NLE Paediatric Nursing — Paediatric Hematologic, Oncologic & Genetic DisordersStudy Notes

The rapid deterioration of paediatric patients in respiratory distress demands that nurses develop a systematic approach to assessment. Children cannot simply 'tell' you they are in trouble — their non-verbal cues and vital sign changes are the primary language of distress. Understanding the spectrum from early (compensating) to late (pre-arrest) signs is fundamental to Maslow-based prioritization and NCM competency. **Early/Compensating Signs (Child is attempting to maintain oxygenation):** Restlessness and anxiety (child senses inadequate oxygen) Tachypnea (rapid breathing to increase minute ventilation) — note reference to IMCI fast-breathing thresholds Tachycardia (sympathetic response; heart rate increases to maintain cardiac output and oxygen delivery) Nasal flaring (use of accessory muscles of inspiration to increase airway diameter) Mild intercostal retractions (inward drawing of the skin between ribs during inspiration, indicating increased work of breathing) The child remains alert and responsive; skin perfusion is warm, pink, and dry. **Worsening/Progressive Signs (Compensation is failing; workload becomes unsustainable):** Progressive retractions: intercostal (between ribs), subcostal (below ribs), and suprasternal (above sternum) — these indicate the child is using accessory muscles heavily Grunting (expiratory grunt — an attempt to maintain positive airway pressure and keep small airways open during expiration) Head-bobbing (rhythmic anterior movement of the head with each breath; uses neck accessory muscles) Increased use of accessory muscles: sternocleidomastoid, scalenes, abdominal muscles Stridor (high-pitched, musical breathing sound from upper airway obstruction — may be inspiratory, expiratory, or biphasic) Wheeze (high-pitched whistling from lower airway narrowing/bronchospasm) The child may become irritable or restless; feeding difficulty develops. **Late/Ominous Signs (Respiratory failure imminent; cardiopulmonary arrest risk):** Cyanosis (central — bluish discoloration of lips, tongue, mucous membranes; indicates arterial oxygen saturation <85%) Bradycardia (dangerous sign — heart rate decreases as hypoxia becomes severe and myocardial perfusion fails) Decreased or absent breath sounds (lungs 'tired out,' ventilation severely impaired) Lethargy or unresponsiveness (cerebral hypoxia) Apnea (cessation of breathing — absolute emergency) Pale, mottled, or cool skin (shock) **IMCI Fast-Breathing Thresholds (Important for Community and Clinic Settings):** Children <2 months: ≥60 breaths/minute Children 2–12 months: ≥50 breaths/minute Children 12 months–5 years: ≥40 breaths/minute These thresholds help nurses in primary health centres and community settings rapidly identify when a child with cough/difficult breathing warrants urgent referral or admission. **Nursing Assessment Framework:** Position the child upright or in the parent's lap; do not agitate with excessive handling. Count respiratory rate for a full 60 seconds (not 15 seconds then multiply). Observe chest wall movement, use of accessory muscles, and retractions. Listen for stridor, wheeze, or grunting without a stethoscope first (general observation). Palpate pulses and assess capillary refill; check skin temperature and moistness. Note mental status: alert, restless, irritable, lethargic, or unresponsive. Assess oxygen saturation if pulse oximetry available; however, do not delay assessment waiting for equipment.

Congenital heart defects are structural abnormalities present at birth due to failure of normal cardiac development in utero. They occur in ~8–10 per 1,000 live births and are a leading cause of childhood morbidity and mortality if not identified and managed. The two major classifications — acyanotic (left-to-right shunt) and cyanotic (right-to-left shunt) — fundamentally determine the pathophysiology, presentation, and nursing priorities. **ACYANOTIC DEFECTS (Left-to-Right Shunt — No Initial Cyanosis)** In left-to-right shunts, oxygenated blood from the left side of the heart is diverted back into the pulmonary circulation instead of the systemic circulation. The child is *not* cyanotic because the oxygenated blood entering the systemic circulation is sufficient to saturate haemoglobin. However, the lungs receive excessive blood flow (pulmonary overcirculation), leading to pulmonary oedema and eventually congestive heart failure (CHF). Over time, if untreated, prolonged left-to-right shunting can cause irreversible pulmonary vascular disease (Eisenmenger syndrome), after which the shunt may reverse to become cyanotic. **1. Ventricular Septal Defect (VSD) — Most Common CHD Overall** Pathophysiology: A hole in the ventricular septum allows blood to shunt from the high-pressure left ventricle into the low-pressure right ventricle. Size determines severity: small VSDs may produce only a murmur, moderate/large VSDs lead to CHF. Classic finding: Loud holosystolic (pansystolic) murmur best heard at the left lower sternal border; the murmur is present throughout systole because there is pressure gradient between left and right ventricles the entire time. Natural history: Many small VSDs close spontaneously by age 5 years as endothelial tissue grows to close the defect; moderate/large VSDs may require surgical closure. Nursing priorities for VSD with CHF: — Monitor for signs of heart failure (see below). — Facilitate efficient feeding: small, frequent feeds using soft/enlarged nipples; limit feed duration to 20–30 minutes to avoid tiring the infant. — Cluster care to minimize oxygen demand. — Position with head elevated 30–45 degrees. — Administer digoxin (if prescribed) with strict apical pulse monitoring (see digoxin section). — Administer diuretics as prescribed; monitor urine output and daily weights. — Teach parents feeding technique, signs of worsening CHF, and medication adherence. **2. Atrial Septal Defect (ASD)** Pathophysiology: An opening between the right and left atria allows shunting of oxygenated blood from the left atrium back into the right atrium. Presentation: Often asymptomatic in childhood; discovered incidentally during a cardiac workup for murmur or on routine screening. Auscultatory findings: A systolic ejection murmur at the pulmonary area and fixed (unchanging with respiration) splitting of the second heart sound (S2). Long-term consequence: Atrial fibrillation in adulthood due to chronic volume overload and right atrial enlargement. Many ASDs are managed conservatively (monitored) in childhood; surgical or catheter-based closure occurs if indicated by cardiac catheterization studies. **3. Patent Ductus Arteriosus (PDA) — Unique for Two Opposite Management Strategies** Pathophysiology: The ductus arteriosus is a normal foetal vessel connecting the pulmonary artery to the aorta, allowing foetal blood to bypass the fluid-filled (non-functional) lungs. After birth, as pulmonary vascular resistance drops and systemic vascular resistance increases, the pressure gradient reverses and the ductus closes (usually by 48–72 hours postnatal). In PDA, the ductus fails to close, resulting in continuous left-to-right shunting from the aorta (high pressure) into the pulmonary artery (lower pressure). Classic clinical findings: — Continuous "machinery" or "diamond-shaped" murmur heard throughout systole and diastole (unique because of continuous pressure gradient). — Bounding pulses (hyperdynamic pulses) — full and rapid, palpable at wrists and femoral pulses; parents may notice a prominent pulsation. — Widened pulse pressure (difference between systolic and diastolic BP); diastolic BP is low (run-off into the pulmonary artery). — In premature infants: PDA may lead to left heart failure, pulmonary oedema, and feeding intolerance. **PDA Management — Critical Point: CLOSURE vs. PATENCY** *Closure of PDA (when PDA is unwanted):* — Indomethacin or ibuprofen: Inhibits prostaglandins, which promote ductal closure. Given to premature infants with symptomatic PDA; success rate ~70–80%. — Acetaminophen: Emerging alternative to NSAIDs; may be used if renal function compromised. — Surgical ligation or catheter-based closure: For PDA refractory to medical management. *Patency of PDA (when PDA is lifesaving):* — Prostaglandin E1 (PGE1) infusion: KEEPS the ductus OPEN by maintaining prostaglandin levels. — Used in "duct-dependent" lesions where pulmonary or systemic blood flow depends on the open ductus: — Pulmonary duct-dependent: Tetralogy of Fallot, pulmonary atresia, critical pulmonary stenosis (ductus delivers blood to the lungs). — Systemic duct-dependent: Hypoplastic left heart syndrome, coarctation, interrupted aortic arch (ductus delivers blood to the body). — PGE1 infusion is a critical bridge to surgery; it may cause apnea (so ventilatory support is often needed), fever, and flushing. This distinction is **extremely high-yield for the NLE**: indomethacin CLOSES PDA; prostaglandin E1 OPENS/KEEPS PDA open. **4. Coarctation of the Aorta** Pathophysiology: Narrowing of the thoracic aorta, usually just beyond the origin of the left subclavian artery (beyond the ductus arteriosus). This narrows the lumen and increases resistance to blood flow distal to the coarctation. Classic clinical findings: — **Discrepancy between upper and lower body blood pressures and pulses.** — **Arms:** High blood pressure, bounding/strong pulses (radial, brachial). — **Legs:** Low blood pressure, weak/diminished/absent femoral and pedal pulses. — This pulse differential may be subtle in neonates but becomes obvious in older infants/children. — Murmur: Systolic ejection murmur heard best over the left infraclavicular area and back (if the coarctation is accessible to the stethoscope). — In neonates with critical coarctation, PGE1 infusion is given to keep the ductus open, allowing blood to bypass the narrowed aorta and perfuse the lower body. Nursing assessment pearls: — Always compare pulses in all four extremities and blood pressures in both arms and legs. — Be alert to weak/absent femoral pulses in a newborn as a possible sign of critical coarctation (emergency). — Post-operatively after coarctation repair, monitor for rebound hypertension, spinal cord ischaemia (paraplegia — rare but devastating), and paradoxical hypertension in the years following surgery. **CYANOTIC DEFECTS (Right-to-Left Shunt — Cyanosis at Rest or with Exertion)** In right-to-left shunts, deoxygenated blood bypasses the lungs and enters the systemic circulation directly. Because deoxygenated blood (with lower oxygen saturation) is mixing with systemic blood, the overall arterial oxygen saturation is reduced, producing *cyanosis* — a bluish discoloration of the skin, lips, and mucous membranes (though cyanosis is a late sign and is less obvious in anaemic children). Cyanosis in congenital heart disease is classically **unrelieved by oxygen administration** (whereas cyanosis from lung disease improves with oxygen) because the problem is mixing of deoxygenated and oxygenated blood, not lung oxygenation. **The "5 T's" of Cyanotic CHD (High-Yield Mnemonic):** 1. **Tetralogy of Fallot** 2. **Transposition of the great arteries** 3. **Tricuspid atresia** 4. **Truncus arteriosus** 5. **Total anomalous pulmonary venous return (TAPVR)** **1. Tetralogy of Fallot (TOF) — Most Common CYANOTIC CHD** Pathophysiology: Four cardiac defects occurring together: 1. **Pulmonary stenosis** (narrowing of the pulmonary valve/outflow tract) 2. **Ventricular septal defect (VSD)** (hole in the ventricular septum) 3. **Overriding aorta** (the aorta is positioned over the VSD instead of solely over the left ventricle, so it receives deoxygenated blood from the right ventricle) 4. **Right ventricular hypertrophy (RVH)** (the RV is thickened and muscular from chronically pumping against increased resistance from pulmonary stenosis) The degree of cyanosis depends on the severity of the pulmonary stenosis: severe stenosis forces more deoxygenated blood through the VSD into the aorta, worsening cyanosis. Classic chest X-ray finding: **"Boot-shaped" or "coeur en sabot" heart** — the silhouette resembles a boot due to RVH and a small pulmonary artery. Clinical presentation: — Mild to moderate cyanosis ("blue baby" appearance), often noticed within the first weeks of life. — Dyspnea on exertion (older infants/children) — **Hypercyanotic spells** ("Tet spells"): Acute episodes of increased cyanosis, breathlessness, and altered consciousness, often triggered by exertion, crying, defecation, feeding, or even nappy changes. The pulmonary stenosis temporarily worsens (spasm), forcing more right-to-left shunting. — Squatting posture: Older children spontaneously squat during Tet spells (increasing systemic vascular resistance reduces the right-to-left shunt gradient; see intervention below). — Poor feeding and failure to thrive — Clubbing of fingers (chronic hypoxia causes thickening of the distal phalanges) **CRITICAL NURSING INTERVENTION FOR TET SPELL: KNEE-CHEST POSITION** When a Tet spell occurs: 1. **Immediately place the infant in the KNEE-CHEST position** (knees pulled toward the chest while supine or in the parent's lap); in older children, encourage SQUATTING. — Rationale: This position increases systemic vascular resistance (SVR). Recall the shunt gradient: RV pressure > LV pressure + resistance of shunt pathway. By increasing SVR acutely, you decrease the pressure gradient driving the right-to-left shunt, reducing the amount of deoxygenated blood entering the systemic circulation. 2. **Administer oxygen** (though remember, oxygen may not fully relieve cyanosis due to right-to-left shunting, it may help). 3. **Calm the child** — agitation worsens spells; ask the parent to comfort the child; minimize handling. 4. **Administer morphine** (0.1–0.2 mg/kg IV/IM) as prescribed — morphine reduces anxiety, causes mild sedation, and may reduce infundibular spasm. 5. **Administer IV fluids** if dehydrated — dehydration increases blood viscosity, worsening cyanosis. 6. **Notify the physician immediately.** This knee-chest position manoeuvre is an **extremely high-yield NLE topic**; many questions test whether nurses know this specific, lifesaving intervention. **2. Transposition of the Great Arteries (TGA)** Pathophysiology: The aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle — the opposite of normal. This is incompatible with life unless there is mixing of blood between the systemic and pulmonary circulations. In utero, the foetus relies on mixing through the foramen ovale (ASD) and ductus arteriosus (PDA). After birth, if these are small or closing, severe cyanosis and acidosis ensue. Presentation: — Severe cyanosis within the first hours to days of life (most cyanotic defect to present early). — Dyspnea, poor feeding, weak cry. — Chest X-ray: "Egg on string" appearance (narrow mediastinum due to abnormal vascular arrangement). **Critical neonatal management:** — **Prostaglandin E1 (PGE1) infusion** to KEEP the ductus arteriosus OPEN, allowing mixing. — Oxygen (though cyanosis may not fully resolve due to mixing limitation). — **Balloon atrial septostomy (Rashkind procedure)** at the bedside: A catheter with a balloon is threaded into the right atrium, the balloon is inflated, and the catheter is pulled back to tear the foramen ovale open, creating a larger ASD for better mixing. — Definitive surgical repair (arterial switch operation) in the first weeks of life. Nursing priorities: Keep the child NPO for potential emergency surgery; administer PGE1 carefully (monitor for apnea, fever); ensure IV access; monitor oxygenation, perfusion, and metabolic status closely. **Congestive Heart Failure (CHF) in Paediatric CHD** CHF develops when the heart cannot pump sufficient blood to meet the metabolic demands of the body. In infants, signs are subtle: Classic signs of infant CHF: — **Tachycardia** (heart rate >150–160 bpm at rest in infants) — **Tachypnea** (RR >60/min) — **Feeding difficulty and diaphoresis with feeds** — the infant sweats while feeding (high metabolic work) — **Poor weight gain or failure to thrive** — caloric intake insufficient; excessive energy expended on breathing — **Hepatomegaly** — liver engorgement from venous congestion (always palpate liver edge; normal is 1–2 cm below costal margin; >2 cm is abnormal) — **Periorbital or dependent oedema** — fluid accumulation around the eyes or in dependent areas — **Frequent respiratory infections** — pulmonary oedema predisposes to infection Nursing management of CHF in paediatric cardiac patients: 1. **Feeding:** Offer small, frequent feedings (6–8 per day instead of 4) to prevent fatigue. Use a soft or cross-cut nipple to reduce sucking effort. Consider bottle-feeding if breastfeeding causes excessive work. Limit feeds to 20–30 minutes; stop if the infant becomes tired or tachypneic. Some infants may need calorie-dense formula or feeds (fortified breast milk, higher-calorie formula) to meet growth needs with smaller volumes. 2. **Cluster care:** Group all care activities (nappy change, bath, assessment) at one time; allow long periods of rest to reduce oxygen demand. 3. **Positioning:** Head elevated 30–45 degrees to ease breathing; avoid prone positioning (restricts chest expansion). 4. **Medications:** — **Digoxin:** Increases myocardial contractility (stronger heart contractions) and slows heart rate. See detailed section below. — **Diuretics (e.g., furosemide):** Reduce fluid overload. Monitor electrolytes (especially potassium and sodium) as these are lost with diuresis. Monitor accurate intake and output; calculate daily weights to assess fluid balance. — **ACE inhibitors (e.g., captopril, enalapril):** Vasodilators; reduce afterload (resistance the heart must pump against), making it easier for the failing heart to eject blood. 5. **Fluid management:** Fluid restriction may be ordered (e.g., 130 mL/kg/day instead of 150 mL/kg/day in infants). Record all intake (feeds, medications, IV fluids) and output (urine, stool, emesis). 6. **Monitoring:** Daily weights (morning, same time, nude weight, before feeds); monitor urine output; monitor breath sounds for crackles (sign of pulmonary oedema); watch for signs of worsening CHF (increased respiratory rate, poor feeding, new hepatomegaly). 7. **Parent education:** Teach medication administration (with correct dosing, frequency, and syringe measurement — NOT estimated); signs of worsening CHF to report (poor feeding, rapid breathing, swelling); importance of antibiotic prophylaxis if indicated (for endocarditis prevention); follow-up cardiology appointments. **DIGOXIN IN PAEDIATRIC PRACTICE — CRITICAL DRUG KNOWLEDGE** Digoxin is a cardiac glycoside that: — **Increases the force of myocardial contraction (positive inotropic effect)** → stronger heart contractions → increased cardiac output. — **Slows the heart rate** by enhancing vagal (parasympathetic) tone and slowing AV node conduction → reduces oxygen demand. In CHF, digoxin improves cardiac output and reduces compensatory tachycardia, allowing the heart to work more efficiently. **Critical Safety Points — APICAL PULSE MONITORING:** 1. **Count the APICAL pulse for a FULL 60 SECONDS before every dose.** (Many nurses make the error of counting for 15 seconds and multiplying by 4, which misses irregular rhythms or slow rates.) — Locate the apical impulse: 5th intercostal space at the midclavicular line. — In infants, the apical impulse is higher (4th or 5th ICS) and more lateral than in older children/adults. — Place your stethoscope directly over the impulse; count "lub-dub" (one heartbeat) for 60 seconds. 2. **HOLD the dose if the heart rate is below the specified threshold:** — Infants: Hold if apical HR <90–100 bpm (some protocols use <100 bpm). — Children 1–5 years: Hold if apical HR <80–90 bpm. — Children >5 years: Hold if apical HR <70 bpm. — The exact threshold should be verified in your facility protocol, but the key principle is: **slower rate = hold the dose.** 3. **NOTIFY the physician immediately if the heart rate is below threshold.** Do not give the dose and assume you will give the next one; report it for possible dose adjustment or discontinuation. 4. **Teach parents:** They must count the apical pulse at home before giving digoxin; if they cannot feel/count the pulse accurately (common in infants at home), teach them to observe the child's general activity and feeding, and to call the clinic if the child seems unusually sleepy, feeds poorly, or vomits. **Signs of Digoxin Toxicity (High-Yield for NLE):** — **Bradycardia** (first sign; heart becomes too slow) — **Nausea, vomiting, anorexia** (GI effects) — **Visual disturbances** (in older children, yellowing of vision — rare in paediatric cases) — **Dysrhythmias** (ectopic beats, heart block) — In infants: irritability, lethargy, poor feeding **CRITICAL: Hypokalemia increases the risk of digoxin toxicity.** When a child is on both digoxin and a diuretic (e.g., furosemide), potassium is lost in the urine. Low serum potassium makes the myocardium more irritable and more sensitive to digoxin's toxic effects. Always monitor potassium levels; administer potassium-sparing diuretics (e.g., spironolactone) or potassium supplementation as prescribed. **Digoxin Administration Points:** — Give at regular, evenly-spaced intervals (usually once daily or twice daily). — **If the child vomits immediately after a dose, do NOT repeat the dose** — assume some absorption occurred; giving a replacement dose risks toxicity. Notify the physician. — **Do not mix digoxin with food or formula.** Give with a small amount of water or as a direct oral liquid; mixing with food may affect absorption. — Teach parents to use a **proper syringe or measuring device**, never an estimated "spoon." Digoxin's narrow therapeutic window (therapeutic dose close to toxic dose) makes accuracy essential. — Store digoxin in a locked drawer away from children (liquid digoxin tastes sweet and is attractive to children; accidental ingestion is toxic). — Provide a written medication card with the dose, frequency, and how to give it. **Monitoring for Drug Interactions:** — Certain medications interact with digoxin (e.g., diuretics causing hypokalemia, some antibiotics increasing digoxin levels). Always review the medication list. — Serum digoxin levels can be checked (therapeutic range ~0.5–2 ng/mL) if toxicity is suspected or if the child is not responding as expected.

Upper airway obstructions (croup and epiglottitis) present with stridor and potential for rapid airway compromise. While croup is usually self-limiting and managed conservatively, epiglottitis is a medical emergency requiring airway expertise and antibiotics. Distinguishing between them is critical for appropriate triage and intervention. **CROUP (Laryngotracheobronchitis)** Pathophysiology: Viral inflammation of the larynx and trachea, causing subglottic edema and narrowing. Most common causative agent: **Parainfluenza virus type 1** (responsible for ~80% of cases); also adenovirus, influenza, RSV. Age most commonly affected: **6 months to 3 years**, with peak at 12–24 months. Seasonal: Most common in autumn and winter. Clinical presentation — Classic Triad: 1. **Barking or seal-like cough** — distinctive, often described by parents as a seal's bark; the cough is dry initially, may become productive. 2. **Inspiratory stridor** — musical, high-pitched breathing sound heard on inspiration (upper airway narrowing); may be absent at rest but prominent when the child cries or is agitated. 3. **Hoarseness or dysphonia** — voice sounds hoarse due to vocal cord inflammation. Other findings: — Mild to moderate fever (usually <39°C) — Symptoms often **worse at night** — chill air in the bedroom may worsen stridor; parents often report waking the child with severe stridor (parent was sleeping; cool night air and lying down worsen symptoms) — Mild respiratory distress (retractions, nasal flaring) in mild-to-moderate cases; severe cases may have significant retractions and hypoxemia — The child may appear alert and playful between episodes of coughing — Prodrome: Often 1–2 days of upper respiratory infection symptoms (cough, congestion) before the characteristic croup cough develops Chest X-ray (if obtained to rule out other diagnoses): — **"Steeple sign"** — narrowing of the subglottic trachea, creating a narrowed column of air instead of the normal wider subglottic space. The steeple sign is characteristic but not pathognomonic (also seen in epiglottitis and laryngeal papillomatosis). Nursing assessment: — Observe the child in a non-threatening position; do not force the child to lie down or perform invasive procedures, as agitation worsens obstruction. — Assess stridor at rest vs. with agitation; if stridor is only present with agitation, the croup is mild; if present at rest, it suggests moderate-to-severe croup. — Monitor respiratory rate, effort (retractions), oxygen saturation, and mental status. — Assess hydration status — the child may refuse fluids due to sore throat or may lose fluid through increased insensible losses from tachypnea and fever. Management — Supportive Care is Primary: 1. **Cool humidified air (mist therapy):** — Cool moisture reduces subglottic edema and soothes the inflamed airway. — Methods: **Croup tent** (cool mist generated over the child), **humidifier at the bedside**, or **taking the child outside into cool night air** (surprisingly effective; parents often report sudden improvement when a child with night-time croup is taken outside). — Cool mist is more effective than warm steam (contrary to older practices). — Administer for 20–30 minutes at a time; can be repeated as needed. — Ensure child is hydrated (inhaling mist may dry secretions; encourage sips of water or cool fluids). 2. **Oxygen:** — Administer if oxygen saturation <90% or if signs of respiratory distress are present. — Deliver humidified oxygen (cool, not hot) to prevent further airway drying. — Avoid agitating the child by forcing oxygen administration; allow the child to hold the mask or tubing if possible. 3. **Medications:** a) **Nebulised Racemic Epinephrine (L-epinephrine):** — Vasoconstrictor that reduces airway mucosal edema. — Indicated for croup with **stridor at rest** (moderate-to-severe croup) or significant respiratory distress. — Dosing: **0.05 mL/kg of 2.25% solution (max 0.5 mL) in 3 mL normal saline**, nebulised over 10–15 minutes. — **Onset:** Relief within 10–15 minutes; effects last 2–6 hours. — **Rebound phenomenon:** Some children may have recurrence of symptoms 1–2 hours after epinephrine wears off. Monitor for this; if stridor returns, the dose can be repeated or the child admitted for observation. — **Caution:** Epinephrine can cause tachycardia, tremor, and anxiety; monitor heart rate. Avoid in children with significant cardiac disease. — Not used for mild croup (only cool mist needed). b) **Corticosteroids (Dexamethasone):** — Reduces airway inflammation and edema over hours. — Dosing: **Single dose of 0.6 mg/kg** (max 10 mg) IM or IV, or given orally. — **Onset:** Slower than epinephrine (takes 30 min–2 hours), but effects last 12–24 hours. — Indicated for **moderate-to-severe croup or any croup requiring nebulised epinephrine**. — Evidence supports routine use in moderate-to-severe croup; many guidelines now recommend a single dose of dexamethasone for any croup with stridor at rest. — **Combination therapy:** Dexamethasone + nebulised epinephrine is used for moderate-to-severe cases. 4. **Fluids and feeding:** — Encourage oral fluids and soft foods; the child may have a sore throat. — Avoid spicy, hot, or irritating foods. — Maintain hydration to keep secretions thin. 5. **Keep the child calm:** — **Agitation and crying increase airway resistance and worsen stridor.** This is crucial: the child who is crying loudly may have MORE stridor, not because the condition is worsening, but because agitation worsens the obstruction. — Encourage the parent to stay with the child; allow comfort items (toy, blanket). — Minimize unnecessary procedures or interventions. — Do NOT perform throat examination with a tongue depressor (unlike epiglottitis, this is less concerning, but unnecessary agitation should still be avoided). **Disposition:** — **Most cases of croup are managed at home** with cool mist and fluids; parents are advised to use a humidifier at night, take the child outside in cool air if stridor worsens, and return if stridor develops at rest, feeding becomes difficult, or the child becomes lethargic. — **Hospital admission** is considered if: — Stridor at rest that does not respond to initial nebulised epinephrine and dexamethasone. — Respiratory distress with retractions or hypoxemia. — Inability to maintain hydration. — Toxic appearance or altered mental status. — Immunocompromised child (higher risk of severe disease). **Home care teaching for parents:** — Use a humidifier in the child's room at night. — If acute stridor develops at night, take the child outside into cool air for 10–15 minutes; often, the stridor resolves, and the child can return to sleep. — Keep the child calm; avoid making a big fuss, which escalates crying and stridor. — Ensure adequate fluid intake; offer water, juice, or popsicles. — Fever management: Acetaminophen or ibuprofen as directed; fever itself does not worsen the condition, but the child may be more comfortable. — Return immediately if: the child develops significant difficulty breathing, seems lethargic, has a high fever with drooling or difficulty swallowing (concerning for another diagnosis), or stridor does not improve over 48–72 hours. --- **EPIGLOTTITIS — AIRWAY EMERGENCY** Pathophysiology: Acute bacterial inflammation of the epiglottis and surrounding structures (aryepiglottic folds), causing rapid onset of stridor and airway obstruction. The epiglottis is located at the base of the tongue and normally covers the larynx during swallowing; when inflamed and swollen, it can completely obstruct the airway. Causative agent: Classically **Haemophilus influenzae type b (Hib)**, but now less common in countries with routine Hib vaccination (such as the Philippines, where Hib vaccine is part of the immunisation schedule). Other organisms: Group A Streptococcus, Staphylococcus aureus (including MRSA), pneumococcus. Age: Can occur at any age but classically **school-age children (3–7 years)**. Much rarer in the post-Hib vaccine era in developed countries, but remains a concern in unvaccinated or incompletely vaccinated populations. **Clinical Presentation — The Classic "4 D's" (Must Know for NLE):** 1. **Drooling** — Copious saliva; the child cannot swallow secretions due to throat pain and potential airway obstruction if the child swallows. 2. **Dysphagia** (difficulty swallowing) — Refuses to eat or drink; swallowing is extremely painful. 3. **Dysphonia** — Muffled or "hot potato" voice (sounds like the child is holding a hot potato in the mouth); voice is thick and unclear, not the hoarse voice of croup. 4. **Distress** — Acute, severe respiratory distress; the child is noticeably ill and toxic-appearing. **Additional critical signs:** — **Tripod or sniffing position** — The child sits upright, leaning forward, with neck extended (trying to keep the airway as open as possible). This is a sign of severe upper airway obstruction. — **High fever** (often >39.5°C or >103°F) — **Rapid onset** — Unlike croup, which has a prodrome of URI symptoms, epiglottitis comes on acutely, often within hours. — **Toxic appearance** — The child looks very ill; pale, listless, or anxious depending on oxygenation. — **Absence of cough** — Unlike croup (which has a barking cough), epiglottitis is NOT accompanied by a significant cough. — **Inspiratory AND expiratory stridor** (biphasic stridor) — Due to the fixed obstruction from a swollen epiglottis. Chest X-ray (if obtained): — **"Thumb sign"** — The enlarged epiglottis appears as a thick, thumb-shaped soft tissue shadow at the base of the tongue on a lateral neck X-ray. — Subglottic narrowing may also be present. **Critical Nursing Principle: DO NOT AGITATE THE CHILD; DO NOT EXAMINE THE THROAT** This cannot be overstressed. An agitated child will cry, strain, and increase intrathoracic pressure, which can precipitate **sudden, complete laryngospasm and total airway obstruction.** Some of the most tragic cases of epiglottitis have occurred when a nurse or physician examined the child's throat with a tongue depressor, triggering complete obstruction and necessitating emergency intubation/tracheostomy under dire circumstances. **What NOT to do:** — **Do NOT use a tongue depressor to visualise the throat.** — **Do NOT take a throat culture or swab.** — **Do NOT lay the child down (unless preparing for intubation).** — **Do NOT force the child to drink or eat.** — **Do NOT separate the child from the parent if the parent is keeping the child calm.** **Immediate nursing management:** 1. **Keep the child calm and upright:** — Position the child sitting upright or in the tripod position. — Allow the parent or carer to remain with the child; the child's anxiety increases intrathoracic pressure and can precipitate obstruction. — Do not force the child into a supine position or perform invasive procedures. — Speak softly; avoid sudden movements or loud noises. — Allow the child to drool (do NOT insist on swallowing); place a towel under the child if needed. 2. **Prepare for emergency airway management:** — **Notify the physician immediately.** This is an airway emergency. — Ensure suction equipment is at the bedside. — Have **emergency airway equipment available**: laryngoscopes, endotracheal tubes of multiple sizes, manual resuscitation bag, oxygen. — **Prepare for possible intubation or tracheostomy.** In severe cases, the epiglottis may be so swollen that even an experienced anaesthetist will have difficulty intubating, and an emergency surgical airway (tracheostomy) may be needed. — Notify anaesthesia or ENT (ear, nose, throat) specialist immediately. 3. **Administer oxygen:** — Humidified oxygen should be available and administered cautiously. — Do not force oxygen administration; if the child will not tolerate a mask, allow the child to breathe oxygen-enriched air passively (e.g., oxygen held near the face). — High-flow oxygen via non-rebreather mask is ideal if the child tolerates it. 4. **Establish IV access (if possible without agitating the child):** — Secure IV access for fluid administration and medication (antibiotics, corticosteroids). — If IV access is difficult to obtain, do NOT pursue it aggressively in a critically ill child; focus on airway. 5. **Avoid examination and diagnostic procedures that agitate the child:** — Lateral neck X-ray may be obtained to confirm diagnosis, but only if it does NOT delay intubation. — Blood cultures and throat culture should NOT be obtained (risk of agitation and airway obstruction); diagnosis is clinical. 6. **Administer antibiotics (after airway is secure):** — Once the airway is secured (intubated) or the child is stable, initiate **broad-spectrum IV antibiotics** covering Hib, streptococci, and staphylococci: — **Ceftriaxone 50–80 mg/kg/day** (divided into 2–4 doses) OR — **Ampicillin + gentamicin** (for Hib coverage when cephalosporin allergy) — Plus **rifampin** (for improved epiglottic penetration) in some protocols. — Antibiotic course typically 7–10 days; repeat blood culture after 48 hours of antibiotics to ensure eradication. 7. **Supportive care:** — Once intubated or airway is secure, the child will be in the ICU on mechanical ventilation for 24–72 hours until the epiglottitis resolves and the child can be extubated. — NPO (nothing by mouth) until airway is secure and extubated. — Maintain sedation if intubated; manage anxiety and discomfort. — Monitor vital signs closely; watch for signs of sepsis. — Once extubated, gradually introduce fluids and soft foods as tolerated. **Parent/Family Communication:** — Epiglottitis is frightening for parents; they have often brought the child to the hospital with what seemed like a sore throat, and now the child is on a ventilator. — Explain that **quick action and securing the airway has prevented a tragedy; with antibiotics, the prognosis is excellent.** — Explain the intubation is temporary, usually 24–72 hours. — Allow parents to visit in the ICU; their presence is calming once the child is sedated and stable. — Discuss the importance of **Hib vaccination for siblings and contacts** to prevent future cases. **Outcome:** With prompt airway management and antibiotics, mortality has dropped from ~30% (pre-antibiotic era) to <5% in developed settings. However, any delay in recognition or airway management can be fatal; missed or delayed diagnosis remains a significant contributor to epiglottitis-related deaths. **Prevention:** — **Haemophilus influenzae type b (Hib) vaccination is the key.** The Hib vaccine, part of the routine childhood immunisation schedule in the Philippines, has made epiglottitis rare in vaccinated populations. — Ensure all children receive the Hib vaccine series (at 6, 10, and 14 weeks of age, or as per current PRC/DOH schedule). — Check vaccination status in all children with epiglottitis; unvaccinated or incompletely vaccinated children are at risk. **Croup vs. Epiglottitis — Quick Comparison Table (High-Yield for NLE):** | Feature | Croup | Epiglottitis | |---------|-------|---------------| | Cause | Viral (parainfluenza) | Bacterial (Hib, streptococci, staphylococci) | | Onset | Gradual (URI prodrome 1–2 days) | Acute (hours) | | Age | 6 months–3 years (peak 1–2 yr) | School-age (3–7 years), but any age | | Appearance | Alert, playful between coughing episodes | Toxic, ill-appearing; tripod position | | Fever | Mild-moderate | High (>39.5°C) | | Cough | Barking, seal-like | Absent or minimal | | Voice | Hoarse | Muffled, "hot potato" | | Drooling | Absent | Copious | | Stridor | Inspiratory (at rest or with agitation) | Biphasic or inspiratory (at rest, fixed) | | X-ray | Steeple sign (subglottic narrowing) | Thumb sign (enlarged epiglottis) | | Throat exam | Safe; not recommended but not dangerous | **CONTRAINDICATED — risk of complete obstruction** | | Management | Cool mist, racemic epinephrine, dexamethasone, supportive care | **Airway management (intubation/tracheostomy), IV antibiotics, ICU care** | | Disposition | Mostly home; some hospital admission | **ALWAYS ICU admission** |

Lower airway diseases (bronchiolitis and asthma) present with wheezing, tachypnea, and respiratory distress due to bronchial/bronchiolar narrowing and obstruction. While bronchiolitis is primarily a viral illness in infants with supportive management, asthma is a chronic inflammatory disease requiring controller and reliever medications. Understanding the distinction and appropriate pharmacological interventions is essential for NLE and clinical practice. **BRONCHIOLITIS (Respiratory Syncytial Virus — RSV)** Pathophysiology: Viral inflammation of the bronchioles (small airways) with bronchiolar edema, mucus plugging, and bronchospasm. Mucus-plugged bronchioles create air trapping and atelectasis (collapse of distal alveoli), leading to ventilation-perfusion (V/Q) mismatch and hypoxemia. Causative agent: **Respiratory Syncytial Virus (RSV)** is the most common; also parainfluenza, influenza, adenovirus, metapneumovirus. Age most affected: **Infants <2 years; peak incidence 2–6 months.** Infants are uniquely vulnerable because their airways are smallest and mucus plugging has the most impact; their collateral ventilation is immature (cannot bypass plugged airways as well). Seasonal: Winter months (Northern Hemisphere: November–March; varies by geography). Prodrome: 3–5 days of upper respiratory infection symptoms (congestion, sneezing, cough, low-grade fever) followed by **lower respiratory signs.** **Clinical Presentation:** — **Persistent cough** (often worse at night or with feeds) — **Wheezing and/or crackles** on auscultation (wheezing indicates bronchiolar obstruction; crackles indicate secretions in smaller airways) — **Tachypnea** (often >60/min) — **Intercostal and subcostal retractions** (indicates increased work of breathing) — **Nasal flaring** (accessory muscle use) — **Feeding difficulty** — infants tire quickly when trying to breathe and feed simultaneously — **Copious nasal secretions** (often green or cloudy) — **Low oxygen saturation** (may drop to 85–92% or lower, especially with exertion) — **Apnea** — in severe cases or in very young infants (<3 months), prolonged apnea may occur, particularly during sleep or feeding — **Fever** — usually low-grade (if high fever, consider bacterial superinfection or other diagnosis) — **Lethargy or poor feeding** — signs of significant hypoxemia or fatigue Chest X-ray findings (if obtained): — **Hyperinflation** — overinflated lungs due to air trapping — **Atelectasis** — patchy areas of collapsed lung — **Peribronchial thickening** — inflammation of the bronchiolar walls — **Bronchial wall thickening** Laboratory: — RSV is diagnosed by **rapid RSV antigen test (nasal wash/swab), RT-PCR, or viral culture.** The rapid antigen test is commonly used in clinical settings for quick diagnosis. — **Chest X-ray is NOT routinely needed** if diagnosis is clinically clear (to avoid radiation exposure). **Critical Infection Control: RSV is HIGHLY CONTAGIOUS** RSV is transmitted by **droplet and contact precautions**: — **Droplet precautions:** RSV is spread by respiratory droplets; droplet isolation should be used (door can be open; no special air handling needed). — **Contact precautions:** RSV survives on surfaces and can be transmitted by touching contaminated surfaces then touching the face; hand hygiene is critical. — **Cohort or private room:** Ideally, RSV-positive infants are placed in a private room or cohorted with other RSV-positive patients. — **Hand hygiene:** Hand washing (soap and water, not alcohol-based hand rub which is less effective against RSV) is essential before and after patient contact, and after contact with respiratory secretions. — **Gown and gloves:** For direct care involving contact with secretions. — **Respiratory hygiene:** Cover coughs/sneezes; dispose of tissues appropriately. — **Restrict visitors:** Siblings, especially young children who may be shedding RSV, should be restricted from visits (to protect the RSV-positive infant and also to prevent spread of RSV to other patients). Nursing priorities for infection control in bronchiolitis: — This is a **Maslow-level priority** — infection control (safety) must be implemented rigorously to prevent nosocomial spread. RSV in an neonatal ICU can spread to vulnerable premature infants, causing severe disease or death. — Ensure all staff and visitors understand droplet/contact precautions. — Hand wash before and after each contact; educate parents and siblings on hand hygiene. — Designate equipment (stethoscope, pulse oximeter) for this infant; do not share devices between patients without disinfection. **Management — Supportive Care is Primary** 1. **Airway clearance — Gentle suctioning:** — **Bulb syringe suctioning** of the nose (not deep into the nasopharynx) to clear secretions and improve air entry. Vigorous deep suctioning can cause airway trauma and bronchospasm; use gentle pressure. — **Nasal saline drops or spray** before suctioning to loosen secretions. — **Limit suctioning frequency** — suction only as needed to maintain airway patency, not routinely every few hours (excessive suctioning can damage mucosa and increase inflammation). — **Position the infant** upright or semi-upright to facilitate drainage of secretions and ease breathing. — Avoid **deep endotracheal suctioning unless intubated**; the infant's own cough should be allowed to clear secretions. 2. **Oxygenation:** — Administer **humidified oxygen** to maintain SpO2 ≥90–95%. — Oxygen delivery method depends on severity: nasal cannula for mild-moderate hypoxemia; non-rebreather mask for severe hypoxemia; mechanical ventilation if the infant fails to oxygenate or develops apnea. — Humidification is important; dry oxygen can further irritate airways and thicken secretions. 3. **Hydration:** — **Feeding difficulty** is common; assess feeding ability and offer small, frequent feeds. — Many infants with severe bronchiolitis are **NPO (nothing by mouth) and given IV fluids** to avoid aspiration risk and to conserve energy. — IV hydration: **Maintenance fluids (~100–150 mL/kg/day for infants) minus any oral intake.** — Monitor urine output (should be ~1–2 mL/kg/hour for infants); output <1 mL/kg/hour suggests inadequate hydration. — Avoid overhydration, which can worsen pulmonary oedema in infants with respiratory distress. 4. **Medications:** — **Supportive care is the mainstay; there is no specific antiviral treatment for RSV bronchiolitis.** — **Bronchodilators (salbutamol/albuterol):** May be used in infants with **audible wheezing**, though evidence for efficacy is mixed. If administered, observe for improvement in work of breathing and oxygen saturation. Some infants may not respond, and some may have paradoxical bronchospasm. — **Corticosteroids:** Generally **NOT recommended** for routine bronchiolitis; evidence does not support routine use. May be considered in infants with recurrent wheezing (suggesting reactive airway disease) or atopy. — **Antibiotics:** **NOT used for uncomplicated viral bronchiolitis.** Antibiotics are only given if there is evidence of bacterial superinfection (purulent sputum, focal infiltrate on chest X-ray, clinical deterioration). — **Ribavirin:** An antiviral previously used for severely immunocompromised infants with RSV; rarely used today due to cost and teratogenicity concerns. 5. **Supportive measures:** — **Cool mist** or humidified air: May soothe airway irritation (similar to croup management). — **Cluster care:** Minimize handling and procedures to reduce oxygen demand; schedule assessments, feeds, and care together, with long rest periods between clusters. — **Positioning:** Head elevated 30–45 degrees to ease breathing; prone positioning may be used if not contraindicated (though some institutions avoid prone due to risk of sudden infant death syndrome — SIDS — concerns; use institutional protocols). — **Monitoring:** Continuous pulse oximetry or frequent oxygen saturation checks; monitor respiratory rate, effort, and mental status; assess feeding tolerance; monitor I&O and weight. 6. **Mechanical ventilation (if needed):** — For infants with **severe respiratory distress (RR >80/min, severe retractions), hypoxemia refractory to oxygen, apnea, or altered mental status**, intubation and mechanical ventilation are indicated. — Ventilatory support allows the infant's respiratory muscles to rest; sedation and sometimes paralysis may be used. — Duration of mechanical ventilation varies; some infants may need only a few days, while severely affected infants may require weeks. — Complications of mechanical ventilation in bronchiolitis include **barotrauma (pneumothorax), volutrauma, ventilator-associated pneumonia (VAP), and subglottic stenosis** (from prolonged intubation). **Palivizumab — Important for Prophylaxis (NOT Treatment)** **Palivizumab is a monoclonal antibody against RSV.** It is used for **PROPHYLAXIS (prevention) of RSV in HIGH-RISK infants during RSV season**, NOT for treatment of acute bronchiolitis. Indications for palivizumab prophylaxis: — **Premature infants:** Born ≤32 weeks gestation; given monthly during RSV season (typically November–April in the Northern Hemisphere) for up to 5 doses. — **Chronic lung disease (bronchopulmonary dysplasia — BPD):** Premature infants with BPD who still require supplemental oxygen or respiratory support. — **Congenital heart disease:** Infants with haemodynamically significant CHD. — **Immunocompromised infants:** Those with primary or acquired immunodeficiency. — **Down syndrome:** Some guidelines recommend palivizumab for Down syndrome infants. Dosing: **15 mg/kg IM (intramuscularly) once monthly** during RSV season. Mechanism: Palivizumab binds to RSV surface protein (F protein) and prevents viral entry into respiratory epithelial cells; it does **NOT** kill RSV or enhance immune clearance of established infection. It reduces the risk of severe RSV infection requiring hospitalization by ~50% in high-risk groups. **Palivizumab DOES NOT treat acute bronchiolitis.** If a high-risk infant receiving palivizumab develops RSV bronchiolitis despite prophylaxis, management is still supportive care; palivizumab does not improve outcomes in established disease. **Parent/Family Education for Bronchiolitis:** — Explain that RSV is a common, usually self-limiting viral infection; most infants recover completely within 1–2 weeks, though cough may persist for weeks. — Emphasize infection control: hand washing, avoiding sick contacts, keeping the infant away from older siblings with URI, and breast-feeding (if possible, provides some passive immunity). — Teach feeding strategies: small frequent feeds; monitor for poor feeding or refusal (sign the infant is tiring). — Signs to seek immediate care: difficulty breathing, stridor, not feeding, lethargy, blue lips/tongue (cyanosis), or apnea. — Medications at home: Continue any prescribed bronchodilators; explain that these are to ease breathing but may not completely resolve the wheezing. --- **ASTHMA IN CHILDREN** Pathophysiology: **Chronic inflammatory disease of the airways** characterized by reversible airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. The pathophysiology involves: — **Bronchospasm** — contraction of bronchial smooth muscle, narrowing the airway lumen. — **Mucosal edema** — inflammation and swelling of the airway lining, further narrowing the lumen. — **Mucus hypersecretion** — excessive mucus production, plugging airways. These three mechanisms combine to reduce airflow, especially during expiration (air trapping), leading to wheezing, dyspnea, and hypoxemia. Triggers for asthma exacerbations (CRITICAL for parent education): — **Allergens:** Dust mites, pet dander, pollen, mold. — **Infections:** Viral upper respiratory infections (most common trigger in children), bacterial infection. — **Environmental irritants:** Smoke, air pollution, strong odours, cold air. — **Exercise:** Exercise-induced asthma; particularly with cold, dry air. — **Emotional stress:** Stress, anxiety, laughing, crying. — **Medications:** Aspirin, NSAIDs, beta-blockers (rare in children). — **Reflux:** Gastro-oesophageal reflux can trigger asthma in some children. **Clinical Presentation of Asthma:** Mild intermittent asthma: — **Wheezing** (whistling sound from narrowed airways, typically **expiratory wheezing — heard as air flows out**; in severe obstruction, wheezing may be biphasic or silent) — **Cough** — often chronic, worse at night, with exercise, or with laughing/crying — **Shortness of breath** or dyspnea — **Chest tightness** (in older children who can describe it; young children may just say "chest hurt") — Symptoms intermittent, not daily Moderate-to-severe asthma exacerbation: — **Prominent wheezing** (or **silent chest — absence of audible wheeze with severe obstruction; the airways are so blocked that little air moves, producing no sound** — this is an **ominous sign** indicating severe obstruction and risk of respiratory failure) — **Marked tachypnea** (RR may be 60–80/min or higher) — **Intercostal and subcostal retractions** (increased work of breathing) — **Accessory muscle use** (neck muscles, abdominal muscles) — **Inability to speak full sentences** — dyspnea is so severe the child can only speak a few words before pausing to breathe — **Cyanosis** — if hypoxemia is severe — **Nasal flaring** (in younger children) — **Fatigue** — respiratory muscles are tiring — **Altered mental status** — if severe hypoxemia or hypercapnia Critical point: **A SILENT CHEST (no audible wheeze) in a child with asthma exacerbation is a SIGN OF SEVERE OBSTRUCTION and indicates risk of respiratory failure.** This is often missed because healthcare providers expect to hear wheezing in asthma; paradoxically, the most severe cases may be quiet. Any child with asthma presenting with respiratory distress and a silent chest requires immediate aggressive intervention (oxygen, nebulised beta-agonists, IV corticosteroids, and consideration of ICU admission). **Asthma Severity Classification (For Reference):** The Global Initiative for Asthma (GINA) and National Asthma Education and Prevention Program (NAEPP) classify asthma severity as: — **Intermittent:** Symptoms ≤2 days/week; nighttime awakenings ≤2 times/month — **Persistent mild:** Symptoms 3–4 days/week; nighttime awakenings 3–4 times/month — **Persistent moderate:** Symptoms most days; nighttime awakenings ≥1 time/week — **Persistent severe:** Symptoms throughout the day; nighttime awakenings often 7 times/week Severity determines treatment intensity (see below). **Asthma Medications — Critical for NLE** Asthma medications are divided into two categories: **1. RELIEVER (RESCUE/QUICK-RELIEF) MEDICATIONS:** Short-acting beta-2 agonists (SABA): — **Salbutamol (albuterol in the US)** is the primary SABA in paediatric asthma. — **Mechanism:** Beta-2 agonists cause smooth muscle relaxation in the bronchi, relieving bronchospasm rapidly (onset 5–15 minutes). — **Administration:** Typically **nebulised (inhaled mist) in young children; metered-dose inhalers (MDI) with a spacer in older children.** — **Dosing (nebulised salbutamol):** 0.15 mg/kg per dose (minimum 2.5 mg, maximum 5 mg) in 3 mL of saline; can be given every 20 minutes for 3 doses, then every 1–4 hours as needed. (Examples: 10 kg child = 1.5 mg per dose; 20 kg child = 3 mg per dose.) — **Side effects:** Tachycardia, tremor, jitteriness, hyperactivity (especially in young children), palpitations (in older children). — **Used for acute relief** of wheezing and dyspnea; also used **before exercise** in exercise-induced asthma. — **Important:** Reliever medications do NOT treat inflammation; they only relieve bronchospasm. A child who needs SABA more than twice per week (excluding pre-exercise use) should be on a controller medication. Other relief agents: — **Ipratropium bromide:** An anticholinergic that works synergistically with beta-2 agonists; often combined with salbutamol for nebulisation in moderate-to-severe exacerbations. — **Magnesium sulphate:** May be used IV in severe exacerbations not responding to initial therapy; mechanism unclear, possibly smooth muscle relaxant. — **Corticosteroids (oral/IV):** For acute exacerbations. See below. **2. CONTROLLER (PREVENTER/LONG-TERM MANAGEMENT) MEDICATIONS:** Inhaled corticosteroids (ICS): — **Examples:** Beclomethasone, fluticasone, budesonide, mometasone. — **Mechanism:** Reduce airway inflammation, mucosal edema, and mucus hypersecretion; also reduce bronchial hyperresponsiveness. — **Onset:** Slower than beta-agonists (takes 24–48 hours to see full effect); therefore, ICS are not used for acute relief. — **Role:** First-line **long-term control medication** for any asthma that is not purely intermittent (i.e., mild persistent or worse). — **Dosing:** Twice daily (morning and evening); child should use a spacer with the MDI. — **CRITICAL:** **Rinse the mouth and gargle with water after each ICS dose.** This is essential to prevent **oral thrush (candidiasis)**, which is a common side effect of ICS inhalation. The ICS particles can deposit on the oral mucosa, creating a environment for candida overgrowth. Rinsing immediately after use removes these particles. — **Spacer use:** A **spacer (or holding chamber)** is an essential device when using MDI in young children. The spacer attaches to the MDI and allows the child to inhale the medication over several breaths, improving drug delivery to the lungs (rather than depositing in the mouth/throat). This is **high-yield:** many NLE questions test whether nurses know that spacers improve MDI efficacy in children. — **Adherence:** ICS must be used regularly (daily), not just when the child has symptoms. Parents often mistakenly stop ICS when the child feels better, leading to rebound inflammation and exacerbations. Long-acting beta-2 agonists (LABA): — **Examples:** Salmeterol, formoterol. — **Onset:** Slower (12–24 hours) but longer-acting (12–24 hours), used for twice-daily dosing as maintenance therapy. — **Role:** Added to ICS in moderate-to-severe asthma not controlled by ICS alone. — **Important:** LABA should NEVER be used as monotherapy; they must always be combined with ICS (risk of asthma deaths with LABA monotherapy). Leukotriene modifiers: — **Examples:** Montelukast, zafirlukast. — **Mechanism:** Block leukotriene receptors, reducing inflammation. — **Role:** Alternative controller (especially useful for exercise-induced asthma or asthma with allergic rhinitis). Can be oral (easier for children than inhalers). — **Onset:** Takes days to weeks. Mast cell stabilisers: — **Sodium cromoglicate, nedocromil.** — **Role:** Prevent asthma symptoms; often used prophylactically before exercise in exercise-induced asthma. — **Less commonly used today** due to inconvenient dosing (4 times daily). **Asthma Action Plan — Critical Parent Education Tool** An **asthma action plan (or written asthma action plan)** is a personalized guide for managing the child's asthma. It should include: 1. **Green Zone (Well-controlled asthma):** — No symptoms, normal activity, normal sleep. — **Action:** Continue maintenance controller medications (e.g., daily ICS). 2. **Yellow Zone (Caution — early symptoms):** — Mild wheezing, cough, or dyspnea; mild retractions. — **Action:** Use reliever (SABA) every 4–6 hours; increase monitoring; contact the doctor if not improving within 24 hours. 3. **Red Zone (Medical emergency):** — Severe dyspnea, continuous wheezing, inability to speak, retractions, cyanosis. — **Action:** Use reliever (SABA) immediately; call emergency services/go to the nearest hospital; give oral/IV corticosteroids if prescribed for emergencies; do NOT delay care waiting for a doctor. **Nursing Management of Acute Asthma Exacerbation in Hospital** 1. **Immediate stabilisation:** — Position upright or semi-upright to ease breathing. — Administer **high-flow oxygen** to maintain SpO2 ≥90–95%; assess if pulse oximetry is available. — Establish IV access for medications and fluids. — Monitor continuously: respiratory rate, heart rate, oxygen saturation, work of breathing (retractions, nasal flaring). 2. **Medications for acute exacerbation:** a) **Nebulised salbutamol:** — Initial dose: 0.15 mg/kg (or 2.5–5 mg) in 3 mL saline, nebulised over 5–15 minutes. — Can repeat every 20 minutes × 3 doses ("back-to-back" nebulisations for severe exacerbations), then every 1–4 hours as needed. — Monitor heart rate and clinical response; if no improvement after 3 back-to-back doses, the child likely needs IV therapy. b) **Ipratropium bromide (anticholinergic):** — 0.25–0.5 mg mixed with salbutamol in the nebuliser. — Synergistic effect with beta-agonists; may improve response in moderate-to-severe exacerbations. c) **Corticosteroids (systemic):** — **Oral prednisolone/prednisone:** First-line for mild-to-moderate exacerbations. Dose: **1–2 mg/kg** (max 50–60 mg) once daily for 5–7 days (or 3–5 days), with or without a taper. — **IV methylprednisolone or hydrocortisone:** For severe exacerbations or inability to take oral medication. Methylprednisolone 1–2 mg/kg IV every 6 hours for acute phase. — Onset: 4–6 hours; reduces inflammation and airway edema. — Reduces risk of relapse and return visits to the ED. d) **Magnesium sulphate:** — 25–50 mg/kg IV (max 2 g) over 10–20 minutes. — Used in **severe exacerbations not responding to initial SABA + steroids**; smooth muscle relaxant effect. e) **IV salbutamol (Continuous terbutaline infusion):** — Used in **life-threatening asthma** (severe distress, silent chest, altered mental status, not responding to nebulised therapy). — Initial bolus: 0.01–0.15 mg/kg IV, then continuous infusion starting at 0.3–1 mcg/kg/min, titrated by clinical response and heart rate. — Risk: significant tachycardia, arrhythmias; requires ICU monitoring. 3. **Ventilatory support:** — If respiratory failure develops (RR >80, severe retractions, hypoxemia <85%, altered mental status, exhaustion), the child requires **intubation and mechanical ventilation.** — Ventilation in asthma is challenging: air trapping and high intrathoracic pressure can develop; permissive hypercapnia (allowing mild elevation of CO2) may be accepted to avoid excessive pressure. 4. **Monitoring and assessment:** — Assess response to treatment: Is the child's respiratory rate decreasing? Are retractions improving? Is oxygen saturation increasing? Is the child calmer/more alert? — Peak expiratory flow rate (PEFR) or FEV1 (forced expiratory volume in 1 second) can be measured in older children/adolescents to assess airflow; values <50% of predicted indicate severe obstruction. — Serial blood gases may be needed in severe cases; normal or elevated CO2 in a tachypnoeic child indicates severe obstruction and impending respiratory failure. 5. **Avoid triggers and irritants:** — Keep the room cool and quiet; avoid agitation. — Encourage slow, deep breathing; some children respond to pursed-lip breathing (breathing out slowly against pursed lips to maintain airway pressure). — Provide comfort; hold/comfort the child as appropriate. 6. **Discharge planning and parent education:** — **Trigger identification and avoidance:** Identify the child's specific triggers (smoke, dust, pets, exercise, viral infections, emotions) and teach avoidance strategies. — **Medication adherence:** Explain the difference between reliever (used for acute symptoms) and controller (used daily for prevention). Many parents stop ICS when the child feels better; reinforce that ICS must be used continuously, even when the child has no symptoms. — **Spacer technique:** Demonstrate proper MDI + spacer technique; incorrect technique wastes medication. — **Asthma action plan:** Provide a written plan with green/yellow/red zones and specific actions for each. — **Monitoring:** Teach parents to monitor for symptoms and to keep a symptom diary if the child has frequent exacerbations. — **Emergencies:** When to call the doctor vs. when to go to the emergency department. — **Avoid aspirin and NSAIDs** in some asthmatics (aspirin-sensitive asthma is a subset; NSAIDs can trigger exacerbations). — **Vaccinations:** Ensure the child receives annual influenza vaccine and pneumococcal vaccine; respiratory infections are common asthma triggers.