Midwife Licensure Exam Infant & Child Health (Growth, Development & IMCI) — Paediatric Respiratory & Cardiac DisordersSummary

Respiratory distress in children progresses through three overlapping phases. Early/compensating signs include restlessness, tachypnea (increased respiratory rate above age-appropriate thresholds), tachycardia, nasal flaring, and mild retractions—these indicate the child's body is attempting to maintain oxygenation. Worsening signs include intercostal, subcostal, and suprasternal retractions; grunting (a sound made during expiration to maintain positive airway pressure); head-bobbing (use of neck muscles); audible stridor or wheeze; and use of all accessory muscles. Late/ominous signs—the pre-arrest phase—include cyanosis, bradycardia, decreased or absent breath sounds (paradoxically, this may indicate severe obstruction with poor air movement), lethargy, altered mental status, and unresponsiveness. Fast-breathing thresholds (from IMCI guidelines used in Philippine primary care) are critical for early detection: ≥60 breaths/min in infants <2 months, ≥50 breaths/min in 2–12 months, and ≥40 breaths/min in 12 months–5 years. Nurses must understand that children progress from early to late signs rapidly, making continuous reassessment essential. The priority nursing diagnosis is often Ineffective Airway Clearance or Impaired Gas Exchange, aligned with Maslow's Physiological Needs (safety of breathing). Intervention timing determines outcomes: early recognition allows non-invasive support; late recognition may require emergency intubation.

Acyanotic defects involve abnormal communication between heart chambers or vessels that allows oxygenated blood from the systemic circulation to recirculate back to the lungs (left-to-right shunt). These children are initially pink/not cyanotic because the blood reaching the body is still adequately oxygenated. However, the increased pulmonary blood flow (pulmonary overcirculation) stresses the lungs and leads to congestive heart failure (CHF), often appearing in the first weeks to months of life. Ventricular Septal Defect (VSD), the most common CHD overall, is a hole between the ventricles causing a loud holosystolic (pansystolic) murmur; many small VSDs close spontaneously. Atrial Septal Defect (ASD) is an opening between the atria; it is often diagnosed later because symptoms are mild. Patent Ductus Arteriosus (PDA) occurs when the ductus arteriosus—a fetal vessel that normally closes after birth—remains open; classic signs are a continuous 'machine-like' murmur, bounding pulses (wide pulse pressure), and left-to-right shunt. Indomethacin or ibuprofen promotes PDA closure; however, in certain 'duct-dependent' lesions (some cyanotic defects that rely on ductal flow for survival), prostaglandin E1 is given to KEEP the duct OPEN. Coarctation of the aorta is a narrowing of the aorta causing higher blood pressure and bounding pulses in the upper extremities but lower blood pressure and weak or absent femoral pulses in the lower extremities—this is a classic nursing assessment finding. All acyanotic defects risk CHF, presenting with tachycardia, tachypnea, feeding difficulty and diaphoresis during feeds, poor weight gain, hepatomegaly (enlarged liver), and periorbital edema. Nursing priorities centre on early detection of CHF, energy conservation (small frequent feeds with soft nipples, rest periods), and digoxin therapy management.

Cyanotic defects involve right-to-left shunting, meaning deoxygenated blood bypasses the lungs and enters systemic circulation directly, causing visible cyanosis unrelieved by supplemental oxygen. The mnemonic '5 T's' helps recall the main types: Tetralogy of Fallot, Transposition of the great arteries, Tricuspid atresia, Truncus arteriosus, and Total anomalous pulmonary venous return. Tetralogy of Fallot (TOF) is the most common cyanotic CHD, comprising four defects: (1) pulmonary stenosis (narrowed pulmonary valve), (2) ventricular septal defect (VSD), (3) overriding aorta (positioned over the VSD), and (4) right ventricular hypertrophy (thickened RV wall from chronic overwork). The classic X-ray finding is a 'boot-shaped' heart. Children with TOF appear cyanotic (blue baby), especially with crying or exertion. A critical acute event in TOF is a 'Tet spell' (hypercyanotic spell)—a sudden episode of severe cyanosis, dyspnea, and distress triggered by increased right-to-right shunting, often during crying, feeding, or defecation. The priority NURSING INTERVENTION for a Tet spell is to place the infant in the KNEE-CHEST position (older children squat)—this increases systemic vascular resistance and reduces the right-to-left shunt, improving pulmonary blood flow. Additional interventions include giving oxygen, calming the child (agitation worsens shunting), administering morphine as ordered, and having emergency equipment at the bedside. Transposition of the great arteries (TGA) is a surgical emergency where the aorta and pulmonary artery are switched; survival depends on mixing between the two circulations, which occurs through a patent ductus arteriosus or atrial septal defect. Infants with TGA present with severe cyanosis shortly after birth and require immediate prostaglandin E1 infusion to keep the ductus arteriosus open until emergency surgery (Rashkind balloon atrial septostomy or arterial switch operation) is performed.

Digoxin is a cardiac glycoside that increases myocardial contractility (making the heart pump more forcefully) and slows the heart rate (negative chronotropic effect) by increasing AV nodal refractoriness. It is a cornerstone therapy for paediatric CHF. The nursing role in digoxin administration is critical because the margin between therapeutic and toxic doses is narrow, and toxicity presents insidiously. Before EVERY dose of digoxin, the nurse MUST count the apical pulse for a full minute. The apical pulse is counted at the left midclavicular line at the 5th intercostal space using a stethoscope, ensuring accuracy. HOLD the dose and notify the physician immediately if the apical heart rate falls below age-specific thresholds: <90–100 bpm in an infant, <80 bpm in a child, or <70 bpm in an older child. A slow heart rate (bradycardia) may be an early sign of digoxin toxicity. Signs of digoxin toxicity include nausea and vomiting (often the first sign), anorexia, abdominal pain, visual disturbances (rare in children), and dysrhythmias (premature ventricular contractions, heart block). Digoxin is given at regular intervals (typically twice daily); if the child vomits shortly after a dose, DO NOT repeat the dose, as vomiting does not necessarily mean the dose was not absorbed. Digoxin should never be mixed with food or formula because it must be given at precise times. Educate parents to administer exact doses using a proper oral syringe (not a household spoon) and to keep the medication locked away from siblings. Hypokalemia (low potassium) potentiates digoxin toxicity because potassium and digoxin compete for binding sites on the sodium-potassium pump; children on loop diuretics like furosemide are at increased risk and require potassium monitoring and supplementation. Calcium levels also affect digoxin binding, so hypercalcemia increases toxicity risk.

Croup is a viral laryngotracheal inflammation most commonly caused by parainfluenza virus, affecting children typically between 6 months and 3 years of age, with a peak incidence in autumn and winter. The infection causes subglottic edema and increased secretions, narrowing the subglottic airway. The classic clinical triad is: (1) a distinctive barking or 'seal-like' cough (croupy cough); (2) inspiratory stridor (a high-pitched musical breathing sound heard during inhalation, indicating upper airway obstruction); and (3) hoarseness of the voice from laryngeal involvement. Symptoms typically worsen at night because children lie flat, increasing airway edema. Many children develop low-grade fever and coryzal symptoms (runny nose). The anteroposterior (AP) neck X-ray shows the characteristic 'steeple sign'—a narrowing of the subglottic trachea resembling a church steeple. Most cases of croup are mild to moderate and managed at home. Nursing management priorities are: (1) keeping the child CALM because agitation and crying increase airway obstruction and distress; (2) providing cool, humidified air (a cool mist from a humidifier or even a steamy bathroom); (3) offering hydration and soft foods; and (4) administering medications as ordered. Medical management includes nebulised racemic epinephrine (a sympathomimetic agent causing vasoconstriction and reducing airway edema) for children with stridor at rest, and corticosteroids such as dexamethasone (typically a single dose of 0.6 mg/kg) to reduce inflammatory airway edema. The child should not be agitated or upset before procedures; parents are encouraged to stay with the child. Hospitalisation is considered only for severe croup with impending airway obstruction, severe hypoxaemia, or in high-risk children (very young infants, immunocompromised). Most children improve within 3–5 days.

Epiglottitis is an acute, life-threatening bacterial infection of the epiglottis (the leaf-shaped cartilage that covers the larynx during swallowing) causing rapid onset of airway obstruction. Classically caused by Haemophilus influenzae type b (Hib), epiglottitis is now rare in countries with high Hib vaccination coverage but remains a medical emergency when it occurs. The presentation is acute and toxic: children appear systemically ill with high fever, difficulty swallowing (dysphagia), drooling from the mouth, muffled or hoarse voice (dysphonia—described as 'hot potato' voice), and severe respiratory distress. The child assumes the tripod or 'sniffing' position (sitting upright, leaning forward, chin thrust forward, mouth open) to maximise airway patency—this is a classic sign. Unlike croup, which develops gradually over days, epiglottitis develops within hours. The lateral neck X-ray shows the 'thumb sign'—the swollen epiglottis appears as a thumb-shaped mass at the base of the tongue. The four classic clinical signs are the '4 D's': Drooling, Dysphagia, Dysphonia, and Distress. CRITICAL NURSING SAFETY POINT: Do NOT examine the throat with a tongue depressor, do NOT take a throat culture, and do NOT attempt procedures that might agitate the child—any manipulation of the posterior pharynx can trigger complete laryngospasm and total airway obstruction, converting a partially obstructed airway into a completely blocked one. The only intervention before intubation is to keep the child calm and upright with the parent present. Management includes immediate preparation for possible intubation or emergency tracheostomy, with appropriate airway equipment at the bedside. Provide humidified oxygen. Establish IV access cautiously. Administer IV antibiotics (typically ceftriaxone or other broad-spectrum agents covering Hib). Do NOT delay antibiotics for X-ray confirmation if clinical suspicion is high.

Bronchiolitis is an acute inflammatory infection of the bronchioles (small airways) causing obstruction and air trapping. The most common causative agent is respiratory syncytial virus (RSV), though other viruses (parainfluenza, influenza, metapneumovirus) can also cause bronchiolitis. The peak age of presentation is 2–6 months, though infants up to 2 years can be affected. RSV is highly contagious, spreading via large respiratory droplets and contact with contaminated surfaces and fomites (objects). The virus causes bronchiolar inflammation, mucus production, and bronchospasm, leading to obstruction of small airways, air trapping, atelectasis (collapse of alveolar units), and ventilation-perfusion mismatch. Clinically, infants present with cough, copious nasal secretions, wheezing, tachypnea, intercostal and subcostal retractions, nasal flaring, and difficulty feeding due to respiratory distress and nasal congestion. Hypoxaemia may be present. The clinical course typically peaks around day 3–5 and improves over 1–2 weeks, though some infants experience prolonged symptoms. Nursing PRIORITY is implementation of STRICT CONTACT PRECAUTIONS: infants with bronchiolitis must be in a private room or cohorted (grouped together) with other RSV-positive patients only. Hand hygiene is essential before and after patient contact, and caregivers should avoid touching their face. Management is entirely supportive: maintain a clear airway via gentle suctioning (bulb syringe nasally, or nasal catheter under careful observation) as needed; provide humidified oxygen to maintain oxygen saturation >90%; ensure adequate hydration (small frequent feeds or IV hydration if necessary); position with head elevated to ease breathing. Fever management and comfort measures are important. Palivizumab is a monoclonal antibody against RSV used for PROPHYLAXIS in high-risk infants (premature infants, those with chronic lung disease, congenital heart disease, or immunodeficiency) during RSV season—it is NOT a treatment for active bronchiolitis. Antibiotics are not indicated unless secondary bacterial superinfection occurs.

Asthma is a chronic inflammatory airway disease characterised by reversible airflow obstruction, bronchial hyperresponsiveness, and inflammation. The pathophysiology involves bronchospasm (contraction of smooth muscle in airways), mucosal edema (swelling of the airway lining), and excessive mucus production—all narrowing the airway lumen. Clinically, children with asthma present with cough (often the only symptom in 'cough-variant' asthma), wheezing (an expiratory sound, though it can be heard throughout the respiratory cycle in severe cases), chest tightness, dyspnea, and prolonged expiration (the child takes longer to exhale). Triggers include allergens (dust, pollen, pet dander), respiratory infections, cold air, exercise, and emotional stress. Asthma medications fall into two categories: RELIEVER/RESCUE drugs and CONTROLLER/PREVENTER drugs. Short-acting beta-2 agonists (SABA) such as salbutamol (albuterol) are reliever medications—they rapidly reverse acute bronchospasm and are used during acute exacerbations or before exercise. Side effects include tachycardia, tremor, and jitteriness. Inhaled corticosteroids (ICS) such as fluticasone or beclomethasone are controller medications—taken regularly (typically twice daily) to suppress chronic airway inflammation and prevent exacerbations. After using an ICS, the child must rinse the mouth with water to prevent oral thrush (Candida infection). Other controller medications include leukotriene receptor antagonists and long-acting beta-2 agonists (LABA). A critical nursing assessment is the recognition of the 'silent chest'—when wheezing is no longer audible despite severe respiratory distress and cyanosis. This is an OMINOUS sign indicating severe airway obstruction with poor air movement; it indicates impending respiratory failure and requires immediate emergency intervention (oxygen, IV steroids, possibly intubation). Nursing management includes teaching correct inhaler technique and the use of a spacer (a tube attached to the metered-dose inhaler that increases drug deposition in the lungs and is especially important in children). Develop a written Asthma Action Plan with traffic-light zones: Green (well-controlled), Yellow (increased symptoms, needs closer monitoring/quick-relief medication), and Red (emergency—seek immediate care). Teach trigger avoidance, when to use the reliever, and when to seek medical care. Family education is crucial for controlling asthma and preventing exacerbations.

Acute rheumatic fever (ARF) is an autoimmune inflammatory disease that develops as a complication of untreated or inadequately treated Group A beta-haemolytic streptococcal (GABHS) pharyngitis (strep throat). The disease occurs 1–5 weeks after the initial streptococcal infection and is most common in school-age children and young adolescents. The pathophysiology involves molecular mimicry: antibodies produced against streptococcal antigens cross-react with cardiac myosin and other cardiac tissue, causing inflammation and tissue damage. ARF is diagnosed using the Jones criteria (major and minor criteria), updated by the American College of Cardiology. Major manifestations include: (1) Carditis (inflammation of the heart—the most serious manifestation, which can cause permanent valve damage); (2) Polyarthritis (migratory joint inflammation, especially in large joints); (3) Chorea (Sydenham chorea—involuntary, purposeless movements); (4) Erythema marginatum (a distinctive pink rash with pale centre and raised borders, appearing on trunk and proximal extremities); and (5) Subcutaneous nodules (small, firm, painless nodules on bony prominences). Minor manifestations include fever, arthralgia (joint pain without inflammation), elevated erythrocyte sedimentation rate (ESR), elevated C-reactive protein (CRP), and prolonged PR interval on electrocardiography (ECG). The DREADED complication of ARF is permanent RHEUMATIC HEART DISEASE (RHD), characterised by valve scarring and stenosis or regurgitation, most commonly affecting the mitral valve. RHD causes chronic heart dysfunction and may require valve replacement later in life. Nursing MANAGEMENT focuses on: (1) Anti-inflammatory therapy—aspirin is given in THERAPEUTIC (anti-inflammatory) doses under careful supervision (different from the analgesic/antipyretic dose); (2) Penicillin therapy to eradicate any remaining streptococcal infection; (3) Rest during the acute phase; (4) Cardiac monitoring for signs of carditis. PREVENTION is the cornerstone of ARF management and is heavily emphasised in Philippine public health. The SINGLE MOST IMPORTANT PREVENTION STRATEGY is complete treatment of streptococcal pharyngitis with a full course of penicillin (typically 10 days); skipping doses or stopping treatment early allows ARF to develop. Long-term secondary prophylaxis with monthly penicillin injections or daily oral penicillin is recommended for at least 5 years after an ARF episode (or until adulthood if carditis occurred) to prevent recurrent ARF episodes.

Kawasaki disease is an acute systemic vasculitis of unknown aetiology affecting primarily young children (typically <5 years, peak age 18 months–4 years). It is the leading cause of acquired heart disease in children in developed countries and is increasing in prevalence in the Philippines. The disease is characterised by acute inflammation of medium-sized arteries, particularly the coronary arteries, and is more common in males and in Asian populations. The clinical diagnosis is made on clinical criteria because there is no specific diagnostic test. Key clinical features include: (1) Prolonged fever (>5 days) that is high (often >39°C) and unresponsive to typical antipyretics (acetaminophen, ibuprofen); (2) Bilateral non-purulent conjunctivitis (redness of the eyes without discharge); (3) Oropharyngeal involvement—a 'strawberry' tongue (red with prominent papillae) and cracked, red lips (often with bleeding); (4) Cervical lymphadenopathy (usually unilateral, >1.5 cm); (5) Polymorphous rash (variable appearance, typically maculopapular, appearing on trunk and proximal extremities, sparing the face); and (6) Extremity involvement—erythema (redness) and edema of the hands and feet in the acute phase, followed by characteristic desquamation (peeling of the skin) of the fingertips and toes in the convalescent phase. The DREADED complication is coronary artery aneurysm (CAA), which can occur in 15–25% of untreated cases and can lead to myocardial infarction, arrhythmias, and sudden death even weeks or months after the acute illness. Earlier recognition and treatment have reduced CAA incidence to <5%. Nursing MANAGEMENT includes: (1) IV Immunoglobulin (IVIG)—a large dose (typically 2 g/kg) given within the first 10 days of illness, which reduces CAA risk dramatically; (2) High-dose aspirin (used therapeutically during the acute phase as an anti-inflammatory agent, a key exception to the rule against aspirin in children)—given in therapeutic doses during acute illness, then switched to low-dose aspirin for antiplatelet effect during convalescence; (3) Cardiac monitoring including electrocardiography and echocardiography (to assess coronary arteries); (4) Symptomatic management of fever, pain, and discomfort. Nursing support for families is crucial: explain that the child may be irritable and crying (due to the systemic inflammation); reassure about the skin peeling in hands and feet (this is expected and will resolve); encourage rest; and arrange close follow-up echocardiography. Long-term antiplatelet therapy is often continued for months after discharge.

Cleft lip and cleft palate are congenital facial malformations resulting from failure of fusion of the maxillary and medial nasal processes (lip) and palatal shelves (palate) during foetal development. They may occur separately (cleft lip only, cleft palate only) or together (cleft lip and palate). The aetiology is multifactorial, involving genetic factors and teratogens (maternal smoking, alcohol, anticonvulsants). The PRIMARY NURSING PROBLEM is feeding difficulty because infants with cleft cannot generate adequate suction (the oral muscles that generate suction insert on intact palate), risking inadequate caloric intake and aspiration. Preoperative feeding strategies include: (1) positioning the infant UPRIGHT during feeding to facilitate gravity-assisted swallowing; (2) using special WIDE NIPPLES or cross-cut nipples that allow easier milk flow (soft silicone nipples work better than rigid ones); (3) using a SQUEEZABLE bottle or special syringe-fed apparatus allowing controlled milk delivery; (4) feeding SLOWLY and patiently (20–30 minutes maximum per feed); (5) BURPING FREQUENTLY because the infant swallows air; (6) allowing adequate rest between feeds; and (7) breastfeeding is often still possible if the mother and infant are taught proper positioning and latch techniques. Surgical repair follows the 'Rule of 10s' for cleft lip: repair is performed when the infant is approximately (1) 10 weeks old, (2) weighs ~10 lb (approximately 4.5 kg), and (3) has a haemoglobin concentration of ~10 g/dL (ensuring adequate reserves for surgery and anaesthesia). Cleft palate repair is typically delayed until 6–12 months of age, allowing better growth and typically performed before the child develops speech, as palatal integrity is essential for normal speech development. Postoperative cleft LIP repair care includes: (1) position SUPINE or on the SIDE (NEVER prone, which would cause rubbing and tension on the suture line); (2) apply ELBOW RESTRAINTS (also called 'no-no' restraints or arm restraints) to prevent the child from touching/rubbing the suture line; (3) keep the suture line CLEAN (gentle cleansing with saline or water as prescribed, never scrubbing); (4) AVOID TENSION and crying (which increases tension on the suture line); (5) keep hard objects away (no pacifiers, spoons, utensils that might trauma the suture line); and (6) monitor for signs of infection (redness, drainage, swelling). Postoperative cleft PALATE care includes similar precautions with additional strictness: (1) NOTHING HARD in the mouth (NO straws, pacifiers, spoons, suction catheters, or rigid tubes near the suture line); (2) feed with a cup (preferred) or soft-tipped spoon (syringe fed if needed); (3) soft/liquid diet; (4) maintain elbow restraints; and (5) position carefully to prevent suture line trauma. Pain management, hydration, and nutrition are ongoing priorities. Parent education must address the cosmetic and functional goals of repair, normal post-operative swelling, and the long-term need for speech therapy, orthodontics, and potential additional surgeries (cleft palate may require secondary surgery in adolescence if speech is not normal).