Learn — Respiratory & cardiac conditions

15 notes · 56 questions on the topic

Cystic fibrosis

Cystic fibrosis is an autosomal recessive disease of the CFTR chloride channel on chromosome 7 in which every exocrine secretion becomes thick and sticky, so the airways clog and become chronically infected while the pancreatic ducts block and stop delivering digestive enzymes. It is uncommon in India but under-diagnosed rather than absent, and it is the standard answer to a child with recurrent pneumonia, bulky greasy stools and failure to thrive despite a good appetite.

The commonest mutation worldwide is F508del, a deletion of phenylalanine at position 508; inheritance is autosomal recessive, so each pregnancy of two carriers carries a 25 percent risk.
Sweat chloride is the diagnostic test: 60 mmol/L or more is diagnostic, 30 to 59 mmol/L is intermediate and needs repeating with genetic testing, and under 30 mmol/L is normal.
Newborn screening where it exists uses immunoreactive trypsinogen on a heel-prick sample, followed by a second sample or mutation panel and then a confirmatory sweat test.
Meconium ileus in the first days of life, with failure to pass meconium and abdominal distension, occurs in about 10 to 20 percent and is often the presenting event.
Pancreatic insufficiency affects around 85 percent, giving steatorrhoea, a voracious appetite with poor weight gain, and deficiency of the fat-soluble vitamins A, D, E and K.
The lungs are colonised first by Staphylococcus aureus and Haemophilus influenzae and later by Pseudomonas aeruginosa, leading to bronchiectasis, clubbing, haemoptysis and nasal polyps.
Salt loss in sweat is heavy, so in Indian summer heat these children develop hyponatraemic, hypochloraemic dehydration with metabolic alkalosis and need extra dietary salt.
Management is daily airway clearance physiotherapy, nebulised bronchodilator, hypertonic saline or dornase alfa, prompt antibiotics for exacerbations, pancreatic enzyme replacement with every meal and snack, fat-soluble vitamin supplements, and a high-calorie high-fat high-salt diet rather than a fat-restricted one.
CFTR modulator drugs treat the underlying channel defect and are mutation-specific, so genotyping decides eligibility; almost all affected males are infertile from congenital bilateral absence of the vas deferens, although they are not sterile in the sense of absent sperm production.

Hypoxia signs

Hypoxia is a fall in oxygen delivery to the tissues below what their metabolism needs, and hypoxaemia is the low arterial oxygen content that usually causes it. In a child the signs appear in a fixed order — restlessness and fast breathing first, then tachycardia, then a falling conscious level, with cyanosis and bradycardia last — so a nurse who waits for a blue child has waited far too long.

The early signs are neurological and respiratory: restlessness, irritability, air hunger, fast breathing, nasal flaring, chest indrawing and grunting; the late signs are cyanosis, bradycardia, hypotension and a falling conscious level.
Fast breathing by the IMNCI age bands is 60 breaths a minute or more under 2 months, 50 or more from 2 to 12 months, and 40 or more from 12 months to 5 years; lower chest indrawing at any of those ages classifies the child as severe pneumonia and needs oxygen and referral.
Pulse oximetry is the bedside test: WHO advises starting oxygen when SpO2 is below 90 percent in room air and keeping it at 90 percent or above, while a child being actively resuscitated is held at 94 percent or above.
Cyanosis needs roughly 5 g/dL of reduced haemoglobin in the capillary blood, so a severely anaemic child can be dangerously hypoxic and still look pink, and a polycythaemic child looks blue at a much higher saturation.
Bradycardia is the pre-arrest sign in paediatrics: a heart rate under 60 a minute with poor perfusion, in a child who is already being oxygenated and ventilated, is the trigger for chest compressions, not for further observation.
Restlessness in a hypoxic child is a call for oxygen, never for a sedative; sedating or restraining that child, or laying a breathless child flat, is the classic examinable error.
The oximeter misleads in carbon monoxide poisoning (falsely high), in methaemoglobinaemia (it plateaus near 85 percent), and whenever the periphery is cold, shut down, moving or covered in nail polish, so a comfortable number in a shocked child is checked against the clinical picture.

Bag-valve-mask ventilation

Bag-valve-mask ventilation is the delivery of positive-pressure breaths through a face mask using a self-inflating bag, a flow-inflating bag or a T-piece resuscitator, and it is the core skill of neonatal and paediatric resuscitation. It matters because the commonest reason a resuscitation fails is not the absence of drugs but ineffective ventilation — a leaking mask, a blocked or badly positioned airway, or too little pressure.

The mask must cover the mouth, the nose and the tip of the chin, and must not press on the eyes or hang over the chin; a mask that is too large leaks at the orbit and a mask that is too small obstructs the nose.
The seal is made with the C-E grip — thumb and index finger form a C on the body of the mask, the remaining three fingers form an E along the bony mandible — and the fingers lift the jaw into the mask rather than pressing the mask down onto the face, which would close the airway.
The rate for a newborn is 40 to 60 breaths a minute, counted aloud as breathe-two-three; in a child with a pulse the rate is roughly 20 to 30 breaths a minute in infants and young children and lower in adolescents, and the volume is only as much as makes the chest rise gently.
Starting inflation pressure in a newborn is about 20 to 25 cm of water, with a pressure-release (pop-off) valve and ideally a manometer in circuit; the response that confirms effective ventilation is a rising heart rate first and chest rise second.
A self-inflating bag for a newborn holds about 240 mL, works without a gas source and is the workhorse of an Indian labour room, but it cannot deliver free-flow oxygen or CPAP reliably and needs an oxygen reservoir to give a high concentration; a flow-inflating bag or T-piece resuscitator can deliver PEEP and a set peak pressure but needs a compressed gas source.
When the chest does not rise, work through MR SOPA in order: Mask readjust and reseal, Reposition the head to neutral or sniffing, Suction the mouth then the nose, Open the mouth slightly, Pressure increase in steps, and Airway alternative meaning an endotracheal tube or laryngeal mask.
Over-vigorous squeezing causes pneumothorax and lung injury, and gastric distension from prolonged mask ventilation splints the diaphragm — pass an orogastric tube and leave it open when mask ventilation continues beyond a few minutes.
Cricoid pressure and routine deep pharyngeal suction are not recommended in the newborn, and suction is applied only to visible secretions that obstruct the airway, briefly, because deep suction causes vagal bradycardia and apnoea.

Cyanotic heart disease — 5 Ts

Cyanotic congenital heart disease is the group of malformations in which deoxygenated blood reaches the systemic circulation through a right-to-left shunt or a mixing lesion, so the child is blue despite normal lungs. The classic memory list is the 5 Ts — Tetralogy of Fallot, Transposition of the great arteries, Truncus arteriosus, Tricuspid atresia and Total anomalous pulmonary venous connection — and the reason the list matters is that a blue newborn who does not pink up on oxygen is a duct-dependent emergency, not a respiratory case.

The 5 Ts in order of the number of the malformed vessels is a workable memory hook: Truncus arteriosus (1 vessel), Transposition of the great arteries (2 vessels transposed), Tricuspid atresia (3 letters in tri), Tetralogy of Fallot (4 features) and Total anomalous pulmonary venous connection (5 words); Ebstein anomaly is the common addition to the list.
Transposition of the great arteries is the commonest cyanotic lesion to present in the first week of life, while Tetralogy of Fallot is the commonest cyanotic lesion overall and beyond infancy — this pair of facts is asked repeatedly and the two are easily confused.
Chest radiograph silhouettes are the classic single-line questions: boot-shaped heart (coeur en sabot) with reduced pulmonary vascularity in Tetralogy of Fallot, egg-on-side or egg-on-string with a narrow pedicle in transposition, snowman or figure-of-eight in supracardiac total anomalous pulmonary venous connection, and a huge box-shaped wall-to-wall heart in Ebstein anomaly.
The hyperoxia test separates cardiac from pulmonary cyanosis: after 100 percent oxygen for about 10 minutes, a post-ductal arterial oxygen tension that stays low (broadly under 100 mmHg) points to a cyanotic cardiac lesion, whereas lung disease usually shows a substantial rise.
Duct-dependent lesions deteriorate as the ductus arteriosus closes over the first days of life; prostaglandin E1 is infused to reopen and hold it open, commonly started around 0.05 to 0.1 microgram/kg/min and reduced to the lowest effective rate, as a bridge to surgery.
Prostaglandin E1 causes apnoea, hypotension, fever, flushing and jitteriness, so the baby is nursed on continuous monitoring with resuscitation equipment and intubation ready at the bedside, and the infusion is never stopped abruptly.
Chronic cyanosis produces clubbing, secondary polycythaemia with a raised haematocrit and hyperviscosity, relative iron deficiency, a risk of cerebral thrombosis when the child is dehydrated, brain abscess and infective endocarditis; these children need adequate hydration, iron when deficient and dental hygiene with endocarditis prophylaxis as advised.
Pulse oximetry screening of the newborn compares the right hand (pre-ductal) with either foot (post-ductal), and a low reading at either site or a persistent difference between the two is the trigger for an echocardiogram before discharge.

Patent ductus arteriosus (PDA)

The ductus arteriosus is the fetal vessel joining the pulmonary artery to the descending aorta, and it is patent when it fails to close after birth, producing a left-to-right shunt from aorta to pulmonary artery. It matters in two opposite ways: in a preterm baby a large duct floods the lungs and steals from the systemic circulation, while in a duct-dependent congenital lesion the same vessel is the only thing keeping the baby alive.

Functional closure normally occurs within 24 to 72 hours of birth in a term baby, with anatomic closure over the following 2 to 3 weeks, driven by the rise in oxygen tension and the fall in circulating prostaglandins; prematurity, hypoxia and high altitude delay it.
The classic signs are a continuous machinery murmur below the left clavicle, bounding pulses with a wide pulse pressure, a hyperactive precordium and, when the shunt is large, tachypnoea, poor feeding, failure to thrive and recurrent chest infections.
It is the lesion of the preterm baby with respiratory distress syndrome: a duct that reopens as the lung compliance improves shows up as a rising oxygen requirement, worsening apnoeas, a widened pulse pressure and difficulty weaning from support.
Congenital rubella syndrome is the classic association, along with prematurity and birth at high altitude; a maternal history of rash and fever in the first trimester, with cataract and deafness in the baby, is the examination hook.
Medical closure in the preterm uses a prostaglandin synthesis inhibitor — ibuprofen or indomethacin, with oral paracetamol as an alternative in some units — and it is withheld when there is renal impairment, active bleeding, thrombocytopenia or necrotising enterocolitis; fluid is restricted and diuretics are used for the pulmonary overload.
Definitive closure is by transcatheter device in most older children and by surgical ligation when the device route is unsuitable or the baby is very small, after which the murmur disappears and the pulse pressure narrows.
Untreated, a large duct causes pulmonary hypertension and eventually Eisenmenger physiology with shunt reversal, which produces differential cyanosis — blue clubbed toes with pink unclubbed fingers, because the desaturated blood enters the aorta beyond the origin of the arm vessels.
The opposite situation must never be forgotten: in transposition, pulmonary atresia, critical coarctation and hypoplastic left heart, closure of the duct is fatal, and prostaglandin E1 is given to keep it open until surgery.

Cyanosis — central vs peripheral

Cyanosis is the bluish discolouration of skin and mucous membranes that appears when the capillary blood contains about 5 g/dL or more of reduced haemoglobin. The distinction that decides the management is central versus peripheral: central cyanosis involves the warm mucous membranes and means the arterial blood itself is desaturated, while peripheral cyanosis spares the tongue and means the blood is simply flowing too slowly through cold or constricted extremities.

Central cyanosis is seen in the tongue, the buccal mucosa, the lips and the conjunctivae, with warm extremities, and it means arterial desaturation from a cardiac, respiratory or haemoglobin cause; peripheral cyanosis affects the hands, feet, nail beds and nose tip with cold extremities and a pink tongue, and it means poor perfusion, cold or vasoconstriction.
Cyanosis depends on the absolute amount of reduced haemoglobin, not the percentage saturation, so a severely anaemic child may never look blue however hypoxic, while a polycythaemic child with a high haemoglobin looks blue at a saturation that would not worry you in another child.
Acrocyanosis of the hands and feet with a pink trunk and tongue is normal in the first 24 to 48 hours of life and after cold exposure; it needs warming and reassurance, not oxygen and investigation.
The bedside separation in a newborn is oxygen: peripheral cyanosis and lung disease improve when oxygen is given, while cyanotic congenital heart disease does not, and the formal version is the hyperoxia test with 100 percent oxygen for about 10 minutes and a post-ductal blood gas.
Differential cyanosis, with blue lower limbs and pink upper limbs, indicates a right-to-left shunt through the ductus as in coarctation or persistent pulmonary hypertension; reverse differential cyanosis, with a blue upper body and pink legs, is the rare pattern of transposition with coarctation or pulmonary hypertension.
Methaemoglobinaemia is the trap: the child is blue with chocolate-brown blood that does not turn red on exposure to air, the oxygen tension on the blood gas is normal, the oximeter plateaus around the mid-80s and gives a saturation gap, oxygen does not help, and the antidote is methylene blue.
Newborn pulse oximetry screening compares a pre-ductal probe on the right hand with a post-ductal probe on either foot, and a low value at either site or a persistent difference between them prompts echocardiography before discharge.
In dark-skinned Indian children, cyanosis is looked for in the tongue, buccal mucosa, conjunctivae, palms and nail beds under natural light, because it is easily missed on the skin of the face and trunk.

Tetralogy of Fallot (TOF)

Tetralogy of Fallot is the combination of pulmonary (right ventricular outflow) stenosis, a ventricular septal defect, an aorta that overrides the septum and right ventricular hypertrophy, all arising from a single embryological error of anterior malalignment of the outflow septum. It is the commonest cyanotic congenital heart disease beyond infancy, and it is examined mainly through the hypercyanotic tet spell, which is a bedside emergency a nurse must be able to break.

The four components are pulmonary stenosis, ventricular septal defect, overriding aorta and right ventricular hypertrophy; the degree of pulmonary stenosis, not the size of the septal defect, decides how blue the child is, because it sets how much blood is shunted right to left.
The murmur is the pulmonary stenosis, not the septal defect — a harsh ejection systolic murmur in the left second and third intercostal spaces with a single second heart sound; paradoxically, the murmur becomes softer or disappears during a spell because almost no blood is crossing the outflow tract.
Squatting is the classic sign in an older child: it kinks the femoral arteries and raises systemic vascular resistance, which reduces the right-to-left shunt and pushes more blood through the lungs, and the knee-chest position is the infant equivalent used in treatment.
The chest radiograph shows a boot-shaped heart (coeur en sabot) with an uplifted apex, a concave pulmonary bay and reduced pulmonary vascular markings; a right-sided aortic arch is present in about a quarter of cases, and the electrocardiogram shows right axis deviation with right ventricular hypertrophy.
A tet spell is a sudden increase in right-to-left shunting, typically on waking, after crying, feeding or straining: the child becomes deeply cyanosed, hyperpnoeic and irritable, then limp, and may have a syncope or seizure; untreated spells cause hypoxic brain injury and death.
The nursing sequence in a spell is knee-chest position (or holding the infant over the shoulder with the knees drawn up), calm quiet handling, oxygen, and then the medical steps of morphine to abolish the hyperpnoea, an intravenous fluid bolus to raise preload, sodium bicarbonate for acidosis, and a vasoconstrictor such as phenylephrine or beta blockade with propranolol to relax the infundibular spasm.
Drugs that lower systemic vascular resistance make a spell worse and are contraindicated during it; propranolol is used orally between spells to reduce their frequency while awaiting surgery.
Complications of the unrepaired lesion are polycythaemia with hyperviscosity, relative iron-deficiency anaemia (which paradoxically increases spell risk), cerebral thrombosis when the child is dehydrated, brain abscess, infective endocarditis and growth failure; management is a modified Blalock-Taussig shunt for palliation when needed and complete intracardiac repair, usually within the first year of life.

Mitral stenosis

Mitral stenosis is narrowing of the mitral valve orifice that obstructs filling of the left ventricle, raising left atrial pressure and driving it back into the pulmonary circulation. In Indian children and young adults it is almost always rheumatic, following acute rheumatic fever, and the aggressive juvenile form can produce severe stenosis before the age of 20, which is why it sits in a paediatric syllabus at all.

The normal mitral valve area is about 4 to 6 square centimetres; symptoms on exertion appear once it falls below about 2, and severe stenosis is generally taken as an area of about 1 square centimetre or less, at which point the patient is breathless at rest.
Rheumatic fever is the cause in the overwhelming majority; it follows a group A streptococcal throat infection, is diagnosed on the revised Jones criteria, and the mitral valve is the valve most often damaged, followed by the aortic valve.
The murmur is a low-pitched rumbling mid-diastolic murmur with presystolic accentuation, best heard at the apex with the bell, in the left lateral position, on expiration; it is accompanied by a loud first heart sound and an opening snap, and a shorter interval between the second sound and the opening snap means tighter stenosis.
Symptoms are exertional dyspnoea progressing to orthopnoea and paroxysmal nocturnal dyspnoea, fatigue, haemoptysis from ruptured bronchial veins, palpitations from atrial fibrillation, and the malar flush of a low cardiac output; the left ventricle stays small, so the apex is tapping rather than displaced.
Left atrial enlargement leads to atrial fibrillation, and a fibrillating left atrium forms clot, so systemic embolism and stroke are the feared complications; anticoagulation with warfarin is standard once atrial fibrillation appears in rheumatic mitral stenosis.
Anything that shortens diastole worsens it — tachycardia, fever, exercise, anaemia, pregnancy and atrial fibrillation with a fast ventricular rate — so rate control with a beta blocker, treatment of anaemia and careful fluid management are the medical mainstays alongside diuretics for congestion.
Definitive treatment is percutaneous transvenous mitral commissurotomy (balloon valvotomy) for a pliable non-calcified valve with no left atrial clot and no significant mitral regurgitation, and open or closed surgical valvotomy or valve replacement when those conditions are not met.
Secondary prophylaxis prevents further attacks and further valve damage: benzathine penicillin G by deep intramuscular injection every 3 to 4 weeks, at 1.2 million units for a child over about 27 kg and 600,000 units below that, continued for years — longest, often into adult life, in those with established valve disease.

Coarctation of aorta

Coarctation of the aorta is a localised narrowing of the aorta, usually just beyond the origin of the left subclavian artery at the site of the ductus arteriosus, which obstructs flow to the lower half of the body. It matters because it is a treatable cause of hypertension in a child, it is missed whenever the femoral pulses are not felt, and in the critical infantile form the baby collapses in shock as the ductus closes.

The bedside diagnosis is made in the femoral pulses: they are weak, delayed or absent, with a palpable radio-femoral delay, and the arm blood pressure is higher than the leg blood pressure — the reverse of the normal relationship, where the leg pressure is the higher of the two.
Four-limb blood pressure is the confirming measurement, and a systolic gradient of more than about 20 mmHg between the upper and lower limbs is significant; the same measurement is the reason every child found to be hypertensive must have the femoral pulses felt.
The child presents with upper limb hypertension, headache, epistaxis, cold legs, leg pain on exercise (claudication) and a systolic murmur heard between the shoulder blades in the interscapular area.
The classic radiographic signs are notching of the undersurfaces of the posterior third to eighth ribs from dilated collateral intercostal arteries, which takes years of collateral growth and so is not seen in infants, and the figure-of-3 sign at the coarctation site on the aortic shadow.
The commonest association is a bicuspid aortic valve; Turner syndrome, ventricular septal defect, patent ductus arteriosus and berry aneurysms of the circle of Willis are the others, so a short girl with webbed neck, widely spaced nipples and absent femoral pulses is Turner syndrome until proved otherwise.
Critical coarctation in the newborn is duct-dependent for the lower body: as the ductus closes in the first days or weeks, the baby presents with shock, poor feeding, acidosis, absent femoral pulses and renal failure, and prostaglandin E1 must be started to reopen the duct as a bridge to surgery.
Definitive treatment is surgical — resection with end-to-end anastomosis, or subclavian flap aortoplasty in infants — with balloon angioplasty and stenting used for older children and for re-coarctation.
After repair, watch for paradoxical hypertension in the first days, for mesenteric arteritis presenting as abdominal pain and distension, and in the long term for residual or recurrent hypertension, so blood pressure follow-up continues for life even after a technically perfect repair.

Normal respiratory rate by age

The respiratory rate in a child is counted over a full 60 seconds while the child is quiet or asleep and before any disturbing procedure, because a child's breathing is irregular and a 15-second count multiplied by four is unreliable. It matters more than any other single number in paediatrics: fast breathing is the most sensitive sign of pneumonia in a child, and in primary care the WHO cut-offs decide who gets an antibiotic and who is referred, without any radiograph or blood test.

Normal resting ranges per minute: newborn 30 to 60, infant 30 to 50, toddler 24 to 40, preschool child 22 to 34, school-age child 18 to 30, and adolescent 12 to 20. The rate falls steadily with age as tidal volume rises.
The WHO and Integrated Management of Neonatal and Childhood Illness cut-offs for FAST BREATHING are age-banded and must be memorised exactly: 60 per minute or more under 2 months, 50 per minute or more from 2 to 12 months, and 40 per minute or more from 12 months to 5 years.
Under the current WHO classification, a child with cough or difficult breathing plus fast breathing OR chest indrawing is classified as pneumonia and treated at home with oral amoxicillin (dispersible tablets) twice daily for 5 days; severe pneumonia requiring urgent referral is defined by a general danger sign, stridor in a calm child, central cyanosis, or oxygen saturation below 90%.
General danger signs that mean referral whatever the respiratory rate: inability to drink or breastfeed, vomiting everything, convulsions, and lethargy or unconsciousness. In a young infant under 2 months, fast breathing itself is treated as possible serious bacterial infection and referred.
Technique: count the abdominal movements in an infant, because infants are diaphragmatic breathers; count for a full minute with the chest exposed; and if the first count is at or above the cut-off, repeat it, because a crying or feeding child will always breathe fast.
Periodic breathing in a newborn - pauses of less than 20 seconds with no colour change and no fall in heart rate - is normal. A pause of 20 seconds or more, or ANY pause accompanied by bradycardia below 100 per minute, cyanosis or desaturation, is apnoea and is abnormal at any gestation.
The rate is only half the assessment. Nasal flaring, grunting, head bobbing, tracheal tug, subcostal, intercostal and suprasternal retractions, see-saw paradoxical breathing and an inability to complete a sentence or a feed all indicate increased work of breathing; the Silverman-Andersen score grades neonatal distress from 0 to 10 and the Downes score is used in older infants.
A respiratory rate that is falling in a child who is working harder, becoming drowsy or developing a silent chest is exhaustion and impending respiratory arrest, not recovery; bradypnoea, gasping and irregular breathing in a sick child are pre-arrest signs.
Fever raises the respiratory rate by roughly 5 breaths per minute for each degree Celsius, so the rate is reassessed after the temperature is brought down before a borderline count is acted on.

Primary apnoea

When a fetus or newborn is deprived of oxygen, breathing first becomes rapid and then stops altogether - this first pause is primary apnoea, during which the heart rate falls but the blood pressure is maintained, and tactile stimulation or oxygen alone will restart breathing. If the hypoxia continues the baby begins to gasp, the gasps weaken and stop, and the baby enters secondary or terminal apnoea, in which heart rate and blood pressure fall together and only positive-pressure ventilation will restore breathing; because the two look identical at the bedside, every apnoeic newborn is treated as secondary apnoea from the outset.

The initial steps of resuscitation - provide warmth, dry, position the head in the neutral sniffing position, clear the airway only if needed, and stimulate - take about 30 seconds. If the baby is apnoeic or gasping, or the heart rate is below 100 per minute, positive-pressure ventilation must be started, and the whole sequence must be complete within the first 60 seconds of life, the Golden Minute.
Positive-pressure ventilation is given at 40 to 60 breaths per minute with an initial inflating pressure of about 20 to 25 cm of water in a term baby and positive end-expiratory pressure of 5 cm of water, starting in 21% oxygen at 35 weeks gestation and above and 21 to 30% below 35 weeks, then titrating to the pre-ductal saturation targets.
A RISING HEART RATE is the primary indicator that ventilation is effective - not chest movement, not colour and not the saturation, which lags behind. If the heart rate is not rising, the ventilation is not working.
Target pre-ductal saturations rise slowly and deliberately after birth: about 60 to 65% at 1 minute, climbing through the first minutes to 85 to 95% by 10 minutes. Chasing an adult saturation in the first minutes causes hyperoxic injury.
When ventilation is not effective, work through the MR SOPA corrective steps in order: Mask adjustment, Reposition the airway, Suction mouth and nose, Open the mouth, Pressure increase, and finally an Alternative airway (endotracheal tube or laryngeal mask).
Chest compressions are started only if the heart rate remains below 60 per minute after 30 seconds of EFFECTIVE ventilation, preferably through a secured airway and with the oxygen increased to 100%. Use the two-thumb encircling technique on the lower third of the sternum, compressing one third of the anteroposterior diameter, coordinated 3 compressions to 1 breath, giving 90 compressions and 30 breaths a minute.
Adrenaline is given if the heart rate stays below 60 per minute despite effective ventilation and compressions: 0.02 mg/kg intravenously, preferably through an umbilical venous catheter, repeated every 3 to 5 minutes, with a higher endotracheal dose used only while access is being obtained.
Suction does not come before ventilation. Routine suctioning of a vigorous baby is not done, and routine intubation for tracheal suction of a non-vigorous meconium-stained baby is no longer recommended - drying, stimulation and ventilation come first.
Apnoea of prematurity is a different entity from perinatal apnoea: a pause of 20 seconds or more, or any pause with bradycardia or desaturation, in a preterm baby; it may be central, obstructive or mixed. Treatment is caffeine citrate 20 mg/kg as a loading dose then 5 to 10 mg/kg daily, with continuous positive airway pressure and tactile stimulation, always after excluding sepsis, hypoglycaemia, anaemia, intraventricular haemorrhage, necrotising enterocolitis and cold stress.

Croup syndrome

Croup, or acute laryngotracheobronchitis, is a viral infection that inflames the larynx, trachea and bronchi and causes oedema at the subglottic region under the cricoid ring, the narrowest part of a young child's airway. Because resistance rises steeply as that ring narrows, a few millimetres of swelling turn a coryzal child into one with a barking cough, inspiratory stridor and hoarseness, typically worse at night, and the nurse's calmness is part of the treatment because crying worsens the obstruction.

Parainfluenza virus type 1 is the commonest cause, followed by parainfluenza 2 and 3, respiratory syncytial virus, influenza and adenovirus. It affects children from 6 months to 3 years with a peak in the second year, and most episodes are mild and settle in 3 to 5 days.
The Westley croup score grades severity from 0 to 17 using level of consciousness, cyanosis, stridor, air entry and retractions: a score of 2 or less is mild, 3 to 5 moderate, 6 to 11 severe and 12 or more indicates impending respiratory failure.
The steeple sign of subglottic narrowing on an anteroposterior neck radiograph supports the diagnosis but is not needed; a child with stridor at rest is never sent to the radiology department, because the diagnosis is clinical and the journey is dangerous.
A single dose of dexamethasone 0.6 mg/kg orally (maximum 16 mg) is given to EVERY child with croup including mild cases, because it reduces return visits, admission and the length of illness; nebulised budesonide 2 mg is an alternative if the child is vomiting, and prednisolone is an accepted substitute where dexamethasone is unavailable.
Nebulised adrenaline 1:1000 at 0.5 mL/kg, to a maximum of 5 mL, is added for moderate to severe croup. It works within 10 to 30 minutes but wears off in about 2 hours, so any child who receives it is observed for at least 2 to 4 hours for rebound before being considered for discharge.
Humidified air, steam and mist tents have NO proven benefit and are no longer recommended; oxygen is given for saturations below about 92%, and the child is left undisturbed on the parent's lap because agitation and crying increase the airway obstruction.
Antibiotics have no role in viral croup, and throat examination with a spatula is avoided in any child with stridor until epiglottitis has been excluded.
The differential is the classic examination question. Acute epiglottitis (Haemophilus influenzae type b, now rare because of the vaccine in the national schedule) comes on within hours with high fever, drooling, dysphagia, a muffled hot-potato voice and distress, the child sitting forward in the tripod position with NO barking cough, and a thumb sign on the lateral neck film; the throat is never examined and the child is never laid flat except in theatre with an anaesthetist present.
Other mimics: bacterial tracheitis (toxic-looking, high fever, thick purulent secretions, poor response to adrenaline, needs antibiotics and often intubation), inhaled foreign body (sudden onset in a previously well, afebrile child), retropharyngeal abscess (neck held stiffly, drooling, fever), spasmodic croup (recurrent, at night, no fever, settles quickly) and angio-oedema.
Discharge criteria after treatment: no stridor at rest, normal air entry and colour, at least 2 to 4 hours since the last dose of nebulised adrenaline, the child drinking, and a parent who has been taught to return for stridor at rest, difficulty breathing, drooling or drowsiness.

Asthma — paediatric

Asthma is a chronic inflammatory disease of the airways with variable expiratory airflow limitation, producing recurrent wheeze, cough that is worst at night and in the early morning, breathlessness and chest tightness that vary in intensity over time and are at least partly reversible. In children under 5 the diagnosis is clinical and probabilistic because most wheeze is viral, while from about 5 or 6 years spirometry with bronchodilator reversibility supports it - and the whole of modern management rests on the fact that inhaled corticosteroids, not relievers, change the outcome.

Suspect asthma when wheeze, cough, breathlessness or chest tightness are recurrent, are worse at night or with exercise, cold air, viral infections, dust, smoke or pets, occur with a personal or family history of atopy (eczema, allergic rhinitis, food allergy), and respond to a bronchodilator.
Objective support from about 5 to 6 years of age: an increase in FEV1 of more than 12% predicted after a bronchodilator, or average daily peak expiratory flow variability of more than 13% in children. A normal spirometry between attacks does not exclude asthma.
Current global strategy no longer accepts treatment with a short-acting beta-2 agonist alone, at any severity, because reliever-only treatment increases exacerbations and asthma deaths; every child with asthma needs inhaled corticosteroid-containing treatment, with the reliever used alongside it.
The device is chosen by age: a pressurised metered-dose inhaler with a spacer and a face mask under about 4 years, a spacer with a mouthpiece from about 4 to 6 years, and a dry powder inhaler only from about 6 years and above once the child can generate the inspiratory flow. Technique is checked at every single visit, because most treatment failure is device failure.
In an acute attack a metered-dose inhaler with a spacer is at least as effective as a nebuliser and causes less tachycardia and less hypoxaemia, so a spacer is the first choice unless the child needs continuous oxygen-driven nebulisation.
Acute management: oxygen to keep saturations 94 to 98%, salbutamol by spacer (commonly 6 puffs under 6 years and up to 12 puffs above, one puff at a time with 5 tidal breaths each) or nebulised salbutamol 2.5 mg under 5 years and 5 mg above, repeated every 20 minutes for the first hour; add nebulised ipratropium bromide for severe attacks; give oral prednisolone 1 to 2 mg/kg (maximum 40 mg in children under 12) for 3 to 5 days; and give intravenous magnesium sulphate 40 to 50 mg/kg (maximum 2 g) over 20 minutes for a severe or life-threatening attack.
Life-threatening features: a SILENT chest, cyanosis, poor respiratory effort, exhaustion, confusion or drowsiness, saturation below 92% despite oxygen, and bradycardia or hypotension. A silent chest is more dangerous than a loud wheeze, because there is no longer enough airflow to make a sound.
Rinsing the mouth and spitting after every dose of inhaled corticosteroid prevents oral candidiasis and hoarseness, and using a spacer reduces both. Low-dose inhaled corticosteroids reduce growth velocity by roughly half a centimetre to a centimetre in the first year of treatment with little effect on final adult height, so height is plotted at every visit rather than the drug being stopped.
Every child needs a written asthma action plan in the parent's language stating the daily controller, the reliever dose in an attack, the signs that mean going to hospital, and who to call; and a trigger review covering household smoke, biomass cooking fuel, dust mite, cockroach, pets, pollen and unnecessary aspirin or non-steroidal anti-inflammatory drugs.
Comorbidities that keep asthma uncontrolled must be treated in their own right: allergic rhinitis, gastro-oesophageal reflux, obesity, obstructive sleep apnoea and poor adherence. Annual influenza vaccination is recommended, and asthma is not a contraindication to any vaccine in the national schedule.

Pulmonary atelectasis — lobe involvement

Atelectasis is incomplete expansion or collapse of alveoli so that a part of the lung becomes airless, blood continues to flow past unventilated alveoli, and the resulting intrapulmonary shunt causes hypoxaemia that oxygen alone corrects poorly. Children collapse a lobe far more readily than adults because their airways are narrow and plug easily, their collateral ventilation through the pores of Kohn and canals of Lambert is poorly developed, and their compliant chest wall gives little outward recoil to hold the alveoli open.

Types by mechanism: obstructive or resorptive, which is much the commonest in children (mucus plug, aspirated foreign body, thick secretions in asthma or cystic fibrosis, an endotracheal tube pushed into the right main bronchus, or extrinsic compression by tuberculous lymph nodes); compressive (pleural effusion, pneumothorax, tumour, gross abdominal distension); adhesive from surfactant deficiency in respiratory distress syndrome; and cicatrisation from fibrosis after infection.
The right middle lobe collapses most often in children - right middle lobe syndrome - because its bronchus is long, narrow and angled and is surrounded by lymph nodes that compress it when they enlarge. An aspirated foreign body also lodges on the right more often, because the right main bronchus is wider, shorter and more vertical.
Physical signs on the affected side: reduced chest expansion, a dull percussion note, and diminished or absent breath sounds, with reduced vocal resonance.
The discriminator is the direction of mediastinal shift. Collapse loses volume and pulls the trachea and mediastinum TOWARDS the affected side; a pleural effusion or a tension pneumothorax adds volume and pushes them AWAY. That single observation separates the two commonest causes of a dull, quiet hemithorax.
Chest radiograph shows opacity WITH signs of volume loss - displaced fissures, crowded ribs, an elevated hemidiaphragm and shift of the mediastinum towards the lesion. Pneumonic consolidation occupies the same space without losing volume and usually contains an air bronchogram.
Treatment is to re-expand the lung and remove the cause: chest physiotherapy with postural drainage and percussion, deep breathing, effective coughing, early mobilisation, adequate humidification and hydration to loosen secretions, suction, and continuous positive airway pressure or added positive end-expiratory pressure in the ventilated child. Flexible bronchoscopy is used when a plug or a foreign body will not clear.
Incentive spirometry works only in a child old enough to cooperate, from about 5 years; in a younger child the same effect is obtained with play - blowing bubbles, blowing a pinwheel or party blower, or blowing a ping-pong ball across a table.
Pain control is part of chest physiotherapy: a child who is guarding a surgical wound will not take a deep breath or cough, so analgesia is given before physiotherapy, not after it.
Positioning differs by age, which is a favourite trap: in adults and older children oxygenation improves with the healthy lung dependent, but in an infant the reverse holds, because the very compliant chest wall and small functional residual capacity mean the dependent lung is compressed rather than better perfused.
Atelectasis is the commonest cause of fever in the first 24 to 48 hours after an abdominal or thoracic operation, and it is prevented by early mobilisation, deep breathing and adequate analgesia rather than by antibiotics.

Bronchopulmonary dysplasia

Bronchopulmonary dysplasia, or chronic lung disease of prematurity, is the need for supplemental oxygen for at least 28 days in a preterm baby, with the severity graded by the respiratory support still needed at 36 weeks postmenstrual age in babies born before 32 weeks (or at 56 days of life in those born later). The new bronchopulmonary dysplasia of the surfactant era is a disease of arrested alveolar and pulmonary vascular development rather than the airway scarring of the pre-surfactant era, which is why these babies have fewer, larger alveoli and grow out of it only slowly.

Severity by the classification in general use: MILD is breathing room air at 36 weeks postmenstrual age, MODERATE needs less than 30% oxygen, and SEVERE needs 30% or more oxygen or any positive pressure support at 36 weeks postmenstrual age.
Risk factors: extreme prematurity and very low birth weight are the dominant ones, followed by mechanical ventilation with volutrauma and barotrauma, oxygen toxicity, chorioamnionitis and postnatal sepsis, a patent ductus arteriosus, excess fluid administration and poor nutrition.
Prevention is the treatment that works: antenatal corticosteroids to the mother, early nasal continuous positive airway pressure in preference to intubation, surfactant given by a minimally invasive route when it is needed, volume-targeted ventilation with permissive hypercapnia, early caffeine citrate (20 mg/kg loading then 5 to 10 mg/kg daily), careful fluid and calorie provision, and avoiding hyperoxia by keeping saturation targets in the recommended preterm range rather than at 100%.
Established disease needs calories above the normal requirement, often 120 to 150 kcal/kg per day or more, because the work of breathing consumes them; growth is the single best marker that the lungs are being managed well, and a baby who is not growing is not being fed enough or is working too hard to breathe.
Drug treatment is supportive and selective: diuretics for episodes of pulmonary oedema and fluid overload, bronchodilators only where there is demonstrable reversible airway obstruction, and a short low-dose course of dexamethasone reserved for the baby who cannot be weaned from the ventilator, because systemic steroids in the first week harm neurodevelopment.
Once bronchopulmonary dysplasia is established the oxygen saturation is kept in the low to mid nineties rather than allowed to run low, because chronic hypoxaemia drives pulmonary hypertension, poor growth and more frequent apnoea.
Complications to watch for: pulmonary hypertension progressing to cor pulmonale (screened with echocardiography), recurrent respiratory infection and rehospitalisation especially with respiratory syncytial virus, asthma-like airway disease in later childhood, gastro-oesophageal reflux with feeding difficulty, growth failure, and the neurodevelopmental and sensory problems shared with extreme prematurity.
Immunisation follows CHRONOLOGICAL age, not corrected age, and doses are never reduced for prematurity; annual influenza vaccination is given to the child from 6 months and to the household, and monthly palivizumab is offered in the respiratory syncytial virus season where it is available and affordable.
Discharge planning is a nursing task in its own right: the parents must be able to use the home oxygen and saturation monitor, recognise increased work of breathing and cyanotic spells, hold and feed the baby safely, keep the home free of tobacco smoke and biomass cooking smoke, and know exactly who to telephone and where to go at night.

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