Breathless Baby Flashcards
What questions do you want to ask about poor feeding?
- Ask about volume of milk taken before and now
- Timescale of decline in feeding - important to get idea of duration of illness as feeding is often important first sign
- Why they stopped feeding e.g. child is breathless, goes pale and clammy
- Sleepiness = very worrying sign - need to explore this more especially if affecting feeding (sleeping longer at night, not crying for usual feed)
- Does mum have any other ideas about precipitating factor - parents often have more time than you do to think around the problem - may not know medical reasons but can give other clues e.g. we have all had a cold
How is the milk requirement calculated?
- Until a baby meets their birth weight, continue using their BW for calculation, not current weight
- Up to a month of age the minimum milk requirement to provide enough calories to grow is 150mls/kg/day
- After 1 month this can be down to 100mls/kg minimum so long as they are gaining weight
What is asked in the antenatal history?
- Scans and screening - maybe congenital disease
- Maternal health - looking for congenital infections, vascular episodes following antenatal bleeds, trauma, medication, teratogenic agents including high sugar
- Delivery - looking for increased risk of infection with prolonged rupture of membranes
- The gestation, mode of delivery and weight
- Post delivery - any time on the neonatal unit, looking at respiratory causes, hypoglycaemic screening, concerns around sepsis
- Routine immunisation schedule starts at 2 months
What are the differentials and presentations of a breathless baby?
- Vascular: symptomatic on exercise I.e. feeding, clammy, sleepy; no hx of antenatal/perinatal trauma, normal anomaly scan
- Infective, inflammation, immune: sleepy, snuffly, poor feeding, not yet immunised; new borns at increased risk as immature immune system
- Traumatic: includes child protection, non accidental injuries
- Autoimmune: FH of anything
- Metabolic (includes inborn errors of metabolism): consanguinity, sleepy, poor feeding
- Iatrogenic/idiopathic: teratogenic medications
- Congenital/genetic: antenatal screening and scans
- Developmental/degenerative: sleep and poor feeding, encouraging factors include normal development up until now
- Endocrine/environment: FH e.g. diabetes, thyroid
- Functional: post-natal depression
What do you look for on inspection of a child?
- General dysmorphism
- Neurology I.e. alert, happy, interacting, responding to voice, pain, unresponsive - also look at muscle tone and abnormal movements
- Colour: check if jaundiced, mottled/pale or cyanosed (sats need to be <85% for cyanosis to show)
- Extra noises: grunting, stridor, wheeze, crying, coughing
- Signs of pain: abdominal posturing, grimacing or relaxed
- Obvious marks/rashes: marks/bruises around face/ears/lips/orbital swelling
- Any secretions: any crusting in eyes? Any nasal secretions
- Signs of increased work of breathing: nasal flaring, head bobbing, subcostal recession, tracheal tug etc
- RR
- Measure length, head circumference, BP and check body for bruises
What are possible causes of abnormal respiratory breathing in neonates?
- Primary respiratory disease e.g. bronchiolitis
- Congenital abnormalities, like diaphragmatic hernia
- Cardiac disease e.g. heart failure
- Shock due to hypovolaemia (compensating for poor perfusion, hypoxia) e.g. sepsis
- Acute blood loss secondary to injury I.e. subdural
- Metabolic issues with compensatory breathing like acidosis/metabolic alkalosis
- Endocrine e.g. DKA - Kussmaul breathing (laboured, deeper breathing rate)
- Always consider sepsis
What are possible causes for tachycardia?
- Upset/fear (stranger fear)
- Pyrexia
- Pain
- Cardiac arrhythmia I.e. SVT = HR >220
- Increased work e.g. accessory muscles for breathing or exercise
- Cardiac/circulatory failure e.g. increased CRT, enlarged liver, cool peripheries, clammy on feeding
- Shock including hypovolaemia secondary to accidental or non-accidental injury
- Shock hypovolaemia secondary to third space loss such as sepsis - cool extremities
- Endocrine e.g. hypothyroid
What congenital heart defects cause a large heart?
- Large left to right shunts
- VSD (cardiomegaly with pulmonary plethora), PDA
- TGA
- Tricuspid atresia
- Single ventricle
- Truncus Arteriosus
- Ebstein’s anomaly
What congenital heart defects cause a small heart?
- Fallot’s tetralogy (boot shaped) - dark lung fields due to pulmonary oligemia
- TAPVD - infradiaphragmatic
What congenital heart defects cause a normal sized heart?
- TGA
- Pulmonary atresia
What does plethoric mean?
Too much blood going into lungs - left to right shunts e.g. VSD, PDA, cardiac failure
What does oligarchic mean?
Very dark XR due to less blood going into lungs - Fallot’s tetralogy, pulmonary atresia/stenosis
Describe VSD
- Pansystolic/holosystolic murmur - lower left sternal border
- Blood shifted from left to right ventricle down pressure gradient
- Hole can form in membranous septum (higher up in ventricle wall) or in muscular septum (lower down). Can hear membranous septum more clearly on auscultation.
- If hole is small then typically asymptomatic so can be left alone but if hole is large can be fixed by surgery
- Not unusual to have normal fetal anomaly scans and then have VSD postnatally (maternal obesity makes scanning difficult)
- Murmur is often absent at the baby check done at a few hours of age due to the changes in pressure within the heart as it changes from foetal to adult circulation.
What heart conditions can present with no murmurs?
- Transposition of great arteries (TGA)
- Total anomalous pulmonary venous drainage (TAPVD)
What causes systolic murmurs?
- Fallot’s tetralogy
- VSD
- Pulmonary/aortic stenosis
What causes diastolic murmurs?
- Truncus arteriosus
- Mitral stenosis
- Pulmonary/aortic regurgitation
What are the signs and symptoms of cardiac failure in children?
- SOB - tachypnoea and dyspnoea
- Poor feeding - weight stays same or decreases
- Tachycardia
- Hepatomegaly
- Poor pulses
- Acidosis
- Sweating
- Oedema - after 2/yrs
What is the management of cardiac failure in children?
- Diuretics: furosemide, amiloride
- ACEi: captopril, enalapril (shorter acting for children)
- Oxygen: not in duct dependent conditions
- Prostaglandins: prostin
- Diet/fluid intake
- Inotropes: dopamine, dobutamine
- Catheter intervention e.g. balloon angioplasty etc.
- Surgery
What is the dietary intake in cardiac failure?
- Increased energy requirements
- Increased calorie feeds: infratini, SMA high energy milk
- Calorie supplements: polycal, duocal
- Small, frequent feeds
- NG tube feeds
- Gastrostomy
What heart problems are there in children?
- Congenital: acyanotic, cyanotic
- Acquired: myocarditis, rheumatic heart disease
- Inherited: hypertrophic cardiomyopathy (HOCM)
- Marfan’s syndrome etc
What is acyanotic CHD?
Malformation of atrial or ventricular walls, heart valves or large blood vessels.
- Septal defects: VSD or ASD
- Aortic/pulmonary stenosis
- Coarctation of aorta
- PDA
- Mitral/tricuspid stenosis
What is the management of VSD?
Pansystolic murmurs:
- Small - no treatment
- Big - increased SOB while feeding and eventually cardiac failure, tx: diuretics, surgery
What are the clinical features of coarctation of aorta?
- Weak/absent femoral pulses
- Systemic hypertension of upper limbs, aorta can be interrupted in severe forms
- Commonly associated with left heart defects like bicuspid aortic valve, VSD
- In newborns - risk of necrotising enterocolitis (reduced blood supply to gut)
What are the clinical features of PDA?
- Persistent opening between 2 major blood vessels leading from the heart (pulmonary artery and aorta)
- Bounding pulses, continuous murmur
- Closes on day 3 - causes acute heart failure and acidosis. Give IV prostin to keep it open (allows time for surgery). Furosemide also given.
What are the clinical features of ASD?
- Ejection systolic murmur, less likely to close spontaneously - arrhythmias, chronic left to right shunt
- Split S2 sound
- Tx: surgery closure
What is cyanotic CHD?
Generalised blueness (central cyanosis):
- Transposition of the great arteries
- Fallot’s tetralogy
- Atrio-ventricular septal defect
What are the clinical features of TGA?
- Central cyanoses at birth
- Usually no murmurs
- Not compatible with life as oxygenated blood > lung, unless mixing e.g. PDA (can keep open with prostin)
What are the clinical features of Fallot’s tetralogy?
- VSD, pulmonary valve stenosis, over-riding aorta (could be just above defect) and RV hypertrophy
- Central cyanosis; pulmonary oligemia on CXR; hyper cyanotic episodes; loud ejection systolic murmur (from pulmonary stenosis)
- Hypercyanotic episodes: patient always has baseline cyanosis but at certain times become very cyanosed which is an emergency - treatment: calm baby down, tuck legs under abdomen, put baby over mums shoulder
What are the clinical features of atria-ventricular septal defect?
- Partial, complete, high incidence in trisomy 21
- Not 2 separate AV valves, tricuspid and mitral commonly fused
- ECG - left axis deviation
What is common in a child with a fever?
Many children have innocent flow murmur when they’re feverish so auscultate heart after fever settles. During activity or stress (like fever), blood flows faster through heart so sounds like a murmur. Children also have thin chest walls so easier to hear the blood flowing through.
What conditions have a congenital heart condition?
- Trisomy 13 - Patau’s Syndrome
- Trisomy 18 - Edwards syndrome
- Turner’s
- Kartagener’s syndrome
- DiGeorge (inherited autosomal dominant)
What does autosomal dominant mean?
- Examples: neurofibromatosis, Marfan’s syndrome, familial adenomatous polyposis
- Males and females equally affected
- Transmitted by both sexes
- Incomplete penetrance
- Variable expression - everyone affected differently
- New mutations
- Risk to offspring is 50%
What can the heel prick test for?
- MCAD (medium-chain acyl-CoA dehydrogenase deficiency) - body can’t convert fats into energy
- HCU (homocystinuria) - body can’t process amino acid methionine (causing build up), can be serious
- Isovaleric academia - body can’t process amino acid leucine (causes build up) - can be serious
- Cystic fibrosis (not diagnostic, sweat and genetic testing needed)
- Hypothyroidism
- Phenylketonuria - body can’t process phenylalanine (can cause learning difficulties and seizures)
What is acquired heart disease?
- Viral pericarditis
- Viral myocarditis - Coxsackie B
- Kawasaki disease
What are the clinical features of Kawasaki disease?
- Inflammatory condition, swinging fevers - resistant to paracetamol
- Lymphadenopathy, red eyes (no pus), rash, red tongue, swollen hands and feet (later peeling from tips of digits)
- Platelet rise in 2 weeks
- Muco-cutaneous lymph node syndrome - can cause coronary artery aneurysms (especially in younger children) - reduced by early aspirin and IV gamma globulin (in first 10 days of illness
What heart problems causes obstruction?
- Coarctation of aorta: present day 3 as duct closes, grey baby, prostin (for PDA) and resus (surgery)
- Aortic stenosis: present in community from 12hrs
- More chance of murmur being pathological under 1yrs
What can you never forget in babies?
- Sepsis
- Metabolic illness
- Always check ammonia, glucose and gas - is the tachypnoea/tachycardia due to primary cardiac or respiratory failure
What urgent treatment do babies with inborn error of metabolism need?
With proprionic acidaemia or ornithine transcarbamylase deficiency will require urgent removal of toxic metabolites e.g. ammonia by specialist treatment in children’s metabolic unit
What is the management for a sick child?
- Inform senior colleagues
- Oxygen - caution in duct dependent cardiac lesions
- Start IV maintenance containing glucose
- IV abx - sepsis
- Consider extra respiratory support e.g. CPAP
- Stop oral feeds and consider NGT feeds when more stable
