC2 | After clinical/imaging diagnosis |
Clinical syndrome recognition by family history, symptoms and ECG findings → Schwartz score guides genetic testing for LQTS: low (≤ 1), intermediate (1.5–3), high (≥ 3.5) [4].
Identification of LQTS gene mutation is diagnostic; however, only 50% positive for known LQTS gene mutation → negative genetic test has limited diagnostic value [4].
Paediatric-specific point: Cascade genetic screening of first-degree relatives (including asymptomatic siblings and parents) is essential when a pathogenic variant is identified. This is a key family-centred care aspect — the diagnosis in one child may save the life of a sibling or parent. Genetic counselling should be offered before and after testing.
6. Special Diagnostic Scenarios by Age
Syncope is very rare in this age group. Any episode of LOC or an apparent life-threatening event (ALTE) / brief resolved unexplained event (BRUE) must be taken seriously:
- ECG (including QTc measurement) is mandatory
- Blood glucose, electrolytes, blood gas, septic screen
- Echocardiography if any cardiac suspicion
- Consider congenital LQTS (especially Jervell and Lange-Nielsen syndrome if sensorineural hearing loss is present)
- Consider congenital complete heart block (especially if maternal SLE/anti-Ro antibodies)
- Breath-holding spells: diagnosed clinically based on typical history (trigger → apnoea → colour change → stiffness ± LOC → rapid recovery). No investigations required unless features are atypical.
- If atypical: check ECG (r/o LQTS, as pallid breath-holding can rarely be the first presentation of a channelopathy), Hb (iron deficiency is associated with breath-holding spells and iron supplementation may reduce frequency)
- Febrile seizures: diagnosis of exclusion — should perform infection screen for all → r/o meningitis! [1]. LP if meningitis suspected (especially in < 12 months or if Haemophilus/pneumococcal vaccination incomplete).
Standard workup as described in the algorithm above. ECG in every case. Blood tests only if indicated by history. Echocardiography and ambulatory monitoring for cardiac suspicion. Tilt-table test for recurrent atypical syncope.
| Investigation | First-Line (All) | Second-Line (Selected) | Third-Line (Specialist) |
|---|---|---|---|
| History | ✓✓✓ — Most important | ||
| Physical exam (incl. lying-standing BP/HR) | ✓✓✓ | ||
| 12-lead ECG | ✓✓✓ — Mandatory for all | ||
| Blood glucose | If hypoglycaemia suspected | ||
| CBC | If anaemia suspected | ||
| Electrolytes | If dehydration/metabolic suspected | ||
| Echocardiography | Murmur, abnormal ECG, exertional syncope | ||
| Holter / Event monitor | Palpitations, suspected arrhythmia | ||
| Exercise stress test | Exertional syncope, suspected CPVT/LQTS | ||
| Tilt-table test | Recurrent atypical syncope, suspected POTS | ||
| EEG | Seizure features | ||
| MRI brain | Focal neuro signs, ↑ICP, progressive symptoms | ||
| Implantable loop recorder | Unexplained recurrent syncope | ||
| EPS | Suspected arrhythmia, abnormal ECG/echo | ||
| Cardiac MRI | Suspected ARVC, myocarditis, equivocal echo | ||
| Genetic testing | After clinical diagnosis of channelopathy/cardiomyopathy |
High Yield Summary — Diagnosis and Investigation
- Syncope is a symptom, not a disease — the diagnostic process aims to confirm true syncope, identify the cause, and risk-stratify.
- History is the most powerful tool — determines diagnosis in 60–80% of cases.
- ECG is mandatory in EVERY child with syncope — look for prolonged QTc, delta wave, Brugada pattern, deep Q waves (HCM), complete heart block, RV strain.
- A normal resting ECG does NOT exclude cardiac syncope — CPVT has a normal resting ECG; exercise stress testing is required if exertional syncope is suspected.
- Ambulatory ECG monitoring must match symptom frequency — Holter for daily, loop monitor for weekly/monthly, ILR for very infrequent.
- Tilt-table test is for recurrent atypical syncope, suspected POTS, or to distinguish convulsive syncope from epilepsy — it shows predisposition only, not definitive proof.
- Blood tests, neuroimaging, and EEG are NOT routinely needed for typical vasovagal syncope — only order when the history or examination suggests a specific non-reflex cause.
- Breath-holding spells in toddlers: clinical diagnosis — check ECG if atypical, and check Hb (iron deficiency associated).
- Genetic testing for channelopathies/cardiomyopathies + cascade family screening = key family-centred care action.
- Schwartz score guides genetic testing for LQTS: low ≤ 1, intermediate 1.5–3, high ≥ 3.5.
Active Recall - Diagnosis and Investigation of Paediatric Syncope/Dizziness
References
[1] Senior notes: Adrian Lui Pediatrics.pdf (p117 — Febrile seizure investigation: infection screen to rule out meningitis; breath-holding spells diagnosis) [3] Senior notes: Ryan Ho Fundamentals.pdf (p207–211, p323 — Syncope workup, ambulatory ECG types and indications, tilt-table test procedure and interpretation, EPS indications, structural causes of cardiac syncope, neurocardiogenic syncope pathogenesis) [4] Senior notes: Ryan Ho Cardiology.pdf (p62, p65–66, p196 — Palpitation/syncope workup, ambulatory ECG modalities, tilt-table test utility and procedure, exercise-related syncope causes, EPS indications and procedure, LQTS ECG findings and Schwartz score, Brugada syndrome) [5] Senior notes: Ryan Ho Endocrine.pdf (p71, p94 — Adrenal insufficiency diagnosis, hypoglycaemia Whipple's triad) [6] Senior notes: Ryan Ho Haemtology.pdf (p10 — Approach to anaemia, symptoms including dizziness/syncope) [10] ESC 2018 Guidelines on Syncope (adapted for paediatrics) — referenced as standard of care framework [11] Senior notes: Ryan Ho Critical Care.pdf (p17 — Early investigations in shock: ECG, CBC, L/RFT, ABG + lactate)
Management of Paediatric Syncope / Dizziness
The management of syncope in children flows directly from the diagnosis. Since the vast majority (~60–80%) is benign reflex (neurocardiogenic) syncope, the majority of management is education, reassurance, and lifestyle measures rather than pharmacotherapy or procedures [1][3][4].
The overarching goals are:
- Prevent injury from falls during syncopal episodes
- Reduce frequency and severity of episodes
- Treat the underlying cause when one is identified (especially cardiac)
- Prevent sudden cardiac death in the rare cases of cardiac syncope
- Minimise impact on quality of life, school attendance, and physical activity
- Family-centred care: educate the child AND the parents/caregivers — anxiety from the family often exceeds the medical severity of the condition
3. Management by Aetiology
3.1 Reflex (Neurocardiogenic / Vasovagal) Syncope — The Most Common Scenario
This is the bread-and-butter of paediatric syncope management. The key message to families: this is benign, not dangerous, and almost always outgrown or well-controlled with simple measures [3][4].
This is the single most important intervention and alone resolves the problem for many families:
- Explain the mechanism in simple terms: "When your child stands for a long time, blood pools in the legs. The heart then beats very hard on an almost empty chamber, which tricks the brain into thinking the blood pressure is too high. The brain responds by slowing the heart and relaxing the blood vessels — the opposite of what's needed — so blood pressure drops and the child faints. It's a reflex, not a disease."
- Reassure that it is not epilepsy, not a heart attack, and not dangerous (once cardiac causes have been excluded)
- Explain that it is extremely common in adolescents and most children outgrow it or learn to control it
- Educate about prodromal symptoms: teach the child to recognize the warning signs (nausea, lightheadedness, visual dimming, sweating) and act immediately
- What to do during a prodrome: lie down immediately with legs elevated (or at minimum sit down and put the head between the knees) — this rapidly restores venous return and prevents full syncope
- What to do if the child faints: lay them flat, elevate the legs, turn to recovery position if vomiting. They will recover spontaneously within seconds to minutes. Do NOT try to sit them up or give them water while they are unconscious (aspiration risk)
Family Communication — Key Talking Points
In Hong Kong, parental anxiety about "fainting" is often extreme — many fear epilepsy or heart disease. The fact that you have done an ECG and examination and found them normal should be explicitly communicated. A written information sheet (in both Chinese and English) is highly valuable.
These address the underlying physiological predisposition:
| Measure | How It Works | Practical Advice |
|---|---|---|
| ↑Fluid intake | ↑Intravascular volume → ↑venous return → less venous pooling on standing → ↓trigger for Bezold-Jarisch reflex | Aim for 1.5–2.5 L/day depending on age and weight (more in summer, during exercise). In adolescents, this often means doubling their usual intake. Water and electrolyte-containing fluids are preferred over sugary drinks |
| ↑Salt intake | Na⁺ retains water in the intravascular space → ↑blood volume → ↑BP → less orthostatic stress | Add salt to meals, eat salty snacks. Some centres recommend oral salt tablets (1–2 g NaCl tablets) in adolescents. Caution: not appropriate if hypertension or renal disease (very rare in this population) |
| Avoid triggers | Prevent the autonomic cascade from being initiated | Avoid prolonged standing (if must stand, shift weight, cross legs, tense muscles); avoid hot, stuffy, crowded environments; avoid dehydration; do NOT skip breakfast (very common in HK secondary school students) |
| Avoid rapid postural changes | Prevent sudden orthostatic stress | Rise slowly from bed (sit at edge for 30 seconds before standing) |
| Regular exercise | Improves cardiovascular conditioning → better autonomic reflex buffering → less prone to venous pooling | Moderate regular aerobic exercise (swimming, cycling, jogging) — 30 minutes 3–5 times/week. Avoid sudden cessation of vigorous exercise (cool down gradually) |
| Adequate sleep | Sleep deprivation worsens autonomic dysregulation | Aim for age-appropriate sleep duration (adolescents: 8–10 hours). This is a major issue in HK with late-night studying |
| Avoid alcohol and recreational drugs (adolescents) | Both cause vasodilation and impair autonomic reflexes | Anticipatory guidance in older adolescents |
These are first-line acute interventions that the child can perform when they feel the prodrome:
| Manoeuvre | How It Works | How to Teach |
|---|---|---|
| Leg crossing with tensing of leg, abdominal, and buttock muscles | Compresses venous capacitance vessels in the lower limbs and abdomen → ↑venous return → ↑preload → ↑CO → ↑BP | Cross legs at ankles and squeeze thigh/calf muscles hard for 30 seconds; repeat |
| Hand grip / arm tensing | Isometric muscle contraction → ↑sympathetic outflow → ↑SVR + ↑HR | Grip one fist with the other hand and pull apart as hard as possible for 30 seconds |
| Squatting | Compresses lower limb veins + raises intra-abdominal pressure → ↑venous return | Squat down immediately when prodromal symptoms appear |
| Toe-raising / muscle pumping | Activates the skeletal muscle pump in the calves → ↑venous return from lower limbs | Rise onto toes repeatedly; shift weight from one foot to the other |
These manoeuvres have been shown in RCTs (PC-Trial) to reduce syncope recurrence by ~39% and are completely safe with no cost.
Drug therapy is reserved for children with frequent, recurrent, disabling vasovagal syncope that significantly impairs quality of life (school attendance, physical activity, injury risk) despite adequate lifestyle measures and PCM.
Pharmacotherapy is NOT First-Line
A common mistake is to jump to medication before giving lifestyle measures a proper trial. In paediatric vasovagal syncope, education + fluids + salt + PCM should be tried for at least 3–6 months before considering drugs. Most children improve with non-pharmacological measures alone.
| Drug | Mechanism | Dose (Paediatric) | Evidence | Contraindications / Side Effects |
|---|---|---|---|---|
| Midodrine | α₁-adrenergic agonist → ↑SVR via arteriolar and venous vasoconstriction → ↑BP → counteracts the vasodepressor component of reflex syncope | Start 2.5 mg BD–TDS (adolescents); titrate up to 10 mg TDS. Use lowest effective dose. Give last dose ≥ 4 hours before bedtime (to avoid supine hypertension) | Best available evidence in paediatric vasovagal syncope (small RCTs showing reduced recurrence). Currently considered first-line pharmacotherapy | C/I: supine hypertension, severe heart disease, urinary retention, phaeochromocytoma, thyrotoxicosis. S/E: supine hypertension (most important — monitor BP), piloerection ("goosebumps"), urinary retention, scalp tingling |
| Fludrocortisone | Mineralocorticoid → ↑renal Na⁺ and H₂O reabsorption → ↑blood volume → ↑preload → ↑CO | 0.05–0.2 mg daily (paediatric); start low and titrate | Mixed evidence (POST2 trial negative in adults, but still used in paediatrics based on physiological rationale and small positive studies) | C/I: heart failure, renal failure, hypertension. S/E: hypokalaemia (monitor K⁺ — the drug causes kaliuresis), oedema, weight gain, supine hypertension, headache. Need to monitor electrolytes |
| Low-dose β-blockers (e.g., propranolol, atenolol, metoprolol) | Proposed mechanism: ↓the initial vigorous ventricular contraction that triggers the Bezold-Jarisch reflex; also ↓adrenergic overshoot | Propranolol 0.5–1 mg/kg/day in 2–3 divided doses; atenolol 0.5–1 mg/kg/day once daily | Evidence is mixed — the POST trial (adults) was negative. Some paediatric data suggest modest benefit. Avoid in adolescents < 42 years old (per POST trial caveat: may be harmful in young adults) | C/I: asthma (β₂ blockade → bronchospasm), severe bradycardia, heart block, decompensated HF. S/E: fatigue, exercise intolerance, sleep disturbance, hypotension, depression, bronchospasm. Generally avoided in athletic adolescents |
| SSRIs (fluoxetine) | Proposed mechanism: serotonin modulates central autonomic control → may blunt the exaggerated vagal response | Fluoxetine 10–20 mg daily | Limited evidence; used off-label in highly refractory cases | C/I: concurrent MAO inhibitors. S/E: GI upset, agitation, ↑suicidality risk in adolescents (black box warning — close monitoring essential). Not first-line |
| Indication | Rationale | Details |
|---|---|---|
| Documented prolonged asystole ( > 3 seconds) during syncopal episodes (cardioinhibitory type on tilt-table or ILR) in older children/adolescents with recurrent, disabling, injurious syncope refractory to all other measures | If the dominant mechanism is profound bradycardia/asystole (cardioinhibitory), a pacemaker can prevent the heart rate from dropping below a set threshold, preventing LOC | Dual-chamber pacemaker with rate-drop response (DDI with rate hysteresis) — the pacemaker detects the sudden HR drop and provides temporary pacing. Evidence from ISSUE-3 trial (adults) showed benefit in highly selected patients. Very rarely indicated in paediatrics. Lifetime pacemaker commits a child to decades of device management |
Pacing is Last Resort in Paediatrics
Pacing is almost never needed for vasovagal syncope in children. The overwhelming majority can be managed with lifestyle + PCM ± pharmacotherapy. Pacing is only considered when there is documented prolonged asystole ( > 3 seconds) causing recurrent injurious syncope despite maximal medical therapy, AND the child is old enough to provide assent for a lifelong implanted device.
Management: reassurance ± PR diazepam PRN if seizure lasts > 5 min [1] — although this last point applies to prolonged anoxic seizures, which are extremely rare.
| Management Step | Rationale | Details |
|---|---|---|
| Reassurance | The single most important intervention. Parents are terrified their child is having seizures or is going to die | Explain: "This is a reflex, not something your child is doing on purpose. The child cannot control it. It is not epilepsy. It is not dangerous. Your child will NOT die from a breath-holding spell. Almost all children outgrow this by age 5–6 years." |
| What to do during a spell | Prevent injury and allow natural recovery | Place the child on their side (recovery position). Do NOT shake the child, splash cold water on them, or put anything in their mouth. The child will resume breathing spontaneously. Time the episode |
| Check iron status (Hb and ferritin) | Iron deficiency is associated with ↑frequency of breath-holding spells (mechanism unclear — possibly related to altered autonomic function or neurotransmitter synthesis) | If iron deficient or low-normal ferritin ( < 20–30 μg/L): prescribe oral iron supplementation (3–6 mg/kg/day of elemental iron). Studies show iron supplementation reduces frequency of breath-holding spells even in non-anaemic children with low ferritin |
| Behavioural advice | Reduce triggers for cyanotic spells (anger, frustration) | Consistent, calm parenting approach. Avoid reinforcing the tantrum behaviour, but do NOT punish the child for the spells (they are involuntary). Distraction techniques |
| Do NOT give anti-seizure medications | Breath-holding spells are NOT epileptic seizures — anti-seizure drugs are ineffective and expose the child to unnecessary side effects | This is a common parental request driven by fear of "seizures." Reassure firmly |
| Piracetam (some centres) | GABA analogue; proposed to modulate autonomic reflexes | Limited evidence from small RCTs showing reduced frequency. Used in some European and Asian centres. Dose: 40 mg/kg/day in 2 divided doses. Not standard practice |
| Atropine (very rare indication) | Blocks vagal-mediated bradycardia/asystole in severe, recurrent pallid breath-holding spells with documented prolonged asystole | Oral atropine 0.01–0.02 mg/kg/dose BD. Only in severe cases with documented cardiac asystole > 4–6 seconds. Rarely needed. Side effects: anticholinergic (dry mouth, constipation, urinary retention, pupil dilation) |
| Cardiac pacing | Prevent asystole in the most severe pallid breath-holding spells with documented prolonged asystole | Extremely rare; reserved for pallid spells with documented asystole > 6 seconds causing recurrent injuries. Almost never needed — most children outgrow spells |
3.3 Orthostatic Syncope and POTS
| Step | Management |
|---|---|
| Treat the underlying cause | Dehydration → rehydrate (oral or IV as appropriate for severity; see paediatric fluid management guidelines). Drug-induced → review and adjust medications. Adrenal insufficiency → hydrocortisone replacement [5]. Acute blood loss → resuscitate (ABC, IV fluids, blood products) |
| Fluid and salt loading | As per vasovagal syncope measures |
| Rise slowly | Education on slow positional changes |
| Compression garments | Abdominal binder or lower limb compression stockings → ↓venous pooling → ↑venous return |
| Midodrine | If above measures fail (same dosing as vasovagal section) |
POTS management is challenging and requires a multidisciplinary approach. These patients are often significantly debilitated (unable to attend school, reduced quality of life).
| Step | Intervention | How It Works |
|---|---|---|
| 1. Education | Explain the condition and that it is real (not "just anxiety") | Adolescents with POTS often feel dismissed — validation is therapeutic |
| 2. Fluid and salt loading | ↑Blood volume → ↓compensatory tachycardia | 2–3 L/day fluids + 6–10 g salt/day (adolescents) — use electrolyte drinks, salt tablets |
| 3. Graduated exercise programme | Reconditions the cardiovascular system → ↑blood volume, ↑stroke volume, improved autonomic regulation | Start with recumbent exercise (swimming, rowing, recumbent cycling) because upright exercise initially worsens symptoms. Gradually progress over months. This is the single most effective long-term treatment |
| 4. Compression garments | Abdominal binder (more effective than leg stockings) → ↓splanchnic venous pooling | Medical-grade abdominal compression (not just tight clothes) |
| 5. Pharmacotherapy (if above inadequate) | Various options targeting different mechanisms | See table below |
| 6. Psychology/psychiatry support | Comorbid anxiety and depression are very common; chronic illness adjustment; school liaison | CBT for anxiety management; school liaison to arrange modified attendance/PE participation |
POTS Pharmacotherapy:
| Drug | Mechanism | Paediatric Notes |
|---|---|---|
| Midodrine (2.5–10 mg TDS) | α₁-agonist → ↑SVR → ↓compensatory tachycardia | Often first-line. Same precautions as vasovagal section |
| Low-dose propranolol (10–20 mg TDS in adolescents) | ↓HR; ↓excessive sympathetic activation (in hyperadrenergic POTS) | Use LOW doses — high doses worsen symptoms by ↓CO. Avoid in patients with low BP |
| Fludrocortisone (0.05–0.2 mg daily) | ↑Blood volume via renal Na⁺/H₂O retention | Monitor K⁺ and BP |
| IV saline infusions (bolus 10–20 mL/kg) | Acutely ↑blood volume | Sometimes used for acute exacerbations or as a "rescue" treatment in severe flares. Not sustainable long-term |
| Pyridostigmine (30–60 mg TDS) | Acetylcholinesterase inhibitor → ↑cholinergic activity at autonomic ganglia → ↑peripheral vasoconstriction without supine hypertension | Used in some centres. S/E: GI cramping, diarrhoea, sweating |
| Ivabradine (2.5–7.5 mg BD) | Selective Iₓ (funny current) inhibitor in SA node → ↓HR without affecting contractility or BP | Increasingly used off-label in adolescent POTS. Reduces tachycardia without the BP-lowering effects of β-blockers. Not yet universally recommended in paediatric guidelines |
3.4 Cardiac Syncope — Cause-Specific Management
This is where management becomes life-saving. Every child with confirmed or suspected cardiac syncope needs paediatric cardiology involvement.
Treatment: indicated in both symptomatic and asymptomatic individuals [4].
| Treatment | Indication | How It Works | Paediatric Details |
|---|---|---|---|
| β-blocker | First-line for ALL LQTS patients (symptomatic and asymptomatic) | Can prevent cardiac events in ~70% of patients [4] — ↓adrenergic trigger for arrhythmias by ↓sympathetic stimulation to the heart | Nadolol preferred (longest-acting, most evidence). Dose: 1–2 mg/kg/day once daily. Propranolol alternative (0.5–1 mg/kg TDS). Must NOT be abruptly discontinued (rebound sympathetic surge → arrhythmia). C/I: asthma (relative — use cardioselective β₁ if needed), high-degree AV block |
| Lifestyle modification | All LQTS patients | Avoid specific triggers based on subtype | LQTS1: avoid strenuous exercise, especially swimming. LQTS2: avoid sudden auditory stimuli (alarm clocks, phone ringtones — use vibration). LQTS3: avoid sleep (controversial — ensure adequate monitoring). All: avoid QT-prolonging drugs (www.crediblemeds.org — mandatory counselling) |
| Left cardiac sympathetic denervation (LCSD) | Patients with recurrence of cardiac events despite β-blocker | Removal of cervicothoracic sympathetic ganglia (anti-adrenergic) → ↓sympathetic innervation to the heart → ↓trigger for TdP [4] | Surgical procedure. Preserves exercise capacity (unlike β-blockers). Bridge or adjunct to ICD |
| ICD (implantable cardioverter-defibrillator) | Most effective treatment for high-risk patients: previous cardiac arrest, recurrent syncope failing β-blocker + LCSD [4] | Detects VT/VF and delivers shock to restore normal rhythm | Lifelong commitment to device. In children, epicardial leads or subcutaneous ICD may be used. Complications: inappropriate shocks (significant psychological impact in children/adolescents), lead fracture, infection. Decision requires extensive family discussion |
Prognosis: good overall if on β-blocker, very good if on ICD. TdP episodes usually self-terminating with ~4–5% of events being fatal [4].
Drug avoidance in LQTS: Children and families must receive a list of QT-prolonging drugs to avoid. Common paediatric offenders: macrolide antibiotics (azithromycin, erythromycin), ondansetron (commonly used for paediatric vomiting — use with extreme caution or avoid), domperidone, antipsychotics (haloperidol, risperidone), certain antihistamines. Always check www.crediblemeds.org before prescribing.
| Treatment | Details |
|---|---|
| β-blocker (nadolol or propranolol) | First-line. Must achieve high doses (nadolol up to 2.5 mg/kg/day) for adequate adrenergic blockade. Exercise restriction to < 60–80% maximum HR |
| Flecainide (Na⁺ channel blocker) | Add-on therapy if β-blocker alone insufficient. Blocks RyR2-mediated Ca²⁺ release → ↓triggered arrhythmias. Dose: 2–4 mg/kg/day in 2 divided doses |
| LCSD | If recurrent events on β-blocker + flecainide |
| ICD | Cardiac arrest survivors or refractory cases. Same considerations as LQTS |
| Exercise restriction | Avoid competitive sports and strenuous exercise. This is one of the most important counselling points for adolescents |
| Treatment | Details |
|---|---|
| Acute SVT: vagal manoeuvres → IV adenosine | Vagal manoeuvres (ice to face in infants; Valsalva, carotid massage in older children) → if fails: IV adenosine 0.1 mg/kg rapid push (max first dose 6 mg; max second dose 12 mg) → blocks AV node transiently → terminates re-entrant circuit. C/I: pre-excited AF (can accelerate conduction through accessory pathway → VF) |
| Catheter ablation | Definitive treatment. Radiofrequency or cryoablation of the accessory pathway. Indicated for symptomatic WPW, especially with syncope or haemodynamically significant arrhythmia. High success rate ( > 95%). Preferred over long-term antiarrhythmics in children |
| Antiarrhythmics (bridge or if ablation not possible) | Flecainide, propafenone, or amiodarone. Avoid digoxin, verapamil, and β-blockers if pre-excited AF is possible (these slow AV node conduction preferentially, allowing faster conduction down the accessory pathway → can precipitate VF) |
| Treatment | Details |
|---|---|
| Congenital complete heart block (neonatal lupus) | Permanent pacemaker if symptomatic or HR < 50–55 bpm or wide QRS escape rhythm. Even asymptomatic children may need pacing prophylactically depending on escape rate and exercise tolerance |
| Acquired complete heart block (post-cardiac surgery, myocarditis) | Temporary transvenous pacing → permanent pacemaker if no recovery within 7–14 days post-surgery |
| Condition | Management |
|---|---|
| HCM | Avoid competitive sports. β-blocker (first-line) or verapamil/disopyramide for LVOT obstruction. ICD for high-risk patients (family Hx SCD, massive LVH > 30 mm, unexplained syncope, NSVT on Holter). Septal myectomy or alcohol septal ablation for refractory LVOT gradient |
| Severe aortic stenosis | Balloon valvuloplasty (neonates/infants) or surgical aortic valve replacement (older children) when symptomatic or gradient > 50 mmHg |
| Anomalous coronary artery | Surgical re-implantation — this is a surgical emergency when diagnosed after syncope or cardiac arrest |
| Pulmonary hypertension | Pulmonary vasodilators (sildenafil, bosentan, epoprostenol), manage underlying cause (e.g., congenital heart disease repair), consideration of lung or heart-lung transplantation in end-stage disease |
| Cause | Management |
|---|---|
| Hypoglycaemia | Oral glucose/carbohydrate if conscious. IV dextrose if unconscious (D10 2–5 mL/kg in neonates; D10 or D25 in older children). IM glucagon if no IV access (dose: < 25 kg: 0.5 mg; ≥ 25 kg: 1 mg). Treat underlying cause (insulin dose adjustment, adrenal insufficiency treatment, investigation of persistent hypoglycaemia in infants) [5] |
| Anaemia | Iron supplementation for iron deficiency (most common in paediatrics — oral ferrous sulfate 3–6 mg/kg/day of elemental iron). Transfusion if severe/symptomatic. Treat underlying cause |
| Dehydration | Oral rehydration therapy (ORT) for mild-moderate; IV normal saline (10–20 mL/kg boluses) for severe. See paediatric fluid resuscitation guidelines |
| Adrenal insufficiency | Acute crisis: IV hydrocortisone (infant 25 mg, child 50 mg, adolescent 100 mg stat, then Q6–8h) + IV NS boluses for shock. Chronic: oral hydrocortisone 8–10 mg/m²/day in 3 divided doses + fludrocortisone 0.05–0.15 mg daily for primary AI [5] |
| Anaphylaxis | IM adrenaline (epinephrine) 0.01 mg/kg (max 0.5 mg) of 1:1000 in mid-outer thigh — first and most important treatment [12]. Repeat every 5–15 minutes as needed. ABC support. Paediatric doses: < 6 yr: 0.15 mg (EpiPen Jr); 6–12 yr: 0.3 mg; > 12 yr: 0.5 mg. IV fluid bolus 20 mL/kg NS |
| Management | Details |
|---|---|
| Acknowledge the reality of the symptoms | "I can see you're experiencing real symptoms" — do NOT say "It's all in your head." Invalidation worsens outcomes |
| Explain the mechanism | "Your body is generating these episodes because of the way your nervous system is processing stress, not because of a structural problem. This is a recognized medical condition" |
| Psychology / psychiatry referral | CBT is the evidence-based treatment. Address underlying anxiety, depression, or trauma. School liaison |
| Physiotherapy | Graded exercise programme if deconditioning is present |
| Avoid unnecessary investigations | Repeated normal investigations reinforce health anxiety |
| Cause | Management |
|---|---|
| Benign paroxysmal vertigo of childhood (BPVC) | Reassurance. Usually self-limiting. No specific treatment needed. Consider migraine prophylaxis (cyproheptadine, propranolol) if episodes are frequent and disabling |
| Vestibular neuritis | Supportive: antiemetics (ondansetron — caution in LQTS; prochlorperazine not recommended in children < 12 yr due to dystonic reactions), short course of vestibular suppressants, early vestibular rehabilitation exercises |
| BPPV (rare in children) | Epley manoeuvre (canalith repositioning). Safe, effective, immediate |
| Migraine with brainstem aura | Acute: rest in quiet dark room, paracetamol/ibuprofen. Prophylaxis if recurrent: propranolol, topiramate, amitriptyline (paediatric doses) |
| Anxiety/hyperventilation | Reassurance, breathing retraining, CBT. Acute: paper bag re-breathing is NOT recommended (risk of hypoxia) — instead, coach slow diaphragmatic breathing |
| Posterior fossa tumour | Urgent neurosurgery referral |
This is a critically important aspect of paediatric syncope management that directly impacts the child's quality of life and psychosocial development:
| Diagnosis | Activity Recommendation |
|---|---|
| Vasovagal syncope | NO restriction of physical activity or sport. In fact, exercise should be encouraged (it helps). Avoid specific triggers (prolonged standing in heat). If recent syncope, avoid activities where loss of consciousness would be dangerous (e.g., swimming alone, climbing) until stable |
| POTS | Encourage exercise (start recumbent). No restriction once exercise programme is established. Avoid prolonged standing in heat |
| LQTS | Avoid competitive sports (especially swimming for LQTS1, and sudden auditory-stimulus-heavy sports for LQTS2). Recreational exercise generally allowed with β-blocker and AED availability. Decision should be individualized with cardiology |
| CPVT | Avoid competitive sports and strenuous exercise. This is one of the most restrictive diagnoses |
| HCM | Avoid competitive sports if moderate-to-severe hypertrophy or risk factors for SCD. Low-intensity recreational exercise generally permitted after cardiology discussion |
| WPW post-ablation | Full activity after successful ablation (usually cleared at 1–2 weeks) |
| Breath-holding spells | No restrictions — these children are NOT at risk during physical activity |
The Importance of Not Over-Restricting Activity
For vasovagal syncope (the vast majority of cases), over-restriction of physical activity is harmful. It leads to deconditioning, social isolation, school avoidance, and anxiety. Unless there is a diagnosed cardiac cause, the child should be encouraged to participate fully in all activities including sport. The only caveat is to avoid situations where a faint would be dangerous (e.g., swimming alone, working at heights).
| Diagnosis | Follow-Up | Prognosis |
|---|---|---|
| Vasovagal syncope | Review if recurrent or new features. Most need only a single visit with education | Excellent. Most adolescents have ↓frequency with age. ~25% have long-term recurrence into adulthood, but episodes are benign |
| Breath-holding spells | Reassurance at routine well-child visits. Review if features change | Self-resolves by age 5–6 years in the vast majority |
| POTS | Regular follow-up (every 3–6 months) with adolescent medicine/cardiology. Multidisciplinary approach | Variable. ~50% of adolescents improve significantly over 1–3 years. Complete remission in ~20% by 5 years |
| LQTS / CPVT / HCM | Lifelong cardiology follow-up. Regular ECG and echo. Genetic counselling. Cascade family screening | Depends on subtype and treatment compliance. Good if on appropriate therapy |
| Psychogenic pseudosyncope | Psychology/psychiatry follow-up | Variable. Better with early intervention and CBT |
High Yield Summary — Management
Vasovagal syncope (most common):
- Step 1: Education + reassurance (most important)
- Step 2: Lifestyle measures (↑fluids 1.5–2.5 L/day, ↑salt, avoid triggers, regular exercise, adequate sleep)
- Step 3: Physical counter-pressure manoeuvres (leg crossing + tensing, hand grip, squatting)
- Step 4: Pharmacotherapy if recurrent/refractory: midodrine (first-line drug), fludrocortisone, low-dose β-blocker
- Step 5: Cardiac pacing — only for documented prolonged asystole refractory to all else
Breath-holding spells:
- Reassurance is THE treatment
- Check iron status → supplement if deficient (even non-anaemic children with low ferritin benefit)
- Do NOT give anti-seizure medication
- Self-resolves by age 5–6
LQTS:
- β-blocker for ALL patients (nadolol preferred)
- Avoid QT-prolonging drugs (always check crediblemeds.org)
- LCSD if refractory to β-blocker
- ICD for cardiac arrest survivors or recurrent syncope failing β-blocker + LCSD
- Lifestyle: avoid subtype-specific triggers (swimming for LQTS1, auditory stimuli for LQTS2)
POTS:
- Fluid + salt loading
- Graduated recumbent exercise programme (most effective long-term treatment)
- Compression garments
- Pharmacotherapy: midodrine, low-dose propranolol, fludrocortisone, ivabradine
Do NOT over-restrict activity in vasovagal syncope or breath-holding spells — deconditioning worsens outcomes.
Active Recall - Management of Paediatric Syncope/Dizziness
References
[1] Senior notes: Adrian Lui Pediatrics.pdf (p117 — Breath-holding spell management: reassurance ± PR diazepam PRN; vasovagal syncope triggers and features) [3] Senior notes: Ryan Ho Fundamentals.pdf (p207–211 — Syncope workup and management, tilt-table test, neurocardiogenic syncope pathogenesis and consequences, ambulatory ECG types, structural cardiac causes) [4] Senior notes: Ryan Ho Cardiology.pdf (p65–66, p196 — Neurocardiogenic syncope pathogenesis and workup, tilt-table test procedure and interpretation, LQTS treatment including beta-blocker, LCSD, ICD, and prognosis) [5] Senior notes: Ryan Ho Endocrine.pdf (p71, p94 — Adrenal insufficiency acute management with IV hydrocortisone; hypoglycaemia management with oral carbohydrates, IV dextrose, IM glucagon) [12] Senior notes: Ryan Ho Critical Care.pdf (p24 — Anaphylaxis management: IM adrenaline first-line, paediatric dosing 0.01 mg/kg)
Complications of Paediatric Syncope / Dizziness
Complications of syncope in children can be divided into two broad categories: (A) direct complications of the syncopal event itself (i.e., what happens when a child suddenly loses consciousness and falls), and (B) complications of the underlying cause (i.e., the disease producing the syncope may carry its own morbidity and mortality). A third and often-overlooked category is (C) psychosocial and quality-of-life complications, which in paediatrics can be profoundly disabling even when the syncope itself is benign.
Understanding these systematically prevents both over-investigation of benign syncope and under-recognition of dangerous sequelae.
A. Direct Complications of the Syncopal Event
These occur because syncope, by definition, involves sudden loss of consciousness and postural tone. The child collapses without warning (or with only seconds of warning) and cannot protect themselves from the fall.
| Complication | Mechanism | Paediatric-Specific Considerations |
|---|---|---|
| Head injury (most important) | Sudden LOC → unprotected fall → head strikes ground or furniture | Children have proportionally larger heads relative to body size → higher centre of gravity → tend to fall head-first. Concussion is the most common result; intracranial haemorrhage (subdural, extradural, SAH) is rare but possible, especially if the child falls onto a hard surface or from a height (e.g., playground equipment). Always assess for signs of head injury after a syncopal fall: headache, vomiting, GCS change, focal neurology |
| Facial/dental injury | Forward fall with facial impact | Dental avulsion, lip laceration, nasal fracture. Particularly relevant in school settings |
| Long bone fractures | Fall from standing height | Wrist fractures (Colles'-type) from outstretched hand, humeral fractures. Less common in young children (lower height, more flexible bones) but increasing risk in adolescents |
| Soft tissue injury | Contusions, lacerations from impact with objects | Minor but common — bruises, abrasions |
| Burns | Collapse near hot surfaces, stoves, heaters, or while holding hot liquids | Relevant in domestic settings; a child fainting while helping in the kitchen could sustain scalding injury |
| Drowning | Syncope while swimming or in bathtub | Critically important in paediatrics — a child who has syncope in water can drown within seconds. This is a recognised mechanism of sudden death in undiagnosed LQTS type 1, where cold water + exercise is a classic trigger. Even in vasovagal syncope, unsupervised bathing or swimming poses risk. Drowning prevention counselling is essential |
Drowning Risk in Paediatric Syncope
Any child with recurrent syncope of any cause must receive counselling about drowning risk. Children with undiagnosed cardiac channelopathies (especially LQTS1 and CPVT) are at particular risk because exercise + cold water is a potent arrhythmia trigger. Even children with benign vasovagal syncope should never swim alone or unsupervised. A family history of unexplained drowning should always raise suspicion for LQTS [3].
Why does injury risk matter clinically?
The injury risk directly influences management decisions. A child with infrequent vasovagal syncope who has never been injured may need only reassurance and lifestyle measures. A child with frequent syncope who has sustained head injuries or dental trauma needs more aggressive management (pharmacotherapy or, in rare cases, pacing) to prevent further injuries. The frequency, severity, and context of injuries are key factors in escalating treatment.
This was covered in detail in the earlier Clinical Features section but bears repeating as a "complication" because it is frequently misdiagnosed:
- Mechanism: If cerebral hypoperfusion during syncope lasts > 10–15 seconds, the hypoxic cortex generates aberrant electrical discharges → brief (usually < 15 seconds) tonic or tonic-clonic movements.
- Not epilepsy: No epileptiform activity on inter-ictal EEG. Does NOT require anti-seizure medication.
- The complication here is misdiagnosis: Children with anoxic convulsions are frequently misdiagnosed with epilepsy and started on anti-seizure drugs, which expose them to unnecessary side effects (sedation, cognitive impairment, teratogenicity in adolescent females) without any benefit [1][3].
- Prolonged anoxic seizure (rare): In severe pallid breath-holding spells or cardiac syncope with prolonged asystole, the anoxic seizure can last longer and be more frightening. Very rarely, prolonged cerebral hypoperfusion can cause anoxic brain injury, though this is essentially limited to cardiac arrest scenarios rather than simple syncope.
| Activity | Risk |
|---|---|
| Driving (relevant for older adolescents ≥ 16 in some jurisdictions, ≥ 18 in HK) | Syncope while driving → motor vehicle accident. Driving restrictions apply to cardiac syncope and uncontrolled recurrent syncope. In HK, adolescents approaching driving age with cardiac syncope need clear counselling |
| Swimming | Drowning (see above) |
| Cycling | Fall from bicycle → head/facial injury (emphasise helmet use) |
| Using stairs / escalators | Fall down stairs → multiple injuries |
| Cooking / using appliances | Burns, lacerations |
B. Complications of the Underlying Cause of Syncope
These are the complications of the disease producing the syncope, not of the syncope episode itself. They range from trivial (in vasovagal syncope) to fatal (in cardiac channelopathies).
| Complication | Mechanism | Detail |
|---|---|---|
| Recurrence | The autonomic predisposition persists → repeated episodes | ~30–50% of children with vasovagal syncope will have at least one recurrence within 1–2 years. About 25% may have continued episodes into adulthood. Recurrence is higher in those with early onset, frequent initial episodes, and cardioinhibitory type |
| Injury (as above) | Repeated falls | The cumulative risk of injury increases with episode frequency |
| School absenteeism | Episodes at school → sent home; fear of episodes → avoidance behaviour | Can significantly impact academic performance, especially in HK's competitive educational environment |
| Physical deconditioning | Over-restriction of activity (by parents, school, or doctors) → loss of cardiovascular fitness → worsened autonomic regulation → more syncope | This creates a vicious cycle: syncope → restriction → deconditioning → more syncope. A key management goal is to PREVENT this cycle |
| No mortality risk | Vasovagal syncope carries NO risk of sudden death | This is a crucial point for family reassurance — once cardiac causes are excluded, syncope itself is not life-threatening |
| Complication | Mechanism | Detail |
|---|---|---|
| Parental anxiety / overprotection | Dramatic appearance of spells (child turns blue or pale, goes limp, may have convulsion) → severe parental fear | Can lead to overprotective parenting, behavioural reinforcement (if parents "give in" to avoid tantrums), and unnecessary medical investigations. Parental education is the primary intervention |
| Iron deficiency (contributor, not consequence) | Pre-existing iron deficiency → ↑spell frequency → if iron deficiency is not recognised and treated, spells persist longer | Iron deficiency is both a risk factor and a treatable contributor — checking and correcting iron status is important |
| No long-term neurological sequelae | Despite the frightening appearance, breath-holding spells do NOT cause brain damage | Studies have shown no difference in cognitive development between children with breath-holding spells and controls. Reassure parents firmly on this point |
| Very rare: prolonged asystole | In severe pallid breath-holding spells, cardiac asystole can last > 6 seconds | Extremely rarely, this can theoretically cause anoxic brain injury, but in practice this is almost never seen because the child's intrinsic cardiac pacemaker resumes before significant anoxia occurs. If documented prolonged asystole, consider cardiac pacing (as discussed in management) |
This is where the stakes are highest. Cardiac syncope may be a premonitory sign of severe cardiac disease (30% mortality if cardiac cause) [3].
| Complication | Associated Conditions | Mechanism | How to Prevent |
|---|---|---|---|
| Sudden cardiac death (SCD) | LQTS, CPVT, HCM, Brugada syndrome, anomalous coronary artery, ARVC | Sustained VT/VF → cardiac arrest → death within minutes if not defibrillated | Early diagnosis (ECG screening, exercise test, echo, genetic testing), appropriate treatment (β-blockers, ICD), activity restriction, family screening [3][4] |
| Cardiac arrest with anoxic brain injury | Same as above | Prolonged cardiac arrest ( > 4–5 minutes without CPR) → irreversible neuronal death → persistent vegetative state, cognitive impairment, cerebral palsy-like motor deficits | Early recognition, bystander CPR training for families, AED availability in schools, ICD implantation in high-risk patients |
| Recurrent arrhythmias | WPW, LQTS, CPVT, SVT, VT | The underlying electrical substrate persists → recurrent episodes → cumulative injury risk and psychological impact | Definitive treatment: catheter ablation (WPW), β-blockers (LQTS, CPVT), ICD (high-risk) |
| Heart failure | Severe AS, HCM (end-stage), DCM, myocarditis | Chronic haemodynamic compromise → ventricular remodelling → progressive systolic/diastolic dysfunction | Surgical/interventional treatment of structural lesions, medical HF management, transplant if end-stage |
| Eisenmenger physiology | Unrepaired congenital heart disease with pulmonary hypertension | Progressive pulmonary vascular disease → irreversible pulmonary HTN → exertional syncope → eventually RV failure and death | Early repair of congenital heart defects before irreversible pulmonary vascular changes |
Syncope as a Warning Shot
In cardiac disease, syncope is often a "warning shot" before sudden death. This is especially true for:
- HCM: syncope is a recognised risk factor for SCD and is incorporated into risk stratification scores (HCM Risk-SCD)
- LQTS/CPVT: a syncopal episode represents a self-terminating episode of VT/VF — the next episode may not self-terminate
- Anomalous coronary artery: syncope during exercise may be the only warning before fatal arrhythmia
The implication: every child with exertional syncope who is sent home without a cardiac workup is potentially being sent home to die. This is not hyperbole — it is the reason that ECG and cardiac evaluation are mandatory [3][4].
| Complication | Mechanism | Detail |
|---|---|---|
| Chronic fatigue and disability | Persistent orthostatic intolerance → inability to stand for prolonged periods → limitation of all upright activities | Particularly disabling in POTS — some adolescents become essentially housebound. This is a major source of disability in post-COVID POTS |
| School absenteeism / academic failure | Morning worsening of symptoms (POTS is often worst in the morning) → inability to attend school | Can lead to school refusal, social isolation, and academic decline. School liaison and modified attendance are essential |
| Depression and anxiety | Chronic illness → loss of function → social isolation → psychiatric comorbidity | Up to 50% of adolescents with POTS have comorbid anxiety or depression. Screen actively. CBT and SSRIs may be needed |
| Deconditioning vicious cycle | Inactivity → loss of cardiovascular fitness → worsened venous pooling and autonomic function → more symptoms → more inactivity | This is the central obstacle to recovery. The graduated exercise programme breaks this cycle but requires months of commitment |
| Falls and injury | Same mechanism as vasovagal, though frank syncope is less common in pure POTS (presyncope more typical) | Still possible — caution with stairs, bathing |
| Cause | Complications |
|---|---|
| Hypoglycaemia | Prolonged severe hypoglycaemia ( < 2.6 mmol/L for > 15–30 minutes) can cause permanent neuronal injury — hippocampal neurones are particularly vulnerable. In neonates and infants, this manifests as cognitive impairment, seizure disorder, or cerebral palsy. In older children, severe hypoglycaemia causes seizures and coma. Neuroglycopenic symptoms: periorbital and finger paraesthesia, seizures, focal weakness, ↓sensation, clouding of vision, ↓consciousness, drowsiness, coma [5] |
| Severe anaemia | High-output cardiac failure if chronic and severe. Complications: cardiac ischaemia, ↑thrombocytopenic bleeding, ↑mortality [6][13] |
| Adrenal crisis | Shock, coma, death if untreated. Adrenal crisis can be precipitated by intercurrent illness in a child with unrecognised adrenal insufficiency |
C. Psychosocial and Quality-of-Life Complications
These are arguably the most underappreciated complications in paediatric syncope, yet they are often the main reason families seek medical attention and the main source of functional impairment.
| Complication | Mechanism | Paediatric Relevance |
|---|---|---|
| Anxiety about future episodes | Unpredictability of syncope → anticipatory fear → avoidance behaviour | The child may avoid triggers (which is adaptive) but may also avoid normal activities out of fear (which is maladaptive). This can evolve into a generalised anxiety disorder or specific phobia |
| Embarrassment and social stigma | Fainting at school in front of peers → embarrassment, teasing | Adolescents are particularly sensitive to social perception. A child who faints at school assembly may refuse to attend assemblies, and eventually school |
| School avoidance / refusal | Fear of fainting at school → avoidance | This is a significant problem in HK where academic pressure is intense. Some children with POTS miss months of school. Modified school attendance, home tutoring, and school liaison are essential |
| Activity restriction (iatrogenic or parental) | Doctor or parent restricts all physical activity → deconditioning → worsened symptoms | Over-restriction is a common complication of the diagnosis itself. Unless there is a confirmed cardiac cause requiring restriction, children with vasovagal syncope should be ENCOURAGED to exercise |
| Identity / self-concept issues | Being labelled as "sickly" or "fragile" | Particularly relevant in adolescence when identity is forming. Normalise the condition |
| Complication | Mechanism |
|---|---|
| Parental anxiety and overprotection | Witnessing a child lose consciousness (especially with anoxic seizure) is terrifying for parents. If the diagnosis is "benign," parents may not believe it. They may restrict the child's activities, refuse to let them attend school trips, sleep poorly, or develop their own anxiety disorder |
| Repeated emergency department visits | Each episode may prompt an ED visit → disruption to family life, healthcare costs, parental work absence |
| Strained family relationships | Parental disagreement about the severity of the condition or appropriate management; one parent may want more investigations while the other accepts reassurance |
| Sibling effects | Attention focused on the affected child → sibling resentment or anxiety |
| Misdiagnosis | Consequence |
|---|---|
| Vasovagal syncope misdiagnosed as epilepsy | Unnecessary anti-seizure medication → side effects (sedation, cognitive impairment, weight gain, teratogenicity). Child labelled as "epileptic" → social stigma, driving restrictions (when older), insurance implications |
| Cardiac syncope misdiagnosed as vasovagal | Failure to treat a life-threatening condition → risk of sudden cardiac death |
| POTS dismissed as "anxiety" or "school refusal" | No appropriate treatment → progressive deconditioning → worsened disability → actual depression and anxiety develop (self-fulfilling prophecy). Common problem |
| Psychogenic pseudosyncope treated as organic | Repeated investigations reinforce illness behaviour → worsened functional impairment |
Treatments for syncope carry their own complications, which must be weighed against the benefits:
| Treatment | Potential Complications |
|---|---|
| Midodrine | Supine hypertension (most important — instruct last dose ≥ 4h before bedtime), piloerection, urinary retention, scalp tingling |
| Fludrocortisone | Hypokalaemia (requires electrolyte monitoring), weight gain, oedema, supine hypertension, growth suppression if prolonged use in children (mineralocorticoid effect) |
| β-blockers | Fatigue, exercise intolerance (major concern in active adolescents), sleep disturbance, bronchospasm in asthmatic children, depression, bradycardia, hypotension |
| ICD implantation | Inappropriate shocks (very distressing, can cause PTSD in adolescents — up to 20% experience inappropriate shocks), lead fracture/malfunction, infection, device replacement every 5–10 years (lifetime commitment for a child), psychosocial impact (body image, sports restriction, MRI compatibility issues) |
| Cardiac pacing | Lead fracture (higher risk in growing children due to body growth), infection, venous occlusion, device replacement, psychosocial impact |
| Catheter ablation | Procedural risk: AV block (particularly in septal accessory pathways near AV node in WPW — risk ~1%), vascular injury, cardiac perforation, radiation exposure. Overall complication rate ~2–4% in paediatric centres |
| Unnecessary anti-seizure drugs (from misdiagnosis) | Sedation, cognitive impairment, weight gain (valproate), hepatotoxicity (valproate), rash (lamotrigine, carbamazepine, phenytoin), teratogenicity (valproate, carbamazepine) — all avoidable if the correct diagnosis is made |
| Aetiology | Direct Complications of Syncope | Complications of Underlying Disease | Psychosocial Complications | Mortality Risk |
|---|---|---|---|---|
| Vasovagal syncope | Falls → head/dental/bone injury; drowning if in water; anoxic convulsion (not epilepsy) | Recurrence; deconditioning (if over-restricted) | Anxiety, school avoidance, parental anxiety, misdiagnosis as epilepsy | NIL (zero mortality for the syncope itself) |
| Breath-holding spells | Falls; anoxic convulsion | Nil long-term (self-resolves by age 5–6) | Severe parental anxiety; overprotective parenting | NIL |
| POTS | Falls (uncommon — presyncope more than syncope) | Chronic fatigue, disability, deconditioning | School absence, depression, anxiety, social isolation | NIL |
| LQTS | Falls; anoxic convulsion; drowning | Recurrent VT/VF → sudden cardiac death | Activity restriction, ICD-related anxiety | YES — 4–5% per TdP event [4] |
| CPVT | Falls; drowning | Recurrent VT → cardiac arrest | Activity restriction, ICD-related anxiety | YES — high without treatment |
| HCM | Falls during exertion | Heart failure, arrhythmia, SCD | Sports restriction | YES |
| Complete heart block | Falls | Cardiomyopathy from chronic bradycardia if untreated | Pacemaker-related psychosocial issues | YES if untreated |
High Yield Summary — Complications
Direct complications of syncopal events:
- Head injury is the most common and most important traumatic complication — children have proportionally large heads and tend to fall head-first
- Drowning is a critical risk, especially in undiagnosed LQTS1 (cold water + exercise trigger) — counsel ALL children with syncope about water safety
- Anoxic convulsion is NOT epilepsy — misdiagnosis leads to unnecessary anti-seizure medication with avoidable side effects
Complications of underlying cause:
- Vasovagal syncope has ZERO mortality — reassure families firmly
- Cardiac syncope carries up to 30% mortality if cardiac cause is undiagnosed — this is why ECG and cardiac workup are mandatory for every child with syncope
- Syncope in cardiac disease (LQTS, HCM, CPVT) is a "warning shot" before sudden death — the next episode may not self-terminate
- POTS causes chronic disability primarily through fatigue, deconditioning, and school absence rather than through the syncope itself
Psychosocial complications (often the most impactful):
- Anxiety, school avoidance, parental overprotection, activity over-restriction, deconditioning vicious cycle, misdiagnosis
- Addressing psychosocial complications is as important as treating the syncope itself — family-centred care, school liaison, and psychological support are essential
Treatment complications:
- Midodrine → supine hypertension
- ICD → inappropriate shocks (up to 20%), psychosocial impact in adolescents
- Unnecessary AEDs from misdiagnosis → sedation, cognitive impairment, teratogenicity
Active Recall - Complications of Paediatric Syncope/Dizziness
References
[1] Senior notes: Adrian Lui Pediatrics.pdf (p117 — Breath-holding spells: anoxic convulsive seizure from transient decreased brain O2 delivery; febrile seizure differential) [3] Senior notes: Ryan Ho Cardiology.pdf (p62–63 — Syncope: clinically important as premonitory sign of severe cardiac disease with 30% mortality if cardiac cause; cardiogenic vs neurocardiogenic vs seizure differentiation table; causes of exercise-related syncope) [4] Senior notes: Ryan Ho Cardiology.pdf (p196 — LQTS: TdP episodes usually self-terminating with approximately 4–5% of events being fatal; prognosis good overall if on β-blocker, very good if on ICD) [5] Senior notes: Ryan Ho Endocrine.pdf (p94 — Hypoglycaemia: neuroglycopenic symptoms including periorbital and finger paraesthesia, seizures, focal weakness, decreased consciousness, drowsiness, coma) [6] Senior notes: Ryan Ho Haemtology.pdf (p10 — Anaemia symptoms: dizziness/syncope may be postural; complications include cardiac ischaemia, increased thrombocytopenic bleeding, increased mortality) [13] Senior notes: Adrian Lui Pediatrics.pdf (p352 — Paediatric approach to anaemia: symptoms, complications including cardiac ischaemia)
Recurrent Chest Infections
Repeated lower respiratory tract infections in children, often defined as three or more episodes per year, warranting investigation for underlying causes such as asthma, immunodeficiency, cystic fibrosis, or structural airway abnormalities.
Transposition Of The Great Arteries
Transposition of the great arteries is a congenital heart defect, typically presenting in newborns, in which the aorta arises from the right ventricle and the pulmonary artery from the left ventricle, creating two parallel circulations that prevent adequate oxygenated blood from reaching the body.