NLE Paediatric Nursing — Paediatric GI, Genitourinary & Neurologic DisordersRevision Notes

Formulas

Exam tips

• NLE items on paediatric fluids often ask: 'Which assessment finding is MOST reliable for hydration status?' — Answer: DAILY WEIGHT.
• If asked about the Holliday-Segar rule, remember: 100-50-20 (daily) = 4-2-1 (hourly).
• A sunken anterior fontanelle = dehydration; a bulging fontanelle = increased ICP or fluid overload.
• A capillary refill > 2 seconds in a child suggests poor perfusion — escalate immediately.

Key points

• Infants have a HIGHER percentage of total body water (up to 80% in neonates vs. 60% in adults) — making them more vulnerable to dehydration.
• Higher body-surface-area-to-mass ratio means greater insensible fluid loss through the skin.
• Immature kidneys cannot concentrate urine efficiently — limited ability to compensate for fluid deficit.
• Higher metabolic rate increases fluid and caloric demands per kilogram body weight.
• Maintenance fluid calculation uses the Holliday-Segar (4-2-1) rule: 100 mL/kg/day for the first 10 kg + 50 mL/kg/day for the next 10 kg + 20 mL/kg/day for each kg above 20 kg.
• The MOST SENSITIVE indicator of hydration status in infants is DAILY WEIGHT (acute weight change reflects fluid balance).
• Target urine output in infants and children: 1–2 mL/kg/hr.
• Other hydration assessment parameters: fontanelle (bulging = fluid overload; sunken = dehydration), mucous membranes, skin turgor, capillary refill (normal < 2 seconds), and heart rate.
• Dehydration is classified as mild (5% weight loss), moderate (10%), or severe (15%) — these percentages are higher thresholds than used in adults.

Definitions

Common mistakes

• Using adult hydration indicators (e.g., thirst) for infants — infants cannot communicate thirst.
• Forgetting that weight change is the MOST SENSITIVE hydration indicator, not urine colour.
• Applying the adult 30 mL/kg/hr urine output target to infants — paediatric target is 1–2 mL/kg/hr.
• Confusing the 4-2-1 hourly rule with the 100-50-20 daily rule — both give the same result but are expressed differently.

Exam tips

• KEY PATTERN: '3–5 week-old firstborn male + projectile NON-bilious vomiting + olive mass RUQ + hungry infant' = Pyloric Stenosis.
• Metabolic imbalance to remember: ALKALOSIS (not acidosis), because HCl is lost through vomiting.
• Pre-op priority: fluid and electrolyte CORRECTION before pyloromyotomy — this is the number-one priority nursing action.
• Post-op: RIGHT SIDE positioning after feeds — promotes gravity-assisted gastric emptying through the now-open pylorus.
• If the NLE question asks 'what should the nurse do FIRST?' and the child has pyloric stenosis with surgery scheduled — correct fluid and electrolytes FIRST.

Key points

• Hypertrophic pyloric stenosis (HPS): hypertrophy of the pyloric muscle causes gastric outlet obstruction — presents at 2–8 weeks of age (classically 3–5 weeks).
• Demographics: more common in FIRSTBORN MALES; familial tendency.
• Classic presenting sign: PROJECTILE, NON-BILIOUS vomiting (obstruction is ABOVE the bile duct entry in the duodenum — bile cannot mix with vomited content).
• The infant is HUNGRY and feeds eagerly immediately after vomiting (contrast with gastroenteritis where the infant refuses feeding).
• Physical findings: OLIVE-SHAPED, firm, PALPABLE MASS in the right upper quadrant (RUQ); VISIBLE LEFT-TO-RIGHT peristaltic waves across the epigastrium.
• Metabolic consequence of persistent vomiting of gastric acid (HCl): HYPOCHLOREMIC, HYPOKALEMIC METABOLIC ALKALOSIS — classic electrolyte imbalance on the NLE.
• Diagnostic confirmation: ultrasound is the gold standard (shows thickened pylorus).
• Priority pre-operative nursing care: CORRECT FLUID AND ELECTROLYTE IMBALANCE FIRST — surgery is elective and must wait until the child is medically stabilised.
• Definitive treatment: PYLOROMYOTOMY (Fredet-Ramstedt procedure) — surgical splitting of the hypertrophied pyloric muscle without resection.
• Post-operative feeding: start small, frequent feeds (usually 4–6 hours post-op, as ordered); position upright at 30–45° and on the RIGHT SIDE after feeds to promote gastric emptying; monitor incision for signs of infection.
• Parents should be reassured that vomiting may continue briefly post-operatively due to mucosal oedema, but should resolve within 24–48 hours.

Definitions

Common mistakes

• Confusing non-bilious (pyloric stenosis) with bilious vomiting (indicates obstruction BELOW the duodenum — e.g., malrotation, intussusception).
• Proceeding to surgery before correcting electrolyte imbalance — a critical nursing priority error.
• Describing the mass as being in the LEFT upper quadrant — it is always in the RIGHT upper quadrant.
• Thinking the infant has no appetite — in pyloric stenosis, the infant is always hungry ('projects and seeks').

Exam tips

• KEY PATTERN: 'Neonate + no meconium in 48 h + abdominal distension + bilious vomiting' = Hirschsprung Disease.
• DEFINITIVE TEST = Rectal BIOPSY (not barium enema — that only shows the transition zone).
• Ribbon-like stools = the stool is being squeezed through the narrow aganglionic segment.
• If the NLE stem describes 'explosive foul-smelling diarrhoea + fever + abdominal distension' in a known Hirschsprung child — this is HAEC, a medical emergency — report immediately and prepare for IV fluids, antibiotics, and bowel decompression.
• Normal meconium passage within 24–48 hours rules OUT Hirschsprung — a good NLE discrimination point.

Key points

• Also called Congenital Aganglionic Megacolon — ABSENCE of ganglion (Auerbach's and Meissner's plexus) nerve cells in a segment of the distal colon.
• Without ganglion cells, there is NO peristalsis in that bowel segment → functional obstruction → the proximal bowel dilates (megacolon).
• NEONATAL KEY SIGN: FAILURE TO PASS MECONIUM within 24–48 hours of birth — the most important early clue on the NLE.
• Other signs: abdominal distension, BILIOUS vomiting (obstruction is BELOW the pylorus), ribbon-like and foul-smelling stools in older infants.
• Older child presentation: CHRONIC constipation, failure to thrive, abdominal distension.
• DEFINITIVE DIAGNOSTIC TEST: RECTAL BIOPSY — confirms the absence of ganglion cells in the affected bowel segment.
• Other diagnostic tools: barium enema (shows transition zone), anorectal manometry.
• Surgical management: removal of the aganglionic segment. A temporary COLOSTOMY may be created first, followed by a 'pull-through' procedure (Swenson, Soave, or Duhamel technique) to connect healthy bowel to the rectum.
• Most dangerous complication: HIRSCHSPRUNG-ASSOCIATED ENTEROCOLITIS (HAEC) — explosive, foul-smelling diarrhoea, fever, abdominal distension, and sepsis. This is a LIFE-THREATENING emergency. Report immediately.
• Post-colostomy nursing: teach colostomy care to parents, skin care around stoma, and signs of complications.
• Pre-operative rectal irrigations may be ordered to decompress the bowel.

Definitions

Common mistakes

• Saying the diagnostic test is a barium enema — barium enema is CONFIRMATORY but the DEFINITIVE test is rectal BIOPSY.
• Confusing the bilious vomiting of Hirschsprung with the NON-bilious vomiting of pyloric stenosis.
• Forgetting that in Hirschsprung, the AGANGLIONIC segment does NOT dilate — it is the PROXIMAL (normal) bowel that dilates (megacolon).
• Missing HAEC signs — treating simple constipation instead of recognising the emergency.

Exam tips

• KEY PATTERN: '5–9 month old + episodic screaming + knees to chest + sausage mass + currant-jelly stool' = Intussusception.
• Remember: Air or barium enema = DIAGNOSTIC + THERAPEUTIC (reduces intussusception non-surgically).
• Passage of normal brown stool = intussusception REDUCED — report to physician immediately.
• Currant-jelly stool = LATE sign of ischaemia — do not wait for this to make the diagnosis.
• NLE discrimination: the intermittent colicky pain with normal intervals between episodes is the MOST characteristic feature.

Key points

• Intussusception: TELESCOPING of one segment of bowel INTO an adjacent segment — most commonly the ileum telescopes INTO the colon (ileocolic).
• The telescoped bowel causes obstruction, venous congestion, oedema, ischaemia, and can progress to necrosis and perforation.
• Age of onset: 3 months to 3 years; PEAK incidence at 5–9 months; often in previously healthy, well-nourished infants.
• CLASSIC TRIAD (memorise this for the NLE): (1) Sudden COLICKY abdominal pain — infant draws knees to chest and screams intermittently, then has pain-free intervals; (2) Palpable 'SAUSAGE-SHAPED' mass, usually in the RUQ or mid-abdomen; (3) 'CURRANT-JELLY' STOOLS — blood mixed with mucus — this is a LATE sign indicating mucosal ischaemia.
• Between pain episodes, the infant may appear lethargic or in a 'shock-like' state.
• DIAGNOSIS AND TREATMENT: Air (pneumatic) enema OR hydrostatic/barium enema is BOTH diagnostic AND THERAPEUTIC — the pressure from the enema reduces (pushes back) the intussuscepted bowel non-surgically.
• KEY POST-REDUCTION SIGN: Passage of a NORMAL BROWN STOOL signals that the intussusception has been reduced — REPORT this to the physician (it confirms resolution).
• Surgery is indicated if: the enema fails, perforation has occurred, or the bowel is compromised/necrotic.
• Post-reduction nursing: monitor for recurrence (can recur in ~5% of cases), monitor stool output, assess vital signs for signs of peritonitis.
• A possible precipitating factor in older children: a 'lead point' such as Meckel's diverticulum or polyp that initiates the telescoping.

Definitions

Common mistakes

• Thinking currant-jelly stool is an EARLY sign — it is LATE, indicating ischaemia.
• Confusing the therapeutic approach: an enema can REDUCE intussusception — it is not just diagnostic.
• Missing the colicky, episodic nature of the pain — the infant appears normal between episodes, which can mislead caregivers.
• Forgetting to report normal brown stool passage after the enema — this is critical clinical information.

Exam tips

• KEY PATTERN: '2–3 year old + non-tender unilateral abdominal mass (does not cross midline) + found during bathing' = Wilms Tumour.
• MOST CRITICAL RULE: DO NOT PALPATE. Post a sign. This is almost always the correct answer when Wilms tumour is in the NLE stem.
• Distinguish from neuroblastoma: Wilms = does NOT cross midline; Neuroblastoma = DOES cross midline.
• Surgery is FIRST (nephrectomy), followed by chemotherapy ± radiation.
• If NLE asks 'what is the priority nursing intervention?' = DO NOT PALPATE the abdomen + post a sign.

Key points

• Wilms tumour (nephroblastoma) is the MOST COMMON PRIMARY RENAL MALIGNANCY of childhood.
• Typical age of diagnosis: 2–3 years; peak incidence between 3–4 years.
• CLASSIC PRESENTATION: A FIRM, NON-TENDER ABDOMINAL MASS found accidentally by a parent while bathing or dressing the child.
• The mass is UNILATERAL (confined to one side) and does NOT CROSS THE MIDLINE — this distinguishes it from neuroblastoma, which does cross the midline.
• Associated signs: haematuria (blood in urine), hypertension (from renin secretion by the tumour), and abdominal pain (uncommon initially).
• Associated syndromes: WAGR syndrome (Wilms, Aniridia, Genitourinary anomalies, Retardation), Beckwith-Wiedemann syndrome.
• ⚠️ CRITICAL NURSING RULE — THE MOST IMPORTANT NLE POINT: DO NOT PALPATE the abdomen of a child with a suspected or confirmed Wilms tumour. POST A SIGN AT THE BEDSIDE. Palpation can RUPTURE the encapsulated tumour, spreading malignant cells (seeding) and worsening the prognosis.
• Handle the child GENTLY during bathing, positioning, and examinations.
• Management: SURGERY (nephrectomy — removal of the affected kidney) is performed usually within 24–48 hours of diagnosis, followed by CHEMOTHERAPY (vincristine, actinomycin D ± doxorubicin) and RADIATION therapy (for Stage III/IV).
• Prognosis is GENERALLY VERY GOOD with early treatment — overall survival rate > 90% for lower stages.
• Post-nephrectomy nursing: monitor remaining kidney function (urine output, BUN, creatinine), avoid nephrotoxic medications, single kidney precautions lifelong.
• Staging determines treatment intensity: Stage I = confined to kidney, completely resected (best prognosis); Stage V = bilateral (most complex).

Definitions

Common mistakes

• Palpating the abdomen during nursing assessment — this is the most dangerous error with Wilms tumour.
• Confusing Wilms tumour with neuroblastoma: Wilms = unilateral, does NOT cross midline, good prognosis; Neuroblastoma = often crosses midline, catecholamine-secreting, worse prognosis.
• Thinking the mass is painful — Wilms tumour is classically NON-TENDER.
• Delaying surgery — nephrectomy should be done within 24–48 hours of diagnosis.

Exam tips

• KEY PATTERN: '2–7 year old + periorbital oedema (worse on waking) + frothy urine + massive proteinuria + normal/low BP' = Nephrotic Syndrome.
• Contrast with AGN: Nephrotic = proteinuria + oedema + low/normal BP; AGN = haematuria + hypertension.
• Treatment: PREDNISONE first-line for minimal change disease.
• Diet: NORMAL protein + LOW SODIUM — not low protein.
• Monitor DAILY WEIGHT as the most sensitive indicator of oedema change.

Key points

• Nephrotic syndrome: a glomerular disorder causing increased permeability of the glomerular basement membrane to PROTEINS.
• Most common type in children: MINIMAL CHANGE DISEASE (also called nil disease or lipoid nephrosis) — peak age 2–7 years; steroid-responsive.
• CLASSIC TETRAD (memorise all four): (1) Massive PROTEINURIA (>3.5 g/day in adults; >40 mg/m²/hr in children); (2) HYPOALBUMINEMIA (low serum albumin < 2.5 g/dL); (3) Generalised EDEMA (pitting); (4) HYPERLIPIDEMIA (elevated cholesterol and triglycerides).
• Pathophysiology chain: protein lost in urine → low serum albumin → decreased oncotic pressure → fluid leaks from blood vessels into tissue = EDEMA → liver compensates by producing more lipoproteins → HYPERLIPIDEMIA.
• HALLMARK SIGN: PERIORBITAL EDEMA (worst in the morning on waking), then progressing to ascites, scrotal/labial edema, and dependent edema.
• Urine is FROTHY (due to protein content) — parents often describe this as 'bubbly urine.'
• Blood pressure is usually NORMAL OR LOW (unlike AGN where BP is HIGH) — loss of intravascular volume from oedema reduces BP.
• FIRST-LINE TREATMENT: CORTICOSTEROIDS — PREDNISONE. Most children with minimal change disease are steroid-responsive (go into remission).
• Diet during edema phase: NORMAL-PROTEIN (do NOT restrict protein — it is already being lost), LOW-SODIUM diet (to reduce fluid retention). Avoid added salt.
• KEY NURSING MONITORING: Daily WEIGHT (most sensitive), ABDOMINAL GIRTH measurement (for ascites), INTAKE AND OUTPUT, urine protein (dipstick — 3+ to 4+ proteinuria).
• PREVENT INFECTION: These children are immunosuppressed (from steroid therapy AND loss of immunoglobulins in urine) — they are highly susceptible to infections, especially spontaneous bacterial peritonitis. Infection is a MAJOR complication and a common cause of death.
• Skin care: oedematous skin is fragile and prone to breakdown — change position frequently, use pressure-relieving mattress, avoid adhesive tape on oedematous skin.
• Thiazide diuretics or furosemide may be ordered to manage severe oedema.
• Albuminuria may be monitored at home — teach parents to use urine dipstick.

Definitions

Common mistakes

• Restricting protein in the diet — protein should be NORMAL (or occasionally high), not restricted, since protein is being lost in the urine.
• Expecting hypertension in nephrotic syndrome — BP is usually NORMAL OR LOW (contrast with AGN where BP is HIGH).
• Forgetting infection prevention — immunosuppression from steroids AND loss of immunoglobulins makes these children very vulnerable.
• Using tape on oedematous skin — always avoid adhesives on fragile oedematous tissue.

Exam tips

• KEY PATTERN: 'School-age child + cola/tea-coloured urine + hypertension + history of strep throat 1–2 weeks ago' = AGN.
• Priority nursing: MONITOR BP — risk of hypertensive encephalopathy.
• AGN vs Nephrotic Syndrome: Remember 'AGN = A for ALTA BP (high BP) + Haematuria'; 'Nephrotic = N for NO BP issue + massive proteinuria'.
• Treatment: SODIUM and FLUID restriction (not protein restriction).
• Self-limiting with excellent prognosis — reassure families that most children recover completely.

Key points

• Acute post-streptococcal glomerulonephritis (APSGN): occurs 1–2 weeks after Group A beta-haemolytic streptococcal infection (strep throat or impetigo/skin infection).
• Mechanism: immune complex (antigen-antibody) deposition in the glomeruli → inflammation → decreased GFR → oliguria, fluid retention, hypertension.
• Common in SCHOOL-AGE children (5–12 years).
• HALLMARK TRIAD: (1) GROSS HAEMATURIA — tea-coloured, cola-coloured, or smoky urine; (2) HYPERTENSION — due to fluid retention and renin release; (3) Mild periorbital EDEMA — less severe than in nephrotic syndrome.
• Additional signs: OLIGURIA (decreased urine output), mild proteinuria (not massive), elevated ASO titre (anti-streptolysin O), elevated BUN and creatinine, low serum complement (C3).
• KEY PRIORITY NURSING INTERVENTION: MONITOR BLOOD PRESSURE — risk of HYPERTENSIVE ENCEPHALOPATHY (severe headache, altered consciousness, seizures from dangerously high BP).
• Management: SODIUM and FLUID RESTRICTION during the acute oliguric phase; antihypertensives if BP is dangerously high; antibiotics if strep infection is still active (penicillin).
• DAILY WEIGHT and strict I&O monitoring.
• The condition is usually SELF-LIMITING — most children recover fully within 2–4 weeks; prognosis is excellent.
• Bed rest during the acute phase; activity restriction until BP and haematuria resolve.
• Dipstick urine: positive for blood (3+), moderate protein.
• C3 complement is LOW during the acute phase (consumed by immune complex deposition) — C3 normalises as the child recovers.

Definitions

Common mistakes

• Confusing AGN with nephrotic syndrome: AGN = haematuria + hypertension; Nephrotic = massive proteinuria + severe oedema + normal/low BP.
• Missing the 1–2 week lag period between strep infection and AGN onset — parents may not connect the two events.
• Failing to prioritise blood pressure monitoring — hypertensive encephalopathy is the most dangerous complication.
• Restricting protein unnecessarily — AGN does not require protein restriction (unlike nephrotic syndrome, which requires normal protein; AGN restricts SODIUM and FLUIDS).

Exam tips

• If NLE asks 'best urine specimen for culture in a 6-month-old infant' = suprapubic aspiration (gold standard) or catheterisation — NOT bag specimen.
• UTI prevention: front-to-back wiping, increase fluids, avoid bubble baths, complete voiding, cotton underwear.
• Recurrent UTIs in children → think VUR → diagnose with VCUG.
• In infants, fever alone may be the only UTI sign — always get urine culture for unexplained fever.

Key points

• UTI is COMMON in paediatrics, especially in GIRLS (shorter urethra provides less protection against ascending bacteria).
• In INFANTS, signs of UTI are NON-SPECIFIC: fever (may be the only sign), poor feeding, irritability, vomiting, foul-smelling urine, and failure to thrive.
• In OLDER CHILDREN: dysuria (painful urination), frequency, urgency, flank or abdominal pain, and haematuria.
• Most common organism: Escherichia coli (E. coli).
• Urine specimen collection: in non-toilet-trained children, use SUPRAPUBIC ASPIRATION (gold standard) or URETHRAL CATHETERISATION for reliable culture; a clean-catch midstream sample is acceptable in toilet-trained children.
• AVOID bag urine specimens for culture — high contamination rate; not reliable for diagnosis.
• Treatment: FULL COURSE of appropriate antibiotics — emphasise to parents that the FULL COURSE must be completed even if symptoms resolve early.
• VESICOURETERAL REFLUX (VUR): backflow of urine from the bladder into the ureters and kidneys during voiding. Recurrent UTIs may signal VUR.
• VUR is graded I–V (Grade V = most severe — intrarenal reflux); diagnosed by VOIDING CYSTOURETHROGRAM (VCUG).
• Risk of VUR: RENAL SCARRING → chronic kidney disease over time.
• Management of VUR: long-term prophylactic antibiotics (low dose), or surgical ureteral reimplantation for higher grades.
• PREVENTION TEACHING (key NLE health education content): increased fluid intake, front-to-back wiping (girls), cotton underwear, avoid bubble baths (can introduce bacteria), complete and regular voiding (do not hold urine), proper perineal hygiene.

Definitions

Common mistakes

• Using a BAG urine specimen for culture in a non-toilet-trained child — highly contaminated; not diagnostically reliable.
• Stopping antibiotics early when symptoms resolve — incomplete treatment leads to recurrence and resistance.
• Missing UTI in infants because the signs are non-specific — unexplained fever in an infant requires urine culture.
• Forgetting to teach front-to-back wiping — wiping back-to-front transfers fecal E. coli to the urethra.

Exam tips

• KEY PATTERN: 'Infant + rapidly increasing head circumference + bulging fontanelle + sunset eyes + high-pitched cry' = Hydrocephalus.
• Post-op VP shunt: FLAT position on NON-OPERATIVE SIDE — prevent rapid decompression.
• Cushing's Triad = Bradycardia + Hypertension + Irregular respirations = LATE SIGN = EMERGENCY.
• Shunt infection signs: fever + redness along the shunt tract = report immediately.
• Shunt malfunction: RETURN of ICP signs (headache, vomiting, altered LOC, bulging fontanelle) — report and prepare for CT scan.

Key points

• Hydrocephalus: accumulation of excess CSF in the cerebral ventricles, causing increased intracranial pressure (ICP).
• Causes: (1) Obstructive/non-communicating — blockage of CSF flow (e.g., aqueductal stenosis, tumour); (2) Communicating — impaired CSF reabsorption by the arachnoid villi; (3) Overproduction — rare (e.g., choroid plexus papilloma).
• INFANT SIGNS (fontanelles and sutures are still open, allowing skull expansion): INCREASING HEAD CIRCUMFERENCE (measure and plot DAILY), BULGING or TENSE ANTERIOR FONTANELLE, widely SEPARATED SUTURES, 'SUNSET EYES' (sclera visible ABOVE the iris — eyes deviate downward), HIGH-PITCHED CRY, irritability, prominent scalp veins, Macewen's sign ('cracked pot' sound on skull percussion).
• OLDER CHILD SIGNS (skull is rigid, so pressure builds internally): HEADACHE (especially in the morning, worsened by leaning forward), PROJECTILE VOMITING (especially on waking, without nausea), ALTERED LEVEL OF CONSCIOUSNESS, PAPILLEDEMA (on fundoscopy).
• CUSHING'S TRIAD — a LATE and OMINOUS sign of dangerously raised ICP: (1) BRADYCARDIA; (2) HYPERTENSION (widened pulse pressure); (3) IRREGULAR RESPIRATIONS (Cheyne-Stokes or other abnormal breathing pattern). Requires IMMEDIATE intervention.
• Definitive treatment: VENTRICULOPERITONEAL (VP) SHUNT — a surgical tube that drains excess CSF from the ventricle to the peritoneal cavity for absorption.
• POST-OPERATIVE VP SHUNT NURSING CARE:
• — Position the child FLAT initially and on the NON-OPERATIVE SIDE to prevent rapid CSF drainage and avoid subdural haematoma from sudden decompression.
• — Gradually raise the head as ordered by the physician.
• — Monitor for SHUNT MALFUNCTION: return of ICP signs (bulging fontanelle, headache, vomiting, altered LOC, sunset eyes).
• — Monitor for SHUNT INFECTION: fever, poor feeding, redness or tenderness along the shunt tract, meningismus — the most serious complication post-shunt.
• Ongoing nursing care: measure head circumference (plot on growth chart), support the head when lifting the infant (head is heavy), maintain skin integrity of the scalp (reposition frequently).
• Teach parents to recognise signs of shunt malfunction and when to seek emergency care.

Definitions

Common mistakes

• Positioning the post-operative VP shunt child with the HEAD ELEVATED — this causes too-rapid CSF drainage. The correct position is FLAT, on the NON-OPERATIVE SIDE initially.
• Thinking Cushing's triad is an EARLY sign — it is a LATE, ominous, emergency sign.
• Forgetting to measure head circumference DAILY in infants with hydrocephalus.
• Missing sunset eyes as a sign — sclera is seen ABOVE the iris (downward gaze), not below.

Exam tips

• KEY FACT: CP = NON-PROGRESSIVE disorder of movement and posture. Always say 'non-progressive' on the NLE.
• SPASTIC type = most common (~70–80%); scissors gait, hypertonia, hyperreflexia.
• Early signs: delayed motor milestones + persistent primitive reflexes beyond expected age + abnormal tone.
• Management goal = MAXIMISE FUNCTION — multidisciplinary approach (PT, OT, Speech Therapy).
• Aspiration precautions during feeding are a critical nursing safety priority in CP children with dysphagia.

Key points

• Cerebral Palsy (CP): a group of PERMANENT (non-progressive), NON-DETERIORATING motor disorders caused by damage or abnormal development of the IMMATURE BRAIN — prenatal (most common: maternal infection, hypoxia), perinatal (birth asphyxia — a major cause in Philippine settings), or postnatal (meningitis, head injury, hyperbilirubinemia/kernicterus).
• KEY CONCEPT: The brain lesion is STATIC (does not progress), but the CLINICAL MANIFESTATIONS may CHANGE as the child grows and the nervous system matures.
• CLASSIFICATION by motor type:
• — SPASTIC CP (most common, ~70-80%): increased muscle tone (hypertonia), hyperreflexia, scissors gait (legs cross over each other due to adductor spasticity), toe-walking, persistent primitive reflexes beyond expected age.
• — Dyskinetic/Athetoid CP: involuntary writhing, twisting movements (athetosis); decreased tone at rest but increases with activity.
• — Ataxic CP: poor balance and coordination, wide-based gait, intention tremor.
• — Mixed type: combination.
• EARLY CLUES: delayed motor milestones, abnormal muscle tone (hypertonia or hypotonia), persistent primitive reflexes (e.g., Moro reflex beyond 4 months), asymmetric posturing, feeding difficulties (poor suck, tongue thrust).
• CP may be associated with: intellectual disability (not always), epilepsy/seizures, vision/hearing problems, speech difficulties, and feeding problems.
• MANAGEMENT IS SUPPORTIVE AND MULTIDISCIPLINARY (there is NO CURE):
• — Physical Therapy (PT): improve mobility, strengthen muscles, prevent contractures.
• — Occupational Therapy (OT): improve activities of daily living, fine motor skills.
• — Speech Therapy: address communication and feeding/swallowing difficulties.
• — Medications: BACLOFEN (oral or intrathecal) for spasticity; BOTULINUM TOXIN injections for focal spasticity.
• — Assistive devices: braces (AFOs), walkers, wheelchairs.
• — Seizure medications if epilepsy is present.
• ASPIRATION PRECAUTIONS are critical during feeding — many CP children have oropharyngeal dysphagia.
• FAMILY SUPPORT and education: set realistic developmental goals; encourage maximum independence within the child's functional capacity.
• The GOAL of CP management: MAXIMISE FUNCTION and quality of life — NOT cure or normalise function.

Definitions

Common mistakes

• Saying CP is a 'progressive' disease — it is NON-PROGRESSIVE (static brain lesion). Manifestations may change with growth but the underlying lesion does not worsen.
• Assuming all CP children have intellectual disability — many have normal or above-average intelligence; the motor disorder does not equal cognitive impairment.
• Forgetting aspiration risk during feeding — CP children with dysphagia are at HIGH risk for aspiration pneumonia.
• Setting goals of 'cure' or 'normalisation' — the realistic goal is maximising function.

Exam tips

• KEY PATTERN: 'Child + high fever + nuchal rigidity + headache + photophobia + positive Kernig's/Brudzinski's' = Bacterial Meningitis.
• In INFANTS: nuchal rigidity may be ABSENT — look for bulging fontanelle + paradoxical irritability + high-pitched cry.
• PETECHIAL RASH + fever = meningococcal septicaemia — emergency.
• PRIORITY: Droplet precautions FIRST → LP → IV antibiotics PROMPTLY.
• Notifiable disease in the Philippines → report to the Local Health Unit (DOH).
• Most common long-term complication: SENSORINEURAL HEARING LOSS.

Key points

• Bacterial meningitis: inflammation of the meninges (membranes covering the brain and spinal cord) caused by bacterial infection — a MEDICAL AND NURSING EMERGENCY.
• Common organisms by age: Neonates — Group B Streptococcus, E. coli, Listeria; Infants/children — Neisseria meningitidis, Streptococcus pneumoniae; historically Haemophilus influenzae type b (Hib) — now rare with immunisation (Philippines immunises against Hib through the EPI).
• CLASSIC SIGNS IN OLDER CHILDREN: (1) HIGH FEVER; (2) SEVERE HEADACHE; (3) NUCHAL RIGIDITY (stiff neck — resistance to neck flexion); (4) PHOTOPHOBIA; (5) PHONOPHOBIA; (6) Positive KERNIG'S SIGN (inability to extend the knee when hip is flexed to 90°); (7) Positive BRUDZINSKI'S SIGN (involuntary flexion of hips and knees when the neck is flexed); (8) Altered LOC, vomiting, seizures.
• INFANT SIGNS (SUBTLE — no classic nuchal rigidity): BULGING FONTANELLE, HIGH-PITCHED CRY, POOR FEEDING, IRRITABILITY, PARADOXICAL IRRITABILITY (infant cries MORE when held/cuddled — due to meningeal irritation), fever or hypothermia, lethargy.
• PETECHIAL or PURPURIC RASH (non-blanching purple spots): suggests MENINGOCOCCAL SEPTICAEMIA — an extreme emergency with very high mortality. Rash spreads rapidly.
• PRIORITY NURSING CARE (in order):
• 1. INSTITUTE DROPLET PRECAUTIONS IMMEDIATELY (mask, private room) — meningococcal meningitis is transmitted via respiratory droplets.
• 2. Assist with LUMBAR PUNCTURE (LP) — to collect CSF for culture, cell count, glucose, protein (diagnostic gold standard for meningitis).
• 3. Administer IV ANTIBIOTICS PROMPTLY (after blood cultures and LP if possible, but do NOT delay antibiotics to wait for LP).
• 4. NEUROLOGICAL MONITORING — monitor ICP signs, seizures, level of consciousness.
• 5. Provide a QUIET, DIMLY LIT ENVIRONMENT — reduces stimulation and discomfort from photophobia.
• 6. SEIZURE PRECAUTIONS.
• Bacterial meningitis is a NOTIFIABLE DISEASE under Philippine law — report to the Local Health Unit (LHU) / Department of Health (DOH).
• Close contacts of meningococcal meningitis require CHEMOPROPHYLAXIS (rifampicin, ciprofloxacin, or ceftriaxone) — a public health measure.
• Complications: septicaemia, DIC, hearing loss (most common long-term neurological complication), brain damage, hydrocephalus, and death.

Definitions

Common mistakes

• Delaying isolation (droplet precautions) until meningitis is confirmed — institute IMMEDIATELY on suspicion.
• Delaying IV antibiotics to wait for LP results — if LP is delayed, give antibiotics first (cultures may still be positive in early treatment).
• Missing infant meningitis signs because no nuchal rigidity — use bulging fontanelle, paradoxical irritability, and high-pitched cry as clues.
• Forgetting to report meningococcal meningitis to public health authorities — it is notifiable under Philippine law.
• Forgetting chemoprophylaxis for close contacts — this is a public health nursing responsibility.

Exam tips

• KEY PATTERN: 'Newborn + sac on the back + lower limb paralysis + hydrocephalus' = Myelomeningocele.
• PRE-OP PRIORITY: PRONE POSITION + STERILE MOIST NON-ADHERENT DRESSING on the sac.
• LATEX-FREE environment — always use latex-free supplies.
• PREVENTION: Maternal FOLIC ACID before conception and during first trimester.
• Associated condition in 90%: HYDROCEPHALUS (Chiari II malformation) → requires VP shunt.

Key points

• Spina bifida is a NEURAL TUBE DEFECT (NTD) — failure of the vertebral column to close during the 3rd–4th week of gestation.
• TYPES (in order of severity): (1) Spina bifida occulta — defect in the vertebral arch only, spinal cord normal, no visible sac; (2) Meningocele — sac contains only CSF and meninges, spinal cord is intact; (3) MYELOMENINGOCELE — the most severe form — sac contains SPINAL CORD, nerve roots, and meninges → causes lower-limb paralysis, sensory loss, neurogenic bowel and bladder, and is associated with HYDROCEPHALUS (due to Chiari II malformation in ~90% of cases).
• PRE-OPERATIVE PRIORITY NURSING CARE — PROTECTING THE SAC:
• — Position the infant PRONE (face-down) or SIDE-LYING — keep pressure OFF the sac.
• — Cover the sac with STERILE, MOIST (normal saline) NON-ADHERENT DRESSING — prevent drying, rupture, and infection.
• — AVOID DIAPERING OVER THE SAC.
• — Maintain a WARM, MOIST environment for the sac.
• — Handle the infant with EXTREME CARE — avoid any pressure or trauma to the sac.
• — Monitor for SIGNS OF INFECTION (redness, drainage, fever) and RUPTURE.
• — Keep the infant NPO pre-operatively.
• Surgical closure of the defect is done within 24–72 hours of birth to prevent infection.
• LATEX ALLERGY PRECAUTION: Children with myelomeningocele have a HIGH RATE OF LATEX SENSITIVITY — use LATEX-FREE gloves, catheters, and all medical supplies. This is a critical safety NLE point.
• PREVENTION: MATERNAL FOLIC ACID supplementation (400–800 mcg/day) BEFORE CONCEPTION and during the FIRST TRIMESTER dramatically reduces NTD risk by up to 70%. This is a key Philippine public health and DOH recommendation.
• Ongoing management: clean intermittent catheterisation (CIC) for neurogenic bladder, bowel training programme, orthopaedic management of paralysis and scoliosis, monitoring for hydrocephalus (VP shunt).
• Arnold-Chiari II malformation: associated downward displacement of the cerebellum and brainstem through the foramen magnum — causes hydrocephalus in most myelomeningocele patients.
• Developmental and family support: these children can achieve significant independence with appropriate management and assistive technology.

Definitions

Common mistakes

• Positioning the infant SUPINE with a myelomeningocele sac — the sac is on the BACK, so SUPINE puts pressure on it. Correct position is PRONE or SIDE-LYING.
• Using DRY dressing on the sac — the sac must be kept MOIST with normal saline to prevent rupture.
• Using LATEX gloves or latex-containing equipment — these children have high latex allergy risk.
• Forgetting folic acid as the prevention strategy — this is both a public health and NLE teaching priority.
• Thinking all children with spina bifida have myelomeningocele — spina bifida occulta is the mildest form with NO sac and NO deficits.

Exam tips

• PRIORITY during seizure: SIDE-LYING POSITION (protect airway) + DO NOT RESTRAIN + PUT NOTHING IN THE MOUTH.
• Time the seizure — > 5 minutes = Status Epilepticus = IV Lorazepam or Diazepam FIRST-LINE.
• Phenytoin side effect = GINGIVAL HYPERPLASIA → meticulous oral care.
• Febrile seizure: 6 months–5 years; rapid rise in temperature; usually benign; teach fever control.
• Never stop anticonvulsants ABRUPTLY — rebound seizures and status epilepticus.
• Absence seizures: brief staring + eye blinking = NOT daydreaming — EEG confirms; treat with ethosuximide or valproic acid.

Key points

• A seizure is the result of abnormal, excessive, and synchronous neuronal electrical discharge in the brain, causing involuntary changes in movement, behaviour, sensation, or consciousness.
• Causes in children: epilepsy, febrile illness (most common in 6 months–5 years), CNS infection (meningitis, encephalitis), traumatic brain injury, hypoglycaemia, hyponatraemia, hypocalcaemia, hypoxia, and toxins.
• FEBRILE SEIZURES: most common type in paediatrics — ages 6 months to 5 years; triggered by RAPID RISE IN TEMPERATURE (not absolute temperature). Usually brief (< 5 minutes), generalised, tonic-clonic, and benign. Risk of recurrence but very LOW risk of epilepsy development. TEACH PARENTS: fever control (paracetamol), sponge bath, and reassure that febrile seizures are usually harmless.
• CLASSIFICATION: Focal (partial) — originates in one area of the brain; Generalised — involves the whole brain from the onset (tonic-clonic, absence, myoclonic, atonic).
• ABSENCE SEIZURES: brief staring spells, eye blinking — 'blanks out' for seconds; often mistaken for daydreaming; common in school-age children.
• PRIORITY NURSING INTERVENTIONS DURING A SEIZURE (memorise this list for the NLE):
• 1. STAY WITH THE CHILD — do not leave.
• 2. TURN THE CHILD TO THE SIDE (SIDE-LYING / LATERAL POSITION) — to maintain airway patency and PREVENT ASPIRATION.
• 3. LOOSEN TIGHT CLOTHING (especially around the neck).
• 4. EASE TO THE FLOOR if in a chair or bed; PAD HARD SURFACES to prevent injury.
• 5. DO NOT RESTRAIN THE CHILD — restraining can cause musculoskeletal injury.
• 6. DO NOT PUT ANYTHING IN THE MOUTH — NOT A TONGUE BLADE, NOT FINGERS. Contrary to old belief, the tongue cannot be swallowed; forcing objects in the mouth causes oral injuries.
• 7. DO NOT MOVE THE CHILD unless in immediate danger.
• 8. TIME THE SEIZURE — note onset, duration, type of movements, and post-ictal state.
• 9. PROVIDE PRIVACY — protect the child's dignity.
• 10. Have SUCTION and OXYGEN available.
• POST-ICTAL CARE: the child will be drowsy and confused (post-ictal state — normal); monitor vitals, airway, neuro status; allow to rest.
• STATUS EPILEPTICUS: a seizure lasting > 5 MINUTES, or repeated seizures without return to consciousness — a NEUROLOGICAL EMERGENCY.
• — First-line treatment: IV/rectal/intranasal BENZODIAZEPINE — LORAZEPAM (IV preferred) or DIAZEPAM (IV or rectal).
• — If benzodiazepine fails: IV PHENYTOIN or FOSPHENYTOIN.
• — If still refractory: PHENOBARBITAL, or general anaesthesia.
• — Protect the airway; prepare for intubation if necessary.
• MAINTENANCE ANTICONVULSANT MEDICATIONS and NLE-relevant side effects:
• — PHENYTOIN (Dilantin): gingival hyperplasia (overgrowth of gum tissue) → TEACH METICULOUS ORAL HYGIENE; hirsutism, ataxia, nystagmus.
• — PHENOBARBITAL: sedation, cognitive effects, paradoxical hyperactivity in children.
• — VALPROIC ACID (Depakote): hepatotoxicity (monitor LFTs), weight gain, hair loss.
• — CARBAMAZEPINE (Tegretol): monitor CBC (risk of agranulocytosis).
• — LEVETIRACETAM (Keppra): behavioural side effects (irritability, aggression in children).
• CRITICAL TEACHING: NEVER stop anticonvulsants abruptly — abrupt cessation precipitates REBOUND SEIZURES and status epilepticus. Taper doses under physician guidance.
• SAFETY IN THE COMMUNITY: avoid unsupervised swimming and bathing; wear helmets; seizure action plan for school; medical alert bracelet.

Definitions

Common mistakes

• Putting a tongue blade or fingers in the mouth during a seizure — this is DANGEROUS and outdated practice. Never done.
• Restraining the child during a seizure — causes musculoskeletal injuries. Let the seizure run its course.
• Failing to time the seizure — duration determines if it becomes status epilepticus (> 5 minutes).
• Not monitoring phenytoin side effects — gingival hyperplasia is a common NLE question.
• Stopping anticonvulsants abruptly when symptoms resolve — NEVER stop suddenly; taper under medical supervision.