PE5.1-4 | Behavioural Problems — Practice Quiz

GORD is a common cause of feeding refusal and back-arching (Sandifer posture) in infants. Acid reflux causes discomfort during and after feeding, leading to aversion and poor weight gain.

Gastro-oesophageal reflux disease (GORD) is a leading cause of feeding problems in infants under 1 year; hallmarks include post-prandial regurgitation, Sandifer posture (back-arching), and feeding refusal. Conservative measures (smaller feeds, upright positioning) are first-line.

Pyloric stenosis causes projectile vomiting typically from 3-6 weeks and does not cause back-arching. Hirschsprung disease presents with constipation and delayed meconium passage. Celiac disease presents after weaning with gluten-containing foods.

This child has food refusal/neophobia, a normal developmental variant at this age especially with late introduction of solids. Responsive feeding strategies and structured meal times without pressure are the cornerstone of management.

Developmental feeding problems (neophobia, texture selectivity) are common between 9-18 months. Responsive feeding with structured meals, division-of-responsibility approach, and avoiding force-feeding are the mainstay; organic causes must be ruled out but invasive investigation is not the first step.

Appetite stimulants are not recommended as first-line in a child with appropriate weight for age. NG tube feeding and endoscopy are invasive and not indicated without organic pathology or severe malnutrition.

Cyanotic breath-holding spells are triggered by a provoking event (frustration, pain), followed by crying → breath-holding in expiration → cyanosis → brief loss of consciousness. Recovery is rapid and spontaneous. This is the most common type of BHS.

Cyanotic breath-holding spells affect 5% of children, peak at 6-18 months, and are benign. Key diagnostic clues: emotional/painful trigger → cry → apnoea → cyanosis → LOC, all resolving within 1 minute with no post-ictal state. Investigations are not routinely needed. Reassure parents.

Pallid BHS is triggered similarly but involves vagally-mediated pallor and bradycardia rather than cyanosis. Febrile seizures require fever and do not have the typical cry-cyanosis sequence. Absence epilepsy has sudden-onset staring without a triggering event or cyanosis.

Pallid breath-holding spells (reflex anoxic seizures) are vagally mediated and benign. Management is parental reassurance. Iron deficiency anaemia is associated with BHS and should be corrected if present. Anti-epileptic drugs and pacemakers are not indicated.

Pallid BHS are caused by vagal-mediated cardiac slowing triggered by pain/fear. They are benign, self-limiting by age 5-6 years. Iron deficiency anaemia must be sought and corrected; it lowers the threshold for episodes. Parents need clear reassurance that these are not epilepsy.

Anti-epileptics are not indicated as these are not epileptic events. Propranolol is rarely used in very severe refractory cases but is not first-line. Pacemaker is considered only in extremely rare, refractory cardioinhibitory cases with documented asystole.

Temper tantrums peak between 18 months and 3 years and are a normal developmental milestone as the child asserts autonomy. Extinction (planned ignoring), consistent limits, and reward of positive behaviour are the cornerstone of management. No medication is indicated.

Temper tantrums are age-appropriate between 18 months and 3 years, driven by the child's emerging autonomy and limited frustration tolerance. Management is entirely behavioural: parental counselling on consistent boundaries, extinction (ignore the tantrum), and positive reinforcement. Medication and investigation are not indicated for typical tantrums.

Autism screening is warranted if there are social communication concerns (absent eye contact, no pointing, language delay, repetitive behaviours) — none of which are present here. Haloperidol and neurological referral are not appropriate for age-appropriate tantrums.

Pica (eating non-nutritive substances) is strongly associated with lead poisoning, especially when the child eats paint chips from old painted walls (which may contain lead-based paint). Blood lead level is essential to screen for lead toxicity, which can cause cognitive impairment, encephalopathy, and microcytic anaemia.

Pica (persistent eating of non-nutritive substances >1 month, in a child >2 years where this is developmentally inappropriate) is associated with iron deficiency and lead poisoning. When a child eats paint chips or soil, blood lead level must be checked. Lead toxicity causes encephalopathy, cognitive impairment, and microcytic anaemia. Treatment: iron for deficiency, chelation (DMSA or CaNa2EDTA) for significant lead toxicity.

Stool for ova and parasites is relevant but does not address the primary concern of lead poisoning from paint-chip pica. Serum ferritin alone addresses iron deficiency but misses the critical lead exposure. Thyroid function is not directly related to this presentation.

Primary nocturnal enuresis (PNE) is defined as bedwetting in a child ≥5 years of age who has NEVER achieved a period of dryness ≥6 months. This child is 6 years with lifelong bedwetting — the textbook definition of PNE.

Primary nocturnal enuresis (never dry for ≥6 months) must be distinguished from secondary enuresis (regression after dryness — suggests a stressor or new organic cause). Organic causes (UTI, diabetes insipidus, DM) must be excluded with urine analysis and culture before labelling it primary/functional enuresis.

Secondary enuresis requires a prior dry period of ≥6 months. Diurnal enuresis is daytime wetting. Overactive bladder presents with urgency, frequency, and usually daytime symptoms as well.

For secondary enuresis (regression after 2 years of dryness), first-line management is behavioural: motivational therapy (star charts), fluid restriction after 5 PM, voiding before sleep, and an enuresis alarm (bell-and-pad). Stress (parental separation) should be addressed. Medications are second-line.

Secondary enuresis requires identifying and addressing the triggering stressor. Enuresis alarm (bell-and-pad) is the most effective long-term treatment for nocturnal enuresis (60-70% success, low relapse). Desmopressin is second-line (good short-term, higher relapse). Imipramine is third-line due to safety concerns.

Desmopressin and imipramine are used in primary enuresis when alarms fail or are not tolerated; they are not first-line behavioural approaches. Oxybutynin targets overactive bladder with urgency; there is no urgency here.

Cyanotic breath-holding spells (the more common type, 75-80%) are triggered by frustration, pain, or anger; the child cries vigorously, then holds the breath in expiration, becomes cyanotic, and may briefly lose consciousness with rapid recovery. No treatment is needed beyond parental reassurance and iron supplementation if anaemic.

Breath-holding spells affect 5% of children, peak at 6-18 months, and resolve by age 5-6 years. Cyanotic type (75-80%) = expiratory apnoea + cyanosis; pallid type (20-25%) = vagal-mediated pallor + bradycardia. Both are benign. Investigate and treat iron deficiency. Reassure parents. No anti-epileptics needed.

Pallid spells (reflex anoxic seizures) are less common (25%). EEG is NOT routinely recommended in typical BHS as the diagnosis is clinical. Anti-epileptics are not indicated.

Blood lead level 18 mcg/dL (reference <5 mcg/dL) is elevated but below the chelation threshold (≥45 mcg/dL for DMSA; ≥70 mcg/dL for CaNa2EDTA or combined therapy). The priority is iron supplementation (iron deficiency promotes lead absorption) and removing the child from the lead source (environmental intervention).

Pica + lead poisoning: BLL <5 mcg/dL = normal; 5-44 mcg/dL = environmental + iron treatment + monitoring; ≥45 mcg/dL = DMSA chelation; ≥70 mcg/dL = CaNa2EDTA ± DMSA. Iron deficiency must always be treated as it amplifies lead absorption through the divalent metal transporter pathway.

DMSA chelation is indicated when BLL ≥45 mcg/dL; CaNa2EDTA ± DMSA for ≥70 mcg/dL. At BLL 18 mcg/dL, environmental remediation and iron treatment are the priorities. Zinc supplementation alone does not address iron deficiency or lead toxicity.