NLE Paediatric Nursing — Paediatric GI, Genitourinary & Neurologic DisordersDetailed Explanation

Infants and young children are far more vulnerable to fluid and electrolyte imbalances than adults. This is because they have a HIGHER percentage of total body water (up to 75–80% in neonates vs. 60% in adults), a GREATER body-surface-area-to-mass ratio (leading to higher insensible water loss), a HIGHER metabolic rate (producing more metabolic waste requiring water for excretion), and IMMATURE kidneys (poor concentrating and diluting ability). Even a small amount of vomiting or diarrhoea can rapidly lead to dehydration and circulatory shock in infants.

The most widely used formula for estimating maintenance fluid needs is the Holliday-Segar method, also called the '4-2-1 rule':

• First 10 kg of body weight: 100 mL/kg/day (or 4 mL/kg/hr)
• Next 10 kg (11–20 kg): 50 mL/kg/day (or 2 mL/kg/hr)
• Each kg above 20 kg: 20 mL/kg/day (or 1 mL/kg/hr)

For example, a 25 kg child needs: (10 × 100) + (10 × 50) + (5 × 20) = 1,000 + 500 + 100 = 1,600 mL/day.

The MOST sensitive indicator of hydration status is DAILY WEIGHT CHANGE (1 kg ≈ 1 litre of fluid). Other indicators include urine output (aim 1–2 mL/kg/hr), fontanelle status, mucous membranes, skin turgor, and capillary refill. In the NLE, you will often be asked which assessment finding BEST reflects hydration — always choose weight.

Pyloric stenosis is a hypertrophy (abnormal thickening) of the pyloric muscle — the muscular valve between the stomach and the duodenum. As the muscle thickens, it progressively narrows the gastric outlet until the passage is almost completely obstructed. This typically becomes symptomatic between 2–8 weeks of age, with the classic presentation at 3–5 weeks. It is significantly more common in FIRSTBORN MALES and has a familial tendency.

Since the obstruction is ABOVE the duodenum (before bile enters from the common bile duct), the vomiting is NON-BILIOUS — it is NOT green or yellow. Instead, the vomit is only stomach contents: curdled milk or formula. The classic description is PROJECTILE VOMITING — the infant forcefully vomits milk immediately after (or even during) a feed, sometimes projecting it several feet. Despite vomiting, the infant is EAGER TO FEED AGAIN immediately after (unlike a sick infant with infection who refuses to feed).

On physical examination, the nurse or physician can palpate an OLIVE-SHAPED MASS in the RIGHT UPPER QUADRANT (the hypertrophied pylorus). VISIBLE PERISTALTIC WAVES moving from left to right across the upper abdomen may also be seen, especially after a feed.

The metabolic consequence is critical: persistent vomiting of gastric hydrochloric acid (HCl) leads to HYPOCHLOREMIC, HYPOKALEMIC METABOLIC ALKALOSIS. Think of it this way: the stomach loses H+ ions (acid) and Cl- ions continuously. The kidneys try to retain H+ (to correct the alkalosis) by excreting K+ instead — worsening the hypokalemia. The NLE frequently tests this electrolyte imbalance.

MANAGEMENT: The surgical fix is a PYLOROMYOTOMY (Fredet-Ramstedt procedure) — an incision through the hypertrophied muscle to release the obstruction WITHOUT cutting the mucosa. HOWEVER, surgery is NOT done immediately. The FIRST PRIORITY is to CORRECT THE FLUID AND ELECTROLYTE IMBALANCE. Operating on a child with severe metabolic alkalosis is dangerous (anesthesia risk). After electrolytes are corrected, surgery is performed. Post-operatively: begin small, frequent feeds as ordered (usually within 4–6 hours), position upright and RIGHT-SIDE DOWN after feeds (gravity assists gastric emptying through the repaired pylorus), and monitor the incision site.

Hirschsprung disease is a congenital condition in which ganglion cells (nerve cells responsible for coordinating peristalsis) are ABSENT in a segment of the distal colon — most commonly the rectosigmoid region. Without these nerve cells, the affected bowel segment has no coordinated muscular relaxation, creating a FUNCTIONAL OBSTRUCTION. The bowel proximal to the aganglionic segment becomes massively dilated — hence the name 'megacolon.'

The CLASSIC NEONATAL PRESENTATION is:

1. FAILURE TO PASS MECONIUM within the first 24–48 hours of life (meconium is the first stool; healthy neonates pass it within 24 hours)
2. ABDOMINAL DISTENSION (due to accumulation of stool and gas)
3. BILIOUS VOMITING (obstruction is in the lower GI tract, well below where bile enters)

In older infants and children, the presentation includes CHRONIC CONSTIPATION that never responds to standard measures, RIBBON-LIKE or PELLET-SHAPED FOUL-SMELLING STOOLS (only small amounts pass around the obstruction), ABDOMINAL DISTENSION, and FAILURE TO THRIVE.

A classic physical exam finding is the EXPLOSIVE RELEASE OF GAS AND STOOL when a rectal examination is performed (because digital manipulation temporarily relieves the functional obstruction).

DIAGNOSIS: The DEFINITIVE test is a RECTAL BIOPSY confirming the ABSENCE OF GANGLION CELLS in the submucosa. A barium enema may show the transition zone (narrow aganglionic segment with proximal dilation) but is not definitive.

MANAGEMENT: Surgical — RESECTION of the aganglionic segment followed by a PULL-THROUGH PROCEDURE (connecting the normal bowel to the anus). Often, a TEMPORARY COLOSTOMY is created first to decompress the bowel, then closed after the pull-through.

THE MOST DANGEROUS COMPLICATION: HIRSCHSPRUNG-ASSOCIATED ENTEROCOLITIS (HAEC) — a life-threatening inflammation of the bowel that can occur pre- or post-operatively. Signs: EXPLOSIVE DIARRHEA, HIGH FEVER, SEVERE ABDOMINAL DISTENSION, VOMITING, and SEPSIS. REPORT IMMEDIATELY — this is an emergency.

Intussusception occurs when one segment of the intestine TELESCOPES INTO or INVAGINATES INTO an adjacent segment — like a collapsed telescope or a sock being turned inside out. The most common type is ILEOCOLIC (the terminal ileum telescopes into the colon). This creates a mechanical obstruction AND compromises the blood supply to the trapped bowel, leading to ischemia, necrosis, and potentially perforation if untreated.

Intussusception most commonly occurs in OTHERWISE HEALTHY INFANTS aged 3 MONTHS TO 3 YEARS, with a peak incidence at 5–9 MONTHS. It is more common in males. The cause is often unknown; in some cases, enlarged mesenteric lymph nodes (from a preceding viral illness) serve as the 'lead point' that initiates the telescoping.

The CLASSIC CLINICAL TRIAD:

1. SUDDEN, SEVERE COLICKY ABDOMINAL PAIN — the infant suddenly SCREAMS and DRAWS THE KNEES TO THE CHEST (flexes legs), then relaxes for a few minutes before the next episode. This episodic nature reflects intermittent peristaltic waves pushing the telescoped bowel further in.
2. A SAUSAGE-SHAPED (oblong) PALPABLE MASS — usually felt in the RIGHT UPPER or MID ABDOMEN, with a sense of emptiness in the right lower quadrant (Dance's sign).
3. 'CURRANT-JELLY' STOOLS — a mixture of blood and mucus passed rectally. This is a LATE SIGN indicating bowel ischemia and mucosal sloughing. Its presence means the bowel has been compromised for some time — urgent action is needed.

DIAGNOSIS AND TREATMENT: An AIR ENEMA (pneumatic) or BARIUM/HYDROSTATIC ENEMA serves a DUAL PURPOSE — it is BOTH DIAGNOSTIC (confirms the telescoping on imaging) AND THERAPEUTIC (the pressure of the air or fluid can REDUCE/PUSH BACK the intussusception non-surgically). Success rates are high when performed early.

CRITICAL NURSING POINT: After an enema reduction, watch for the PASSAGE OF A NORMAL BROWN STOOL — this signals that the intussusception has been SUCCESSFULLY REDUCED. REPORT THIS IMMEDIATELY — it is a positive sign. Surgery is performed only if the enema fails, if there are signs of bowel perforation, or if the child is haemodynamically unstable.

Wilms tumour (nephroblastoma) is the MOST COMMON RENAL MALIGNANCY OF CHILDHOOD, typically diagnosed between AGES 2–3 YEARS. It arises from embryonic kidney tissue (nephroblasts) that failed to differentiate normally. It can occur in one or both kidneys.

CLINICAL PRESENTATION:

• The child presents with a FIRM, NON-TENDER, SMOOTH, UNILATERAL ABDOMINAL MASS — usually discovered by a parent or caregiver during bathing or dressing. The mass typically does NOT CROSS THE MIDLINE (distinguishing it from neuroblastoma, which often does cross the midline).
• Other signs: HEMATURIA (blood in urine — may be microscopic or gross), HYPERTENSION (from renin secretion by the tumour), abdominal pain, fever, and fatigue.
• The child often looks WELL initially despite the large mass.

THE MOST CRITICAL NURSING RULE — THIS IS HIGHLY NLE-TESTED:
⚠️ DO NOT PALPATE THE ABDOMEN ⚠️
The tumour is encapsulated, and vigorous palpation can RUPTURE the capsule and DISSEMINATE malignant cells throughout the abdomen (tumour spillage), drastically worsening the prognosis. Post a sign on the child's bed: 'DO NOT PALPATE ABDOMEN.' Handle the child GENTLY during all care activities including bathing, diapering, and positioning. Avoid compression of the abdomen.

MANAGEMENT:

• SURGERY (nephrectomy) is performed — usually within 24–48 hours of diagnosis
• Followed by CHEMOTHERAPY (vincristine, dactinomycin ± doxorubicin) ± RADIATION depending on the stage
• PROGNOSIS IS GENERALLY EXCELLENT — Wilms tumour has one of the highest cure rates among childhood cancers, especially when diagnosed early (Stage I survival rate >90%)

Associated syndromes: WAGR syndrome (Wilms, Aniridia, Genitourinary anomalies, intellectual disability Range — formerly mental Retardation), Beckwith-Wiedemann syndrome.

Nephrotic syndrome in children is most commonly caused by MINIMAL CHANGE DISEASE (also called nil disease or lipoid nephrosis) — a glomerular disorder where there is increased permeability of the glomerular basement membrane to proteins. This typically affects children aged 2–7 YEARS and has an EXCELLENT response to corticosteroids.

The classic TETRAD of nephrotic syndrome:

1. MASSIVE PROTEINURIA: Large amounts of protein (especially albumin) are lost in the urine. Urine is frothy/foamy due to protein content.
2. HYPOALBUMINEMIA: Because albumin is lost in the urine, serum albumin levels fall dramatically.
3. GENERALIZED EDEMA: Albumin maintains oncotic pressure in blood vessels. When albumin falls, fluid shifts OUT of the capillaries into interstitial tissue → edema. The classic location is PERIORBITAL EDEMA (puffy eyelids, worst in the MORNING after lying flat). As the condition progresses: ascites, scrotal/labial edema, and pitting edema of the legs.
4. HYPERLIPIDEMIA: The liver compensates by producing more lipoproteins (in response to low albumin) → elevated cholesterol and triglycerides.

KEY CONTRASTING FEATURE WITH AGN: Blood pressure is NORMAL OR LOW in nephrotic syndrome (because of low plasma volume from fluid shift) — there is NO hematuria (unless it is a mixed pattern).

MANAGEMENT:

• CORTICOSTEROIDS (PREDNISONE): First-line treatment; most cases of minimal change disease respond within 4–8 weeks
• DIET: Normal to HIGH PROTEIN (to replace losses), LOW SODIUM (to reduce fluid retention/edema). Note: during the acute edematous phase, restrict sodium; do NOT restrict protein
• DAILY WEIGHT and ABDOMINAL GIRTH measurement — best indicators of fluid status
• URINE PROTEIN monitoring (dipstick or 24-hour urine)
• PREVENT INFECTION: These children are immunosuppressed (steroids + loss of immunoglobulins in urine). INFECTION IS THE MOST COMMON AND SERIOUS COMPLICATION. Watch for fever, deterioration. Common infections: peritonitis (especially spontaneous bacterial peritonitis from Streptococcus pneumoniae), cellulitis, pneumonia.
• SKIN CARE: Edematous skin is fragile and prone to breakdown — reposition frequently, use gentle skin care
• Diuretics (furosemide) may be used for severe edema
• Salt-poor albumin infusions for severe hypoalbuminemia

Acute glomerulonephritis (AGN) in children is most commonly POST-STREPTOCOCCAL — occurring 1–2 WEEKS AFTER A STREPTOCOCCAL INFECTION (strep throat or impetigo/skin infection caused by group A beta-hemolytic Streptococcus). An immune complex (antigen-antibody complex) is deposited in the glomeruli, triggering inflammation that damages the filtration membrane. Affected children are typically SCHOOL-AGE (5–12 years).

The three HALLMARK FEATURES of AGN (memorize as the opposite of nephrotic syndrome):

1. GROSS HEMATURIA — the urine appears DARK (tea-colored, cola-colored, rust-colored). This is because damaged glomeruli leak red blood cells into the filtrate. This is the most striking and alarming sign for parents.
2. HYPERTENSION — elevated blood pressure from: (a) fluid and sodium retention (oliguria reduces excretion), and (b) activation of the renin-angiotensin-aldosterone system from reduced renal perfusion.
3. MILD PERIORBITAL EDEMA and OLIGURIA — some sodium and water retention causes mild facial swelling (less severe than nephrotic syndrome) and reduced urine output.

Other findings: fever, headache, malaise, flank pain, and moderately elevated creatinine/BUN.

MAJOR DANGER: HYPERTENSIVE ENCEPHALOPATHY — the elevated blood pressure can cause brain swelling leading to seizures, altered consciousness, and visual disturbances. This is the MOST SERIOUS ACUTE COMPLICATION.

MANAGEMENT:

• MONITOR BLOOD PRESSURE frequently (every 4 hours or as ordered) — highest nursing priority
• RESTRICT SODIUM AND FLUIDS during the acute oliguric phase (reduces edema and hypertension)
• DAILY WEIGHT to track fluid retention
• MONITOR I&O — track urine output (recovery = increasing urine output and clearing of hematuria)
• ANTIHYPERTENSIVES if BP is significantly elevated
• ANTIBIOTICS (penicillin) to eliminate any residual streptococcal infection — does NOT change the course of AGN but prevents spread
• REST during acute phase
• PROGNOSIS: USUALLY SELF-LIMITING AND EXCELLENT in children (most recover fully within weeks to months)

Hydrocephalus is the accumulation of EXCESS CEREBROSPINAL FLUID (CSF) in the cerebral ventricles, resulting in INCREASED INTRACRANIAL PRESSURE (ICP). It occurs due to one of three mechanisms: (1) OVERPRODUCTION of CSF (rare), (2) OBSTRUCTION of CSF flow (communicating vs. non-communicating/obstructive), or (3) IMPAIRED ABSORPTION of CSF.

CLINICAL SIGNS — differ by age:

INFANTS (fontanelles and sutures are still OPEN — this allows the skull to expand and compensate, but eventually leads to abnormal head enlargement):

• INCREASING HEAD CIRCUMFERENCE (MEASURE DAILY — most important nursing assessment)
• BULGING or TENSE ANTERIOR FONTANELLE (even when the infant is upright and calm)
• WIDELY SEPARATED CRANIAL SUTURES
• 'SUNSET EYES' sign — the eyes are deviated DOWNWARD (sclerae visible above the iris), caused by pressure on the midbrain
• DISTENDED SCALP VEINS
• HIGH-PITCHED CRY, IRRITABILITY
• Poor feeding, lethargy

OLDER CHILDREN (sutures are fused — no room for expansion, so ICP rises faster):

• HEADACHE (worsens in the morning, with position change, or with Valsalva maneuver)
• PROJECTILE VOMITING (often without nausea, worse in the morning)
• ALTERED LEVEL OF CONSCIOUSNESS
• PAPILLEDEMA (disc edema on fundoscopic examination)
• DIPLOPIA (double vision from cranial nerve compression)

CUSHING'S TRIAD — a LATE, OMINOUS sign of severely elevated ICP approaching brain herniation:

1. BRADYCARDIA
2. HYPERTENSION (widening pulse pressure)
3. IRREGULAR RESPIRATIONS

If you see Cushing's triad, the situation is critical — notify the physician IMMEDIATELY.

TREATMENT: VENTRICULOPERITONEAL (VP) SHUNT insertion — a surgical procedure that places a catheter in a lateral ventricle and drains CSF through a valve-regulated tube into the PERITONEAL CAVITY where it is absorbed.

POST-OP VP SHUNT NURSING CARE:

• Position: Keep the child FLAT and on the NON-OPERATIVE SIDE — to PREVENT TOO RAPID CSF DRAINAGE (which can cause subdural haematoma from sudden brain shift/collapse). The head is raised GRADUALLY as ordered.
• Measure HEAD CIRCUMFERENCE daily
• Monitor for ICP SIGNS (shunt malfunction — ICP returns)
• Monitor for SHUNT INFECTION: fever, redness/tenderness along the shunt tract, poor feeding, meningeal signs — the most serious complication
• Support the infant's head when lifting (heavy due to large size)
• Pump the shunt reservoir ONLY if ordered by the physician

Cerebral palsy is a GROUP OF NON-PROGRESSIVE DISORDERS of movement and posture resulting from a non-progressive insult or anomaly of the DEVELOPING BRAIN. The brain lesion DOES NOT WORSEN over time — but the MANIFESTATIONS (functional limitations) may appear to change as the child grows and develops. The insult can occur prenatally (intrauterine infection, genetic, hypoxia), perinatally (birth asphyxia — the most common identifiable cause), or postnatally (meningitis, head trauma, hyperbilirubinemia) up to age 2–3 years.

Risk factors: prematurity, low birth weight, hypoxic-ischemic encephalopathy (HIE), kernicterus, congenital infections (TORCH).

TYPES OF CP:

• SPASTIC CP (MOST COMMON — 70–80%): Increased muscle tone (HYPERTONIA), exaggerated deep tendon reflexes (hyperreflexia), persistent primitive reflexes, and the characteristic SCISSORING GAIT (spastic legs are adducted and cross-over during walking) and TOE-WALKING. The affected muscles feel stiff and resistant.
• DYSKINETIC/ATHETOID CP: Involuntary, writhing, uncontrolled movements (athetosis); fluctuating tone; typically affects the whole body; associated with kernicterus/hyperbilirubinemia.
• ATAXIC CP (LEAST COMMON): Impaired coordination and balance; wide-based gait; intention tremor.
• MIXED TYPE: Combination of the above.

EARLY CLINICAL CLUES:

• DELAYED MOTOR MILESTONES (late head control, sitting, standing, walking)
• PERSISTENT PRIMITIVE REFLEXES beyond expected age (e.g., Moro reflex beyond 6 months, asymmetric tonic neck reflex beyond 6 months)
• ABNORMAL POSTURING (fisting, asymmetric movement)
• FEEDING DIFFICULTY (poor suck, tongue thrust, choking)
• INCREASED MUSCLE TONE or FLOPPINESS (hypotonia in some types)

Associated conditions (not always present): intellectual disability, seizures, speech/language impairment, vision/hearing impairment, learning disabilities.

MANAGEMENT (SUPPORTIVE AND MULTIDISCIPLINARY — there is NO CURE):

• GOAL: MAXIMISE THE CHILD'S FUNCTIONAL INDEPENDENCE AND QUALITY OF LIFE
• Physical therapy: to improve motor function, prevent contractures
• Occupational therapy: for fine motor skills and activities of daily living
• Speech therapy: for communication and SAFE SWALLOWING (aspiration is a major risk)
• ASPIRATION PRECAUTIONS: upright positioning during feeding, thickened feeds as needed, small amounts, pacing
• Medications: BACLOFEN (oral or intrathecal pump for spasticity), BOTULINUM TOXIN injections (focal spasticity), DIAZEPAM; ANTICONVULSANTS for seizures
• Orthotic devices (braces, splints), adaptive equipment, mobility aids (wheelchairs, walkers)
• Family support, counselling, and education

IMPORTANT: CP is NON-PROGRESSIVE. The brain damage does not get worse. However, complications like contractures, scoliosis, and aspiration pneumonia must be prevented.

Bacterial meningitis is an INFLAMMATION OF THE MENINGES (the membranes covering the brain and spinal cord) caused by bacteria — most commonly NEISSERIA MENINGITIDIS (meningococcal meningitis), STREPTOCOCCUS PNEUMONIAE (pneumococcal meningitis), and formerly HAEMOPHILUS INFLUENZAE TYPE B (Hib — now rare due to vaccination). It is a MEDICAL EMERGENCY with high morbidity and mortality if not treated promptly.

CLINICAL FEATURES in OLDER CHILDREN:

• FEVER
• SEVERE HEADACHE
• PHOTOPHOBIA (sensitivity to light — due to meningeal irritation)
• NUCHAL RIGIDITY (stiff neck — the child resists flexion of the neck; a hallmark sign)
• POSITIVE KERNIG'S SIGN: The examiner flexes the hip and knee to 90°, then tries to extend the knee — PAIN and RESISTANCE indicate meningeal irritation
• POSITIVE BRUDZINSKI'S SIGN: Passive flexion of the neck causes INVOLUNTARY FLEXION OF THE HIPS AND KNEES — another sign of meningeal irritation
• VOMITING, ALTERED CONSCIOUSNESS, SEIZURES
• PETECHIAL OR PURPURIC RASH: A non-blanching rash (does not fade with pressure) suggests MENINGOCOCCEMIA — associated with septicaemia and is a sign of meningococcal disease; this warrants immediate emergency treatment

CLINICAL FEATURES in INFANTS (SUBTLE — harder to recognise):

• BULGING FONTANELLE (increased ICP)
• HIGH-PITCHED CRY
• POOR FEEDING, LETHARGY
• IRRITABILITY — classically PARADOXICAL IRRITABILITY (the infant cries MORE when picked up or touched, because movement aggravates meningeal pain)
• TEMPERATURE INSTABILITY (may be hypo- or hyperthermia)
• Neck stiffness may be ABSENT in infants

DIAGNOSIS: LUMBAR PUNCTURE (spinal tap) — CSF analysis showing increased WBCs (neutrophils), elevated protein, decreased glucose, and positive culture/gram stain.

PRIORITY NURSING MANAGEMENT:

1. INSTITUTE DROPLET PRECAUTIONS IMMEDIATELY (for meningococcal and Hib meningitis — transmitted by respiratory droplets). Place the child in a private room. Healthcare workers and close contacts need masks.
2. ASSIST WITH LUMBAR PUNCTURE (positioning, sterile field, post-procedure monitoring)
3. ADMINISTER IV ANTIBIOTICS PROMPTLY — as soon as cultures are obtained; do not delay for results
4. MONITOR FOR INCREASED ICP (altered consciousness, Cushing's triad, worsening headache)
5. MONITOR FOR SEIZURES — have anticonvulsants ready
6. PROVIDE A QUIET, DIMLY LIT ENVIRONMENT — reduces photophobia and stimulation
7. POSITION COMFORTABLY — side-lying with slight head elevation if not contraindicated
8. MONITOR VITAL SIGNS FREQUENTLY

MEINGOCOCCAL DISEASE IS NOTIFIABLE to the Department of Health (DOH) in the Philippines — close contacts (household, healthcare workers) need CHEMOPROPHYLAXIS (rifampicin or ciprofloxacin).

COMPLICATIONS: Hearing loss (most common long-term complication — test with audiogram before discharge), hydrocephalus, intellectual disability, limb amputation (from meningococcemia/purpura fulminans).

Spina bifida is a NEURAL TUBE DEFECT resulting from FAILURE OF THE NEURAL TUBE TO CLOSE during the first 28 days of gestation (before many women even know they are pregnant). The defect occurs along the posterior vertebral column.

TYPES (in order of severity):

• SPINA BIFIDA OCCULTA: Bony defect only (vertebral arch fails to fuse) with NO sac or nerve involvement — often asymptomatic, found incidentally on X-ray; may have a dimple or tuft of hair over the site
• MENINGOCELE: A sac containing MENINGES and CSF protrudes through the defect but contains NO NEURAL TISSUE — may have minimal neurological deficits
• MYELOMENINGOCELE (MOST SEVERE): A sac containing MENINGES + CSF + SPINAL CORD TISSUE and nerve roots protrudes — results in significant neurological deficits including LOWER LIMB PARALYSIS, BOWEL AND BLADDER DYSFUNCTION (neurogenic bowel and bladder), and LOSS OF SENSATION. 80–90% also develop HYDROCEPHALUS.

PRE-OPERATIVE NURSING PRIORITIES (before surgical closure of the sac):

⚠️ PROTECT THE SAC — this is the NUMBER ONE PRIORITY:

1. POSITION THE INFANT PRONE (face-down) or SIDE-LYING — to prevent PRESSURE ON THE SAC from body weight
2. Keep the sac COVERED with a STERILE, MOIST (SALINE-SOAKED) NON-ADHERENT DRESSING — prevents drying and infection
3. AVOID DIAPERING OVER THE SAC — diaper soiling can contaminate the sac with faeces/urine → infection/meningitis risk
4. NO PRESSURE on the sac
5. Keep the infant WARM (prone positioning in incubator)
6. Monitor the sac for LEAKAGE of CSF (clear fluid), signs of RUPTURE, or INFECTION (redness, discharge, increased temperature)
7. Monitor for signs of MENINGITIS and INCREASED ICP (bulging fontanelle — since 80–90% develop hydrocephalus)
8. LATEX-FREE ENVIRONMENT — children with myelomeningocele have a HIGH RATE OF LATEX ALLERGY (sensitised through repeated exposures from surgical/medical procedures; risk is lifelong). All equipment, gloves, and supplies must be LATEX-FREE.

PREVENTION — KEY PUBLIC HEALTH POINT:
Maternal FOLIC ACID supplementation (400–800 mcg/day) BEFORE CONCEPTION and during the FIRST TRIMESTER dramatically reduces (by ~70%) the incidence of neural tube defects. This is a major health education message in Philippine maternal-child health programmes.

Seizures result from ABNORMAL, EXCESSIVE, OR SYNCHRONOUS NEURONAL ACTIVITY in the brain. They can be caused by epilepsy (recurrent unprovoked seizures), fever (febrile seizures), infection (meningitis, encephalitis), metabolic disturbances (hypoglycaemia, hyponatraemia, hypocalcaemia), trauma, hypoxia, or toxins.

FEBRILE SEIZURES are the most COMMON TYPE of childhood seizures, occurring in 2–5% of children aged 6 MONTHS TO 5 YEARS. They are triggered by a RAPID RISE IN BODY TEMPERATURE (not necessarily a very high temperature — the RATE of rise matters). Most are BRIEF (under 5 minutes), GENERALIZED (tonic-clonic), and BENIGN — they stop on their own and the child recovers fully. Parents are understandably terrified; REASSURANCE and FEVER MANAGEMENT teaching are key nursing roles.

SEIZURE FIRST AID — NURSING PRIORITIES:
During a seizure, the priorities are:

1. PROTECT THE AIRWAY AND PREVENT INJURY — this is the FIRST priority
2. TURN THE CHILD TO THE SIDE (SIDE-LYING/LATERAL POSITION) — to keep the airway clear and PREVENT ASPIRATION of secretions; gravity drains secretions from the mouth
3. LOOSEN tight clothing around the neck and body
4. EASE THE CHILD TO THE FLOOR — if in a chair or bed, lower gently to prevent falling
5. PAD HARD OR SHARP SURFACES around the child
6. TIME THE SEIZURE — document onset, type, duration, body parts involved, and postictal period
7. STAY WITH THE CHILD — do not leave
8. Have SUCTION AND OXYGEN available (at the bedside in hospital settings)
9. Ensure PRIVACY

WHAT TO DO: Side-lying. Protect from injury. Time the seizure. Stay with the child. Observe carefully.

WHAT NOT TO DO — CRITICAL:

• DO NOT RESTRAIN THE CHILD'S MOVEMENTS (this can cause fractures or injury; you cannot stop the seizure by holding)
• DO NOT PUT ANYTHING IN THE MOUTH — not your fingers, not a tongue blade, not a spoon, not cloth (this is an old myth; the tongue CANNOT be swallowed; inserting objects can BREAK TEETH, INJURE THE NURSE OR THE CHILD, and cause AIRWAY OBSTRUCTION)
• DO NOT MOVE THE CHILD UNLESS IN DANGER

STATUS EPILEPTICUS: A seizure lasting MORE THAN 5 MINUTES, or TWO OR MORE SEIZURES without recovery of consciousness between them = STATUS EPILEPTICUS — a MEDICAL EMERGENCY. Without treatment, prolonged seizures cause neuronal damage, hypoxia, hyperthermia, and may be fatal.
First-line treatment: IV LORAZEPAM or IV DIAZEPAM (benzodiazepines)
If IV access not available: RECTAL DIAZEPAM (Diastat)
Second-line if benzodiazepines fail: IV phenytoin/fosphenytoin, IV phenobarbital, or IV levetiracetam
SUPPORT AIRWAY, BREATHING, CIRCULATION throughout

MAINTENANCE ANTICONVULSANTS (for recurrent seizures/epilepsy):

• PHENYTOIN (Dilantin): Important side effect = GINGIVAL HYPERPLASIA (gum overgrowth) → teach METICULOUS ORAL CARE (regular brushing, dental check-ups). Also: nystagmus, ataxia, hirsutism; monitor drug levels (therapeutic range 10–20 mcg/mL)
• PHENOBARBITAL: Sedation, behavioural changes, cognitive effects in children
• VALPROIC ACID (Depakene): HEPATOTOXICITY — monitor LFTs; teratogenic (avoid in women of reproductive age)
• CARBAMAZEPINE: Steven-Johnson syndrome, diplopia
• LEVETIRACETAM (Keppra): Well-tolerated, fewer drug interactions

TEACH: NEVER STOP ANTICONVULSANTS ABRUPTLY — this can PRECIPITATE REBOUND SEIZURES or STATUS EPILEPTICUS. Any dose changes must be gradual and under physician guidance.