Accidents and Poisoning in Children

In the management of a seriously injured child, what is the correct sequence of the primary survey, and what life-threatening injuries must be identified during it?

Catastrophic haemorrhage must be addressed FIRST (before the standard ABCDE approach).

Life-threatening injuries to identify during the primary survey include:
Airway obstruction, Tension pneumothorax, Open pneumothorax, Massive internal/external haemorrhage, Flail chest, and Cardiac tamponade.

Cervical spine injury should always be assumed; manual in-line stabilization is preferred over cervical collars (collars are no longer recommended).

What are the indications for an urgent CT scan vs. hospital admission vs. discharge in a child with head injury?

Urgent CT scan is indicated if any of the following are present:
suspicion of non-accidental injury, post-traumatic seizure, GCS <14 initially or <15 after 2 hours, suspected open/depressed skull fracture, signs of basal skull fracture (haemotympanum, panda eyes, Battle sign, CSF leak), focal neurological signs, or child <1 year with bruise/swelling >5 cm.

Admit and observe for ≥6 hours if any of: witnessed LOC >5 min, abnormal drowsiness, ≥3 vomiting episodes, dangerous mechanism (fall >3 m, high-speed RTC), or amnesia >5 min. If only one of these features, a CT scan may still be needed depending on clinical judgment.

What are the primary and secondary mechanisms of brain damage following head injury in children?

Primary damage occurs at the time of injury and includes: focal cerebral contusions and lacerations, diffuse axonal injury, injury to blood vessels (extradural haemorrhage from arterial origin, subdural haemorrhage from venous origin), and penetrating injury.

Secondary damage develops afterward and includes: cerebral oedema, hypotension, hypoxia, seizures, hypoglycaemia, and later infection.

Management aims to prevent secondary damage by maintaining cerebral blood supply and minimizing raised intracranial pressure.

What is SCIWORA, and what are the key features of neck injuries in children?

SCIWORA stands for Spinal Cord Injury Without Radiologic Abnormality.

It occurs because the elasticity of the cervical spine in children allows spinal cord damage without injury to bony structures.

Neck injuries resulting in spinal cord damage are rare and usually associated with high-impact trauma (e.g., high-speed road traffic collisions).

The most common fracture is of the upper two cervical vertebrae (C1–C2).

How should a choking child be managed depending on the severity of airway obstruction and the child's age?

If the cough is effective (mild obstruction):
encourage continued coughing and observe.

If the cough is ineffective (severe obstruction) and the child is conscious:
give 5 back blows followed by 5 abdominal thrusts (Heimlich manoeuvre) for children;
for infants, give 5 back blows followed by 5 chest thrusts (NOT abdominal thrusts, due to risk of liver/spleen injury).

If unconscious: start CPR immediately.
Continue alternating until the obstruction is cleared or the child becomes unconscious.

What are the key principles of first aid for burns, including cooling duration and timing, and what methods are used to estimate burn surface area?

Cool the burn with running water for a total of 20 minutes, within 4 hours of injury (even if cooling was started later, make up the remaining time).

Avoid hypothermia.
After cooling, cling film can wrap the area.

Chemical burns require copious irrigation.

For surface area estimation: use the Lund and Browder chart (most accurate), the child's palm + outstretched fingers = ~1% BSA,
or the Rule of Nines (whole limb = 9%, face = 9%, chest front+back = 18%, etc.).

Purely erythematous (superficial epidermal) burns are NOT included in the BSA calculation.

How are burns classified by depth, and what are the appearance, pain sensation, and healing time for each type?

Superficial (epidermis only): dry, erythematous; painful; heals in ~1 week.

Partial thickness superficial (e.g., scalds): moist, erythematous, blistered; painful; heals in 1–3 weeks.

Partial thickness deep (e.g., scalds, brief flame): moist with white slough, mottled; painful or painless; heals in 3–4 weeks, often requires grafting.

Full thickness (significant flame contact): dry, charred, white; painless; requires skin grafting.

Laser Doppler Imaging (LDI) is a sensitive and specific tool for non-invasive burn depth assessment.

What are the four categories of poisoning in children, and what are the key epidemiological features of accidental poisoning?

The four categories are:
1) Accidental (most common in young children),
2) Deliberate self-harm or recreational experimentation (adolescents),
3) Iatrogenic (drug errors by health professionals),
4) Intentional (by parents or carers — rare).

Accidental poisoning peaks at 30 months of age, typically occurs at home, and serious harm is uncommon since many household substances are of low toxicity and children usually ingest small amounts.

A small number of medicines (e.g., antihypertensives, antidepressants) can be fatal even in small doses.

What substances are considered highly toxic vs. low toxicity in childhood poisoning, with examples from medicines, household products, and garden substances?

Low toxicity —
Medicines: oral contraceptives, most antibiotics, topical hydrocortisone.
Household: liquid soap, lipstick, washing-up liquid, water-based paint.
Garden: animal faeces, slugs, geraniums, compost.

High toxicity —
Medicines: opioids, beta-blockers, tricyclic antidepressants, oral hypoglycaemics, paracetamol, digoxin, iron, salicylates.
Household: strong bleach, concentrated oven cleaner, liquid nicotine (e-cigarettes), ethylene glycol (antifreeze), petroleum distillates.
Garden: laburnum, death cap mushroom, yew, foxglove, organophosphorus pesticides, kerosene.

What is the outline of management of a poisoned child, including the role of activated charcoal and when gastric lavage is used?

Steps:
1) Identify the agent (history, clinical signs per toxidrome table).
2) Determine toxicity (intrinsic toxicity via poisons information service e.g., ToxBase UK; dose reported; symptoms; time since ingestion).
3) Decide on investigations (LFTs, RFTs, FBC, ECG for cardiac drugs; specific blood levels only useful for paracetamol, iron, salicylates, and alcohol; urine toxicology not helpful acutely).
4) Reduce absorption if indicated: activated charcoal is effective within 1 hour of ingestion for many drugs (ineffective for iron, hydrocarbons, pesticides).

Gastric lavage and induced vomiting are NO LONGER recommended.

Describe the clinical features, mechanism, and management of paracetamol poisoning in children.

Clinical features:
Early — abdominal pain and vomiting;
Late (12–24 h) — liver failure.

Mechanism: Toxic metabolite NAPQI is produced when normal liver metabolism is saturated; NAPQI causes hepatocellular damage.

Management: Measure plasma paracetamol concentration 4 hours after ingestion and plot on a nomogram;
if concentration is on or above the treatment line, give IV N-acetylcysteine (acetylcysteine). Monitor liver function and INR.

Describe the clinical features, mechanism, and management of salicylate and tricyclic antidepressant poisoning.

Salicylates (e.g., aspirin):
Early — vomiting, tinnitus;
Late — respiratory alkalosis followed by metabolic acidosis.

Mechanism: stimulates respiratory centre; uncouples oxidative phosphorylation causing metabolic acidosis and hypoglycaemia.

Management: plasma salicylate level 2–4 h post-ingestion;
alkalinize urine to increase excretion;
haemodialysis effective in severe cases.

Tricyclic antidepressants:
Early — tachycardia, drowsiness, dry mouth;
Late — arrhythmias, seizures.

Mechanism: anticholinergic effects and interference with cardiac conduction.

Management: sodium bicarbonate for arrhythmias; support breathing.

Describe the clinical features, mechanism, and management of iron poisoning and organophosphorus pesticide poisoning.

Iron:
Initial — vomiting, diarrhoea, haematemesis, melaena, acute gastric ulceration;
then a latent improvement phase;
6–12 h later — drowsiness, coma, shock, liver failure, hypoglycaemia, convulsions;
long-term — gut strictures.

Serious if >75 mg/kg elemental iron. Measure serum iron at 4 h;
give IV deferoxamine (chelates iron) for moderate-to-severe toxicity.

Organophosphorus pesticides:
Cholinergic effects (SLUDGE: salivation, lacrimation, urination, diarrhoea, vomiting) + muscle weakness, cramps, paralysis, bradycardia, hypotension;
CNS — seizures, coma.

Mechanism: acetylcholinesterase inhibition → acetylcholine accumulation.

Management: atropine (large doses), pralidoxime (reactivates acetylcholinesterase), supportive care.

What are the key features of chronic environmental poisoning in children, focusing on lead toxicity?

Children are particularly vulnerable to chronic environmental poisoning because: they engage in frequent hand-to-mouth activity, their small body size makes them more susceptible to low doses, and their developing brains are at greater risk of permanent neurotoxic damage.

Lead is the most important chronic environmental toxin.

Symptoms of chronic exposure include behavioural changes, hyperactivity or decreased activity, developmental delay/loss of milestones, and chronic lead nephropathy.

Significant exposure adds: abdominal pain, vomiting, constipation, headache, ataxia, lethargy, seizures, and coma.

Management:
prevent further exposure; chelation therapy for acute symptoms (e.g., encephalopathy), though complex due to lead's long half-life in bone.

What special considerations apply to drowning, button battery ingestion, and carbon monoxide poisoning in children?

Drowning: Babies/toddlers drown in domestic settings (baths, paddling pools); older children in canals/lakes/sea.
Cold water hypothermia is protective — resuscitation must continue until child is warmed to normal body temperature even with fixed dilated pupils.

Button batteries: cause abdominal pain, gut perforation, and stricture formation via electrical corrosion of the gut wall.
X-ray to confirm and locate;
endoscopic removal if in the oesophagus, failing to pass, or symptomatic.

Multiple magnets also require urgent surgical referral.

Carbon monoxide:
Early — headache, nausea;
Late — confusion, drowsiness, coma.
Binds haemoglobin causing tissue hypoxia.
Treatment: high-flow oxygen; role of hyperbaric oxygen is unclear.