Midwife Licensure Exam Infant & Child Health (Growth, Development & IMCI) — Paediatric Hematologic, Oncologic & Genetic DisordersDetailed Explanation

Recognising Respiratory Distress in Children

Children have anatomically smaller airways, making even mild swelling or secretions clinically significant. Their high metabolic rate means they need more oxygen per kilogram, and their immature autonomic nervous system means they compensate differently from adults. Recognising respiratory distress early using a systematic approach is the nurse's PRIMARY responsibility under the nursing process (Assessment phase). Respiratory distress in children follows a continuum from early (compensating) to late (decompensating/pre-arrest): **EARLY SIGNS (the body is still compensating):** - Restlessness, irritability (early sign of hypoxia) - Tachypnea (fast breathing — most reliable early indicator) - Nasal flaring (widening of nostrils to increase air intake) - Mild chest retractions (pulling inward of skin between ribs) - Tachycardia **WORSENING SIGNS:** - Intercostal retractions (between ribs) - Subcostal retractions (below the rib cage) - Suprasternal retractions (above the sternum) - Grunting (the infant's attempt to maintain positive end-expiratory pressure) - Head bobbing with each breath - Audible stridor or wheeze - Use of accessory muscles (neck, shoulder muscles) **LATE/OMINOUS SIGNS (pre-arrest — EMERGENCY):** - Cyanosis (bluish discolouration — oxygen saturation critically low) - Bradycardia (in children, bradycardia means the heart is giving out) - Decreased or absent breath sounds - Lethargy or unresponsiveness (brain not getting enough oxygen) - Apnea **IMCI (Integrated Management of Childhood Illness) Fast-Breathing Thresholds — memorise these:** - Less than 2 months old: ≥60 breaths/minute - 2 to 12 months old: ≥50 breaths/minute - 12 months to 5 years old: ≥40 breaths/minute These IMCI thresholds are used in Philippine rural health units and barangay health centres, which aligns with the DOH's primary healthcare delivery system. Filipino nurses in community settings apply these daily.

Congenital Heart Defects (CHD): Acyanotic vs Cyanotic

Congenital heart defects (CHDs) are structural abnormalities of the heart present at birth. They are classified into two major groups based on whether deoxygenated blood enters the systemic circulation, causing cyanosis. **UNDERSTANDING THE SHUNTS:** Normally, oxygenated blood flows: Lungs → Left heart → Body. Deoxygenated blood flows: Body → Right heart → Lungs. **Acyanotic CHDs (Left-to-Right Shunt):** Oxygenated blood from the LEFT side shunts back to the RIGHT side and recirculates to the lungs. The child is NOT cyanotic initially, but the lungs become overloaded (pulmonary overcirculation), leading to CONGESTIVE HEART FAILURE (CHF). **Key Acyanotic Defects:** 1. **Ventricular Septal Defect (VSD)** — THE MOST COMMON CHD OVERALL - A hole (defect) in the wall (septum) between the two ventricles - Blood shunts from LEFT ventricle → RIGHT ventricle → lungs (overcirculation) - Sound: loud HOLOSYSTOLIC (pansystolic) murmur heard at the left lower sternal border - Small VSDs may close spontaneously; large ones require surgical repair or device closure - Signs of CHF if large: poor feeding, diaphoresis, failure to thrive 2. **Atrial Septal Defect (ASD)** - Opening in the wall between the two atria - Left atrium → Right atrium shunt - Often asymptomatic in childhood; soft systolic murmur - May be closed with a catheter-based device (Amplatzer occluder) 3. **Patent Ductus Arteriosus (PDA)** - The ductus arteriosus (a fetal vessel connecting the aorta to the pulmonary artery) fails to close after birth - In fetal life, the ductus allows blood to bypass the lungs (lungs are not yet used) - After birth, it should close within 24-48 hours - If it stays open: blood shunts from aorta → pulmonary artery (overcirculation of lungs) - Classic sign: **MACHINE-LIKE CONTINUOUS MURMUR** (heard throughout systole AND diastole), **BOUNDING PULSES**, **WIDENED PULSE PRESSURE** - Treatment: **INDOMETHACIN or IBUPROFEN** (prostaglandin inhibitors) → promotes closure - If medications fail: surgical or catheter-based ligation - KEY DISTINCTION: **PROSTAGLANDIN E1 is given to KEEP the ductus OPEN** in duct-dependent defects (e.g., TGA) while waiting for surgery — do NOT confuse these! 4. **Coarctation of the Aorta** - Narrowing (coarctation) of the aorta, usually just past the aortic arch - Blood pressure and pulse are HIGHER in the arms (above the narrowing) and LOWER in the legs (below the narrowing) - Classic finding: **BOUNDING pulses and HIGH BP in arms; WEAK or ABSENT femoral pulses and LOW BP in legs** - Think of a garden hose with a kink — pressure before the kink is high, pressure after is low - Treated surgically or by balloon dilation (catheterisation) **Cyanotic CHDs (Right-to-Left Shunt):** Deoxygenated blood from the RIGHT side shunts to the LEFT side and enters systemic circulation WITHOUT going to the lungs. Result: CYANOSIS that does NOT improve with oxygen alone. Memory Aid: **5 T's of Cyanotic CHDs** - **T**etralogy of Fallot - **T**ransposition of the Great Arteries - **T**ricuspid Atresia - **T**runcus Arteriosus - **T**otal Anomalous Pulmonary Venous Return **KEY Cyanotic Defects:** 1. **Tetralogy of Fallot (TOF)** — MOST COMMON CYANOTIC CHD Four defects (remember the mnemonic **PROVE**): - **P**ulmonary stenosis (narrowing of the pulmonary valve — the KEY defect) - **R**ight Ventricular Hypertrophy (RVH) (enlarged right ventricle due to working against obstruction) - **O**verriding aorta (aorta sits over both ventricles, receiving deoxygenated blood) - **V**entricular Septal Defect (VSD) (hole between ventricles) - X-ray: **BOOT-SHAPED HEART** (boot = coeur en sabot in French) - **TET SPELLS (Hypercyanotic Spells):** Acute episodes of deep, severe cyanosis triggered by crying, feeding, activity, or morning waking. The infant becomes intensely blue and may lose consciousness. - **PRIORITY INTERVENTION for TET SPELL:** Place infant in **KNEE-CHEST POSITION** (older child SQUATS spontaneously). This increases systemic vascular resistance (SVR), reduces the right-to-left shunt, and forces more blood to the lungs. Also: give oxygen, calm the child, administer morphine as ordered (reduces respiratory drive and spasm). 2. **Transposition of the Great Arteries (TGA)** - The AORTA comes out of the RIGHT ventricle (instead of the left) - The PULMONARY ARTERY comes out of the LEFT ventricle (instead of the right) - Result: two separate, PARALLEL circuits — oxygenated blood goes back to the lungs, deoxygenated blood keeps circulating in the body - This is INCOMPATIBLE WITH LIFE unless there is mixing (through ASD, VSD, or PDA) - **PROSTAGLANDIN E1 (PGE1) infusion is CRITICAL** — it keeps the ductus arteriosus open to allow mixing until surgical correction (arterial switch operation)

Nursing Management of CHF in Children and Digoxin Safety

Congestive Heart Failure (CHF) in infants and children occurs when the heart cannot pump enough blood to meet the body's metabolic needs. In children, CHF most commonly results from large acyanotic CHDs (VSD, PDA, ASD) causing volume overload, or from cardiomyopathy. **RECOGNISING CHF IN INFANTS (different from adult presentation):** Infants CANNOT tell you they have shortness of breath. Instead, look for: - **Tachycardia** (first sign — compensatory) - **Tachypnea** (fast breathing, especially during feeds) - **Diaphoresis (sweating) with feeds** — the infant is WORKING SO HARD to feed that they sweat (feeds = exercise for a sick infant) - **Poor feeding and failure to thrive** — they tire easily and cannot consume enough calories - **Hepatomegaly** (enlarged liver) — from venous congestion (right-sided failure → systemic venous backup) - **Periorbital edema** (swelling around the eyes) — infants show fluid retention here before leg edema - **Weak cry and irritability** In older children, the presentation is more adult-like: dyspnea on exertion, orthopnea, leg edema, and decreased exercise tolerance. **NURSING MANAGEMENT PRIORITIES FOR CHF (Nursing Process: Planning/Implementation):** **1. Reduce Cardiac Workload:** - **CLUSTER CARE** — group all nursing activities together (bathing, assessment, blood draws) to allow uninterrupted rest periods - Position with **head elevated 30-45 degrees** (semi-Fowler's or infant seat) to ease breathing - Provide a **quiet, calm environment** - Maintain **thermoregulation** — temperature extremes increase oxygen demand **2. Optimise Nutrition and Feeding:** - **Small, frequent feedings** every 2-3 hours rather than large feeds - Use a **soft, enlarged, or cross-cut nipple** to reduce the work of sucking - Limit feeding time to **20-30 minutes maximum** — beyond this, the infant burns more calories feeding than they gain - Allow rest mid-feed - **Calorie-enriched formula** may be prescribed to maximise caloric density - Consider nasogastric tube feeds if oral feeds are inadequate **3. Monitor Fluid Status:** - **Daily weight** — the most sensitive indicator of fluid retention (gain >50g/day in infants or >200g/day in older children is significant) - **Strict I&O (intake and output)** - Monitor for signs of fluid overload: worsening edema, increasing tachypnea **4. Medications — DIGOXIN:** Digoxin is a cardiac glycoside that: - **Increases MYOCARDIAL CONTRACTILITY** (positive inotropic effect) — makes the heart pump more effectively - **Slows HEART RATE** (negative chronotropic effect) — reduces cardiac workload - **Slows CONDUCTION** through the AV node (antiarrhythmic effect) **DIGOXIN SAFETY — ABSOLUTE PRIORITY NURSING ACTIONS (HIGH-YIELD NLE):** Before EVERY dose of digoxin: 1. **Count the APICAL PULSE for a FULL MINUTE** — use a stethoscope placed on the chest at the apex of the heart. Do NOT use radial pulse in children (inaccurate due to pulse deficit). 2. **HOLD the dose and NOTIFY the physician if:** - Apical HR is **<90-100 bpm in INFANTS** - Apical HR is **<70 bpm in OLDER CHILDREN** 3. **DOCUMENT** the apical pulse before each dose **Signs of DIGOXIN TOXICITY (CRITICAL to recognise):** - **Bradycardia** (first cardiac sign) - **Nausea, vomiting, anorexia** (GI signs — often the earliest symptoms) - **Dysrhythmias** (in severe toxicity) - **Visual changes** (halos, yellow-green tinge — more common in adults) **Factors that INCREASE digoxin toxicity risk:** - **HYPOKALEMIA** (low potassium) — potassium competes with digoxin at the same receptor; low K+ means more receptor sites open for digoxin → TOXICITY. This is why nurses monitor potassium when patients are also on **furosemide** (a diuretic that causes potassium loss) **Digoxin Parent Teaching (Health Education role per RA 9173):** - Measure the EXACT dose with a syringe (not a household spoon) - Give at the SAME TIME each day - If the child VOMITS, **DO NOT repeat the dose** (risk of double dosing) - **DO NOT mix with food or formula** (absorption is altered) - **STORE LOCKED** away from children - Return to the RHU or hospital if signs of toxicity appear

Croup vs Epiglottitis — Critical Upper Airway Distinction

Croup and epiglottitis both cause upper airway obstruction in children, but they differ dramatically in cause, severity, and nursing management. Confusing them on the NLE — or clinically — can have life-threatening consequences. **CROUP (Laryngotracheobronchitis):** **Cause:** Viral — most commonly **PARAINFLUENZA VIRUS** (types 1 and 2). Other causes include RSV and influenza. **Age Group:** Typically **6 months to 3 years** (but can affect up to age 6) **Onset:** Gradual (over days); often preceded by cold symptoms (rhinorrhea, low-grade fever) **Classic Clinical Picture:** - **BARKING or 'SEAL-LIKE' COUGH** — this is pathognomonic (classic identifying feature) - **INSPIRATORY STRIDOR** — high-pitched crowing sound during breathing IN - **Hoarseness** (voice is affected because larynx is inflamed) - Symptoms worsen at NIGHT (cold air and horizontal position worsen subglottic edema) - Low to moderate fever **Diagnostic Sign:** **'STEEPLE SIGN'** on neck X-ray — the subglottic region appears narrowed like a church steeple due to edema **MANAGEMENT OF CROUP:** 1. **Keep the child CALM** — agitation, anxiety, and crying worsen airway obstruction; a calm child breathes better 2. **Cool humidified air** — traditionally, cool mist (or cool night air) reduces subglottic edema 3. **Oxygen** as needed 4. **Nebulised RACEMIC EPINEPHRINE** — for moderate-to-severe croup with stridor at rest; provides temporary relief (up to 2-3 hours) by constricting mucosal blood vessels; monitor for REBOUND EFFECT (symptoms may return after ~2 hours — child must be observed) 5. **Corticosteroids (DEXAMETHASONE)** — single oral or IM dose significantly reduces airway edema; most cost-effective treatment 6. Most mild croup is managed at HOME with cool mist humidifier and oral fluids --- **EPIGLOTTITIS — AIRWAY EMERGENCY:** **Cause:** BACTERIAL — classically **Haemophilus influenzae type b (Hib)**. Now RARE in countries with widespread Hib vaccination (including the Philippines' Expanded Programme on Immunisation — EPI). Other causes: Streptococcus, Staphylococcus. **Age Group:** Any age, but classically **3-7 years**; CAN occur in adults **Onset:** SUDDEN and RAPID deterioration over hours **Classic Clinical Picture — The '4 D's':** - **D**rooling (child cannot swallow; saliva drips) - **D**ysphagia (difficulty swallowing; complains of severe sore throat) - **D**ysphonia (muffled or 'hot potato' voice — the child sounds like they have a hot object in their mouth) - **D**istress (intense anxiety, appears TOXIC, high fever 39-40°C) **Additional signs:** - Child sits in TRIPOD POSITION or **SNIFFING POSITION** — leaning forward with neck hyperextended, hands on knees — to maximise airway patency - Drooling (cannot swallow saliva) - **HIGH FEVER** and toxic-looking appearance - Does NOT have the barking cough of croup **Diagnostic Sign:** **'THUMB SIGN'** on lateral neck X-ray — the swollen epiglottis looks like a thumb **CRITICAL NURSING MANAGEMENT OF EPIGLOTTITIS:** ⚠️ **ABSOLUTE PRIORITY: DO NOT examine the throat with a tongue depressor. DO NOT attempt to take a throat culture or perform any oral procedure that could stimulate gagging or laryngospasm. This can trigger COMPLETE AIRWAY OBSTRUCTION.** 1. **Keep the child UPRIGHT and CALM** — allow child to stay in the position of comfort (usually tripod); allow the parent to remain with the child 2. **Do NOT place the child supine** — this worsens obstruction 3. **Administer humidified oxygen** via blow-by (avoid tight-fitting mask which causes distress) 4. **Prepare for emergency INTUBATION or TRACHEOSTOMY** — have equipment at the bedside 5. **IV Antibiotics** (ampicillin-sulbactam or cefotaxime) once airway is secured 6. **Do NOT leave the child unattended** 7. Call for the physician, anaesthesiologist, and otolaryngologist immediately **CROUP vs EPIGLOTTITIS — QUICK COMPARISON TABLE:** | Feature | Croup | Epiglottitis | |---|---|---| | Cause | Viral (parainfluenza) | Bacterial (Hib) | | Onset | Gradual | Sudden, rapid | | Cough | Barking/seal-like | Absent or minimal | | Stridor | Inspiratory | Inspiratory | | Fever | Low-moderate | HIGH, toxic appearance | | Position | No specific preference | Tripod/sniffing position | | Drooling | Absent | Present (4 D's) | | X-ray sign | Steeple sign | Thumb sign | | Throat exam | Allowed (visualise) | CONTRAINDICATED | | Treatment | Cool mist, racemic epi, dexamethasone | Emergency airway, IV antibiotics |

Bronchiolitis (RSV) and Asthma

Bronchiolitis and asthma both cause LOWER AIRWAY obstruction, but they differ in age of presentation, cause, and management approach. **BRONCHIOLITIS:** **Cause:** Predominantly **Respiratory Syncytial Virus (RSV)**; also human metapneumovirus, parainfluenza **Age Group:** Infants and children **<2 years old** (peak: 2-6 months) **Pathophysiology:** RSV infects the bronchioles (smallest airways), causing inflammation, edema, mucus plugging, and air-trapping. This leads to WHEEZING (air squeezing past narrowed bronchioles) and TACHYPNEA. **Clinical Presentation:** - Preceding URI symptoms (runny nose, mild fever) for 2-3 days - **Wheezing** (expiratory wheeze) - **Tachypnea** with retractions and nasal flaring - **Copious nasal secretions** (congestion) - Cough - **Poor feeding** (breathless infants cannot feed well) - Hypoxia if severe **INFECTION CONTROL — TOP PRIORITY IN RSV:** - RSV is **HIGHLY CONTAGIOUS** — spread by **LARGE RESPIRATORY DROPLETS** and **DIRECT CONTACT** with secretions - **CONTACT PRECAUTIONS:** gloves and gown for all contact - **Strict HAND HYGIENE** is the single most effective prevention - **COHORT infected infants** or place in a private room - RSV survives on surfaces for hours — clean and disinfect surfaces **MANAGEMENT — SUPPORTIVE CARE (no specific antiviral treatment):** 1. **NASAL/BULB SUCTIONING** — PRIORITY to maintain a patent airway; infants are obligate nose breathers 2. **Humidified oxygen** (for hypoxia) 3. **Hydration** — oral or IV fluids; small frequent feedings 4. **Elevate head of bed** 30-45 degrees 5. Monitor respiratory status closely **PALIVIZUMAB:** - A **monoclonal antibody** that provides passive immunity against RSV - Given as **PROPHYLAXIS** (prevention) to HIGH-RISK infants: - Premature infants (<35 weeks) - Infants with CHD - Immunocompromised children - It is **NOT A TREATMENT** — it does NOT work for a child who already has RSV bronchiolitis - Given as a monthly IM injection during RSV season --- **ASTHMA:** **Definition:** A **CHRONIC REVERSIBLE** inflammatory airway disease characterised by: - **Bronchospasm** (muscle spasm → narrowed airway) - **Mucosal edema** (swelling of the airway lining) - **Excessive mucus secretion** Result: EXPIRATORY WHEEZING (air trapped, expiration prolonged), COUGH, CHEST TIGHTNESS **TRIGGERS (teach families to AVOID):** - Allergens: house dust mites, pet dander, cockroaches (common in Philippine homes) - Air pollutants: smoke, vehicle emissions (common in Metro Manila) - Cold air, strong smells, exercise - Respiratory infections (RSV, influenza) - Strong emotions, stress, crying **ASTHMA PHARMACOLOGY — HIGH-YIELD NLE:** **RELIEVER (Rescue) Drugs — for ACUTE ATTACKS:** - **Salbutamol (Albuterol)** — SHORT-ACTING BETA-2 AGONIST (SABA) - Mechanism: relaxes bronchial smooth muscle → BRONCHODILATION - Use: first-line treatment for acute bronchospasm - Side effects: **tachycardia, tremor, jitteriness** (stimulant-like effects) - Route: inhaled (MDI with spacer, nebuliser) or oral **CONTROLLER (Preventer) Drugs — for LONG-TERM CONTROL:** - **Inhaled Corticosteroids (ICS)** — e.g., budesonide, fluticasone, beclomethasone - Mechanism: reduce airway inflammation (prevent attacks) - Must be taken DAILY even when asymptomatic - Key side effect: **ORAL THRUSH (oral candidiasis)** - **TEACH: RINSE MOUTH with water AND gargle AFTER EVERY ICS USE** to prevent thrush - Long-term systemic effects are minimal with inhaled route, but growth monitoring is needed with high doses **SPACER DEVICE:** - A chamber attached to the MDI to improve drug delivery to the lungs - Especially important for young children who cannot coordinate the MDI properly - Improves drug deposition in the airways and reduces oral thrush risk - **Teach proper inhaler + spacer technique** to parents and children **Other drugs:** - **Ipratropium bromide** (anticholinergic) — adjunct bronchodilator in acute attacks - **Oral/IV corticosteroids (prednisolone)** — for acute exacerbations - **Leukotriene receptor antagonists (montelukast)** — controller for mild persistent asthma **OMINOUS SIGN — SILENT CHEST:** - A child in severe asthma exacerbation who suddenly has NO audible wheeze is NOT better - It means so little air is moving that no wheeze can be produced - **Silent chest = NEAR-COMPLETE OBSTRUCTION = RESPIRATORY EMERGENCY** **ASTHMA EDUCATION (Health Education — RA 9173):** - Written ASTHMA ACTION PLAN (green/yellow/red zones) - Correct inhaler and spacer technique demonstration - Trigger identification and avoidance - Importance of controller medication adherence daily - When to seek emergency care

Rheumatic Fever and Kawasaki Disease

These are two distinct but important ACQUIRED (not congenital) heart conditions in children. Both are inflammatory, both affect the heart, but their causes, presentations, and management are very different. **RHEUMATIC FEVER:** **What it is:** An **AUTOIMMUNE INFLAMMATORY DISEASE** that occurs as a complication of **UNTREATED or inadequately treated Group A Beta-Haemolytic Streptococcal (GABHS) pharyngitis** (strep throat). **Key Concept:** The body's immune system, while fighting strep, produces antibodies that mistakenly attack the heart (and other tissues) through a process called **MOLECULAR MIMICRY** — strep antigens resemble heart tissue antigens. **Timeline:** Rheumatic fever typically develops **1-5 WEEKS after a strep throat infection.** **Age Group:** Most common in **school-aged children (5-15 years)**. Rare in infants/toddlers. **Philippine Context:** Rheumatic fever remains a significant public health problem in the Philippines due to overcrowding, poverty, and inadequate treatment of strep infections. It is a priority concern for community health nurses. **DIAGNOSIS — JONES CRITERIA:** Diagnosis requires evidence of strep infection PLUS 2 major OR 1 major + 2 minor criteria. **MAJOR CRITERIA (high-yield mnemonics):** - **C**arditis — inflammation of the heart (all layers: pericarditis, myocarditis, endocarditis); THE MOST DANGEROUS — can cause permanent valvular damage (RHEUMATIC HEART DISEASE) - **P**olyarthritis — MIGRATORY arthritis (moves from one joint to another; not all joints at once) - **S**ydenham's Chorea — involuntary jerky movements of the face and limbs; also called 'St. Vitus Dance' - **E**rythema Marginatum — pink ring-shaped rash on the trunk (not the face); comes and goes - **S**ubcutaneous Nodules — small, painless, firm nodules over bony prominences Mnemonic: **SPECS** (Sydenham's chorea, Polyarthritis, Erythema marginatum, Carditis, Subcutaneous nodules) **DREADED COMPLICATION — RHEUMATIC HEART DISEASE:** Recurrent attacks of rheumatic fever cause progressive VALVE DAMAGE, especially the **MITRAL VALVE** (most commonly affected), leading to mitral stenosis or regurgitation. This is the primary cause of valvular heart disease in young Filipinos. **MANAGEMENT:** 1. **PENICILLIN** — to eradicate GABHS from the throat (even if throat culture is now negative) 2. **Anti-inflammatory therapy:** Aspirin (salicylates) for arthritis and fever; corticosteroids for severe carditis (Note: this is one of the rare situations where aspirin IS used in children under physician supervision) 3. **Bed rest** during the acute phase 4. **LONG-TERM PROPHYLACTIC PENICILLIN** — to PREVENT recurrence; monthly benzathine penicillin IM or daily oral penicillin V for years (sometimes lifelong if there is valve damage) 5. Monitor for signs of CHF if carditis is present **MOST IMPORTANT PREVENTION POINT:** **TREAT EVERY STREP THROAT COMPLETELY with a FULL ANTIBIOTIC COURSE.** This is the most tested point in the NLE. The antibiotic must be taken for the FULL course (usually 10 days of penicillin) — stopping early because 'the child feels better' allows the strep to persist and trigger rheumatic fever. --- **KAWASAKI DISEASE:** **What it is:** An **ACUTE SELF-LIMITING VASCULITIS** (inflammation of blood vessels) of **UNKNOWN CAUSE**; the most common cause of **ACQUIRED HEART DISEASE in children** in developed countries (including urban Philippine settings). **Age Group:** Children **UNDER 5 YEARS** (peak: 6 months - 5 years) **Why it Matters:** The disease causes inflammation of medium-sized arteries throughout the body, including the **CORONARY ARTERIES** → risk of **CORONARY ARTERY ANEURYSM** (ballooning/dilation of the coronary artery) → risk of myocardial infarction even in young children. **CLINICAL FEATURES — REMEMBER 'CRASH' or the DIAGNOSTIC CRITERIA:** Diagnosis: **FEVER >5 DAYS** + **4 or more of the following 5 features:** 1. **C**onjunctivitis — BILATERAL, NON-PURULENT (no pus, just redness) 2. **R**ash — polymorphous (varied appearance), widespread, especially on trunk/perineal area 3. **A**denopathy — CERVICAL lymphadenopathy (usually unilateral, >1.5 cm) 4. **S**trawberry tongue — **red, 'strawberry' appearance of the tongue; red, cracked, dry LIPS** (very distinctive sign) 5. **H**ands and Feet — red, swollen palms/soles early → **PEELING (desquamation) of the fingertips and toes** in the subacute phase (1-2 weeks after fever) **Key Clinical Feature: FEVER >5 DAYS that does NOT respond to antipyretics** (acetaminophen, ibuprofen will NOT bring this fever down well) **DREADED COMPLICATION: CORONARY ARTERY ANEURYSM** **MANAGEMENT:** 1. **IV IMMUNOGLOBULIN (IVIG)** — large single dose; reduces inflammation and, critically, PREVENTS coronary artery aneurysm if given within the first 10 days of illness 2. **HIGH-DOSE ASPIRIN** — for its anti-inflammatory AND antiplatelet effects - ⚠️ **KEY EXCEPTION:** Kawasaki disease is one of the FEW conditions in CHILDREN where ASPIRIN is INDICATED. (Normally avoided in children due to Reye's syndrome risk.) 3. After the acute phase, aspirin is continued at a LOW dose for antiplatelet effect 4. Echocardiogram to monitor for coronary artery aneurysm 5. Long-term follow-up by a paediatric cardiologist **NURSING EDUCATION FOR KAWASAKI PARENTS:** - The peeling skin is NORMAL and expected — do not panic - The child will be VERY IRRITABLE — this is a hallmark and expected - Give all medications as prescribed, especially aspirin - Watch for signs of cardiac complications: chest pain, shortness of breath

Cleft Lip and Cleft Palate

Cleft lip and cleft palate are among the most common congenital craniofacial malformations. They result from FAILURE OF FUSION of facial structures during fetal development (usually 4-12 weeks of gestation). They can occur together (cleft lip AND palate) or separately. **PATHOPHYSIOLOGY:** - **Cleft Lip:** Failure of the median nasal and maxillary processes to fuse → gap in the upper lip; may be unilateral or bilateral; may extend into the nostril - **Cleft Palate:** Failure of the palatal shelves to fuse → opening in the roof of the mouth; may be incomplete (soft palate only) or complete (soft + hard palate) **PRIORITY NURSING PROBLEMS (NANDA Framework):** 1. **IMBALANCED NUTRITION: Less than body requirements** related to inability to create adequate suction — TOP PRIORITY 2. **RISK FOR ASPIRATION** related to impaired suction and palatal opening 3. **IMPAIRED VERBAL COMMUNICATION** (later, if cleft palate untreated — nasal, hypernasal speech) 4. **RISK FOR OTITIS MEDIA** — the Eustachian tube is dysfunctional in cleft palate → recurrent ear infections 5. **RISK FOR ALTERED BODY IMAGE and PARENTAL ANXIETY** **PRE-OPERATIVE FEEDING MANAGEMENT (Priority — Maslow: Physiological):** The infant with cleft lip/palate cannot generate adequate suction (negative pressure) with normal nipples because the palate is open — air leaks through the cleft instead of creating suction. Feeding strategies: - Hold the infant **UPRIGHT** (nearly vertical) to use gravity and prevent aspiration - Use a **SPECIAL NIPPLE**: wide-based, cross-cut, large nipple OR a **SQUEEZABLE/COMPRESSIBLE BOTTLE** (Haberman feeder, Pigeon feeder, Mead Johnson cleft palate nurser) that allows the caregiver to squeeze the bottle, compensating for the infant's poor suction - Feed SLOWLY and monitor for choking or coughing - **BURP FREQUENTLY** — the infant swallows a lot of air through the cleft → excess gas - Breast-feeding may still be possible (especially for cleft lip only) — the breast can mould to the cleft; encourage and support the mother **TIMING OF SURGICAL REPAIR — RULE OF 10s for CLEFT LIP:** Remember: the infant should be **10-10-10** before cleft lip repair: - **10 WEEKS old** (mature enough for anaesthesia) - **10 POUNDS weight (~4.5 kg)** (big enough for safe surgery and healing) - **Haemoglobin of 10 g/dL** (adequate for anaesthesia and blood loss) **CLEFT PALATE** is repaired **LATER: ~6-12 MONTHS of age**, ideally before the child begins to develop speech patterns (so speech development occurs with a repaired palate). **POST-OPERATIVE CARE — CLEFT LIP REPAIR:** Goal: PROTECT the suture line from tension, rubbing, infection, and mechanical trauma. 1. **POSITION:** Place infant **SUPINE** (on the back) or **LATERAL** (on the side). **NEVER PRONE** (face-down) — this will rub and damage the suture line. 2. **RESTRAINTS: ELBOW (No-No) RESTRAINTS** — prevent the infant from bending the elbows and reaching the face to scratch or rub the suture. Apply BILATERALLY. Check neurovascular status (circulation, sensation) frequently. REMOVE for short periods with supervision and for exercises (range of motion). 3. **SUTURE LINE CARE:** Clean the suture line gently after each feeding with normal saline or hydrogen peroxide as ordered; apply antibiotic ointment as prescribed 4. **FEEDING POST-OP:** No nipple directly against the suture — use a SYRINGE with rubber tubing or a cup to deliver formula to the SIDE of the mouth 5. **AVOID CRYING** — crying puts tension on the suture; keep the infant calm and comfortable; adequate pain management 6. **Nothing hard in or near the mouth** **POST-OPERATIVE CARE — CLEFT PALATE REPAIR:** Goal: PROTECT the palatal suture from mechanical injury and infection. 1. **NOTHING HARD IN THE MOUTH** — absolute restriction: - **NO STRAWS** - **NO PACIFIERS** - **NO SPOONS** (use the SIDE of a spoon only, or a cup) - **NO SUCTION CATHETERS** near the suture line (suction ONLY the front of the mouth) - **NO TONGUE DEPRESSORS** - **NO FINGERS or TOYS** in the mouth 2. **DIET:** Start with liquids/cup feedings; advance to SOFT foods; avoid hard, crunchy, or large pieces of food 3. **ELBOW RESTRAINTS** — same as for cleft lip 4. **POSITIONING:** Prone position MAY be allowed (unlike cleft lip repair) — but check specific physician orders 5. Monitor for **BLEEDING** — any bleeding from the mouth must be reported immediately 6. **Pain management** — adequate analgesia prevents crying and tension on the suture

This problem tests three concepts simultaneously: (1) knowledge of the correct pre-digoxin assessment (apical pulse for 1 full minute), (2) the correct threshold for infants (hold if <90-100 bpm), and (3) the correct action (HOLD AND NOTIFY — not just hold, not just give). The weight-based calculation is included to acknowledge the paediatric pharmacology context, but the main clinical decision point is the heart rate. On the NLE, the most common error students make is giving the medication despite a borderline heart rate or choosing to just 'monitor' instead of reporting.

This prioritisation question tests Maslow's framework applied to a TET spell. The knee-chest position is a non-pharmacological, immediately available nursing intervention that produces the fastest physiological effect (increases SVR → reduces R-to-L shunt). In NLE priority questions, independent nursing actions that address the ABCs come before dependent actions like calling the physician. Oxygen and morphine are also essential but come after positioning. This sequence is directly tested in Philippine NLE board exams.

This problem combines three skills: diagnosis (croup vs epiglottitis differentiation), safety (contraindicated action in possible epiglottitis), and management. The nurse's role in PREVENTING a potentially fatal procedure tests clinical judgment and the advocacy function outlined in RA 9173. A child with epiglottitis could die from an inadvertent throat examination — the nurse must feel empowered to stop this.

This is a comprehensive Kawasaki disease scenario testing: (1) recognition of all diagnostic criteria, (2) the most important complication (NLE favourite), and (3) specific drug treatment (IVIG and aspirin — the aspirin exception). The Philippine setting (PGH) makes it contextually relevant. Kawasaki disease is increasing in recognition in the Philippines, and Filipino paediatric nurses must know this condition thoroughly.

This problem tests multiple competencies simultaneously: priority nursing diagnosis (using NANDA), priority intervention (suctioning in bronchiolitis), and parent education about palivizumab. The NLE commonly combines pharmacology knowledge with nursing process application. The clarification about palivizumab being prophylaxis, not treatment, addresses the most common misconception about this drug.