Paeds Mx Flashcards
Signs, Ix and Management of ASDs?
Sx: Ejection systolic murmur (upper L sternal edge), fixed wide splitting of S2
Ix: (severe, long term cases)ECG: RAD, RBBB for secundum. partial AVSD - the AV node is displaced and therefore it conducts the ventricles superiorly giving a negative reflection of QRS in the AVF lead. Echo will show the abnormality.
Observation is main treatment, as it may close or shrink; measured by ratio of pulmonary to systemic blood flow, where <1.5 is of little prognostic importance. >1.5 = large enough to cause RV dilatation and will require surgical closure at 2-4 years of age.
Secundum ASDs - managed by cardiac catheterisation with the insertion of an occlusive device (percutaneous closure/endovascular closure) but may need
surgical closure under GA.
Partial AVSD - managed by surgical correction
Prophylactic amoxicillin for the first 6m after device insertion
Sx and Mx of VSD?
Signs:
• Pansystolic murmur (lower L sternal edge) (loud murmur = smaller defect) (will be soft/absent in large VSD)
• Quiet P2
• Large VSD will have apical mid-diastolic murmur from increased flow over the mitral valve
• Signs of HF if large VSD (hepatomegaly, SOB, failure to thrive, recurrent chest infections) (From 1 week old)
Ix: ECG will show biventriuclar hypetrophy if LVSD. (Upright t wave in V1 indicates pul HTN).
Management Depends on size! If smaller than AV node diagemeter (~ 3mm), they will close spontaneously, ascertained by the disappearance of the murmur and normal ECG/Echo. While the VSD is present, prevention of bacterial endocarditis is by maintaining dental hygiene. Proph amoxicillin if high risk.
More than 3mm: Drug therapy for HF is with diuretics furosemide, often combined with captopril and digoxin. Additional calorie input is required.
Surgery 3-6months is required to manage HF and prevent lung damage from pul HTN. This procedure (pulmonary artery banding) narrows the pulmonary artery to reduce the blood flow to the lungs. When the child is older, an operation is done to remove the band and fix the VSD with open-heart surgery if the opening is large.
Signs, IX and management of PDA?
Signs: Continuous murmur below L clavicle (cont. as Pa in pul artery always less than aorta)
ECG- Large L-R shunt will cause RVH (+ Pul HTN) and LVH and so indistinguishable from large VSD.
If a cyanotic disease is dependent on a PDAs (e.g. TGA), the patient should start a prostaglandin infusion to keep the PDA open until corrective surgery can be performed
• The duct can be closed using:
o IV Indomethacin – 1st line treatment
o Prostacyclin synthetase inhibitor
o Ibuprofen ( Usually done in premature/VLBW infants)
• If pharmacological methods are unsuccessful, surgical ligation or PCD closure may be used
• Term infants:
o Symptomatic >6mo, PCD closure ASAP
o Usually closed using a coil or occlusive device introduced through a cardiac catheter at ~1yo via femoral.
o Diuretics can be given if delay of closure, to manage symptoms
Acute diagnosis and management of cyanotic heart disease in neonate
Ix: Nitrogen washout test ( The infant is placed in 100% oxygen (headbox or ventilator) for 10 min. If the right radial arterial PaO2 from a blood gas remains low (<15 kPa, 113 mmHg) after this time, a diagnosis of ‘cyanotic’ congenital heart disease can be made if lung disease and persistent pul HTN of newborn have been excluded)
Mx: ABC, artificially ventilate if necessary. Start prostaglandin infusion (PGE, 5 ng/kg per min). Most infants with cyanotic heart disease presenting in the first few days of life are duct dependent; i.e. there is reduced mixing between the pink oxygenated blood returning from the lungs and the blue deoxygenated blood from the body. Maintenance of ductal patency is the key to early survival of these children. Observe for potential side-effects – apnoea, jitteriness and seizures, flushing, vasodilatation and hypotension
TOF Ix and Mx
Sx: loud systolic MURMUR FROM DAY1, murmur will shorten with time and cyanosis will increase. Clubbing in older children. Can present with severe cyanosis on d1 or much later with hypercyanotic spells (squatting on exs).
Ix: CXR: boot-shaped heart (RVH), pul artery ‘bay’ (concavity where the PulA should be). ECG normal at birth. RVH eventually.
Initial mx is medical, with definitive surgery at 6 months. It involves closing the VSD and relieving right ventricular outflow tract obstruction, sometimes with an artificial patch, which extends across the pulmonary valve.
• Infants who are very cyanosed in the neonatal period require a shunt to increase pulmonary blood flow. This is usually done by surgical placement of an artificial tube between the subclavian artery and the pulmonary artery (a modified Blalock–Taussig shunt), or sometimes by balloon dilatation of the RV outflow tract. ±ECMO.
• Hypercyanotic spells are usually self-limiting and followed by a period of sleep. If prolonged (beyond about 15 min), they require prompt treatment with:
– sedation and pain relief (morphine is excellent)
– IV propranolol (or an α adrenoceptor agonist), which probably works both as a peripheral vasoconstrictor and by relieving the subpulmonary muscular obstruction that is the cause of reduced pulmonary blood flow
- bicarb to correct acidosis
Ix & TGA management
Signs: Cyanosis is the main sx and it is always present. Often presents on day 2 when the PDA closes with increased cyanosis. Presentation can be delayed if there are other SDs. Loud S2 that is single. Generally, NO MURMUR. (Can have systolic murmur from pul stenosis -> increased blood flow)
Ix: CXR can show ‘egg on the side’ on cardiac contour, ECG is normal, Echo shows the deformity.
Mx: In a cyanosed neonate, the key is to improve mixing.
• Maintain patency of DA with PG infusion is mandatory.
• A balloon atrial septostomy is a life-saving procedure which may need to be performed in 20% of those with TGA. A catheter, with an inflatable balloon at its tip, is passed through the umbilical or femoral vein and then on through the right atrium and foramen ovale. The balloon is inflated within the left atrium and then pulled back through the atrial septum. This tears the atrial septum, renders the flap valve of the foramen ovale incompetent, and so allows mixing of the systemic and pulmonary venous blood within the atrium.
• All pts need the arterial switch procedure in the neonatal period. In this operation, performed in the first few days of life, the pulmonary artery and aorta are transected above the arterial valves & switched over. coronary arteries have to be transferred across to the new aorta also.
Signs and management of cardiac outflow obstructions in the well infant
Well children (if asymptomatic -> f/u, no intervention) Aortic Stenosis - murmur on UR sternal edge, carotid thrill; Mx is Trans-catheter balloon dilatation (balloon valvulotomy) If severe, transcatheter aortic valve replacement (TAVR) with proph abx and anticoag.
Pul stenosis - Murmur UL sternal edge, no carotid thrill; Transcatheter balloon dilatation 1st line, valvulostomy 2nd line.
Coarctation -Systemic HTN, Stent insertion or surgery
Signs & Mx for outflow obstructions in the sick child
Sick infant (i.e. duct dependent) ALL PRESENT WITH COLLAPSE. ALL NEED ABC + PG.
Coarctations -> Collapse, absent FEMORAL pulses. Abc + PG infusion + Surgery.
Interruption of Aortic Arch - distal aortic arch is attached (via a duct) to pulmonary artery instead of aorta. VSD usually present. Syndromic associations e.g. DiGeorge. Present with collapse, absent LEFT BRACHIAL pulse. Surgical repair and closure of VSD in first few days of life.
Hypoplastic LH syndrome: (MV and AV is small/absent, coarctation, LV is v small -> no flow on left hand side of heart.) Present antenatally or post natally with collapse and severe acidosis. Absence of all peripheral pulses. Surgical management: Norwood procedure (neonatally) and then Glenn/hemi-Fontan (6 months) and Fontan (at 3 yo)
Cardiac arrhythmia management
It is important to differentiate normal and pathological arrhythmias:
Normal sinus arrhythmia are cyclical changes in HR with respiration. Acceleration in inspiration and slowing on expiration (HR can change by 30 beats/min)
SVT - most common arrhythmia (250-350 b/min) due to premature activation of atrium via accesspory pathway (rarely a structural issue), echo needed. Mx depends on severity and whether there are signs of HF on investigation e.g. T wave inversion on lateral precordial leads.
1) Circulatory and resp support, correct acidosis
2) Vagal stimulating maneouvers e.g. carotid sinus massage or cold ice pack to face (v successful)
3) IV adenosine is treatment of choice (safe, effective, induces AV block and terminates tachycardia by breaking re-entry circuit that is set up between AV node and accessory pathway) Given in incrementally in increasing doses
4) If adenosil fails, Electircal cardioversion with synchronised DC shock
Once sinus rhythm is restored -> Maintenance therapy using flecainide (na channel blocker) or sotalol (beta blocker). 90% of children have no further attacks. The eons that do can be treated with cryoablation of accessory pathway.
Rheumatic fever Mx
QUICK RECAP: Rare in developed countries, rare Cx of strep throat infection where pt develops fever, painful joints etc. After several attacks, in 50% of cases there is an autoimmune reaction towards GBS bacteria causing scarring and fibrosis of valve leaflets.
Acute - anti-inflam and bed rest, aspirin in high dosage with monitoring. If inflammation doesn’t resolve-> corticosteroids.
Chronic -ACE inhibitors and diuretics if severe HF.
Anti-strep abx if any evidence of persisting infection
Maintenance: monthly injections of benzathine penicillin is is most effective prophylaxis. Most recommend to treat until 18-21.
Rheumatic fever diagnosis
JONES CRITERIA (2 major or 1 major and 2 minor) Major criteria Polyarthritis: large joints, usually starting in the legs and migrating upwards. Subcutaneous nodules: Painless, firm collections of collagen fibers over bones or tendons. Erythema marginatum: reddish rash that begins on the trunk/arms as macules -> spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance. This rash typically spares the face and is made worse with heat. (RARE) Sydenham's chorea: series of involuntary rapid movements of the face and arms. This can occur very late in the disease for at least three months from onset of infection. Pancarditis: Myocarditis (Inflammation of the heart muscle- can leads to HF & death), Endocarditis (murmur + valve dysfunction), Pericarditis (pericardial friction rub + pericardial effusion) Minor criteria: Fever, polyarthralgia, hx rheumtaic fever, PR interval prolonged, raised acute phase reactant on FBC
Infective endocarditis management
Most common causative organism is alpha haemolytic strep (strep viridans). It is usually treated with a beta-lactam (e.g. high dose penicillin) and aminoglycoside e.g. genta (broad spec abx for g-ve) IV therapy for 6 weeks.
If the causative organism is Staph Aureus, treat as above + clindamycin.
If there is a prosthetic valves/VSD patches shunts etc. This might have been the cause and there is less chance of eradication- surgical removal might be required.
PROPHYLAXIS - good dental hygiene! strongly encouraged in all children with congenital heart disease. Proph abx no longer recommended. Avoid piercings.
Myocarditis /cardiomyopathy management
RECAP: Can be caused by either direct viral infection, secondary to metabolic disease or inherited - any child with enlarged heart and HF should be suspeted to have cardiomyopathy.
Mx: symptomtic with ACE inhibitors and carvedilol (a Beta-adrenoceptor blocking qagent)
Pul HTN Management
Key is to reduce pressure to prevent irreversible damage to the pulmonary vascular bed (which is not correctable other than herat-lung transplant)
Medications that target GMP pathway (inhaled NO) or cAMP pathway (IV prostacyclin) can cause vasodilation and allow transplant to be delayed for many years. Or endothelin antagonists (e.g. oral bosentan).
Causes of pul HTN
1) Arterial HTN (persisnt pul htn of newborn; post tricuspid shunts e.g. VSD, PDA, AVSD; HIV; idiopathic)
2) Venous HTN (L sided heart disease, pul vein stenosis)
3) Systemic HTN + resp diseae
4) Pulmonary thromboembolic disease
5) Pul. inflammatory or capillary disease
Presentations of congenital heat diseae
- BREATHLESS (or asymptomatic) - ASD, VSD, PDA
- BLUE (R-L shunts) TOF, TGA
- BREATHLESS AND BLUE (Common mixing, AVSD, complex congenital heart disease e.g. tricuspid atresia)
- ASYMPTOMATIC (AS, adult type coarc, PS)
- COLLAPSED WITH SHOCK (Coarcation, HLHS)
What is AVSD?
Complete AVSD:
1) Defect in atrial septum
2) Defect in ventricular septum
These in turn then result in the mitral/tricuspid valve being deformed, and is regarded as having one single five leaflet common valve which stretches across tha triovetircular junction that tends to leak. This results in pul HTN.
upper UTI/pyelonephritis management
NICE GUIDELINES:
<3 mnths - refer to hospital asap, IV abx therapy (eg cef)
> 3 mnths
1. Cefalexin (o) 12.5 mg/kg or 125 mg twice a day for 7 to 10 days (If older than a year its 3x a day)
- If can’t tolerate (o) or severely unwell:
IV Co-amoxiclav (only in combo or if culture results available and susceptible) 30 mg/kg three times a day (max 1.2 g 3 times a day)
IV Cefuroxime 20 mg/kg three times a day (max 750 mg/ dose), increased to 50 to 60 mg/kg three or four times a day (maximum 1.5 g per dose) for severe infections
lower UTI management
NICE GUIDELINES:
If under 3 months -> IV abx therapy (3rd gen ceph e.g. cefotaxime or ceftriaxone) and refer to paed specialist
> 3 mnths - oral abx:
Trimethoprim if low risk of resistance, (25 mg twice a day for 3 days)
Nitrofurantoin if eGFR>45ml/min (750 mcg/kg four times a day for 3 days
If no improvement after 48 hrs ->
Nitrofurantoin if not used as first choice
Amoxicillin (only if culture results available and susceptible, 125 mg three times a day for 3 days)
Cefalexin (125 mg twice a day for 3 days, if over 1yo dose is three times a day)
UTI preventative care & follow up
Good perineal hygiene
High fluid intake
Ensuring complete bladder emptying by encouraging children to try a second time
Regular voiding
Lactobacilllus acidophilus - probiotic that reduces pathogen organism
Abx prophylaxis if under 2 and has congenital abnormality of kidneys (trimethoprim 2mg/kg at night)
Followup for children with reflux, recurrent UTIs or scarring:
Urine culture for every non-specific illness
Circumcision in boys can be considered
Annual BP checks if defects are present
Regular assessment of renal growth and function if bilateral defects.
Nephrotic syndrome mx
Steroid sensitive:
60mg/m2 /day of prednisolone (o). After 4 weeks, reduce to 40mg/m2 on alternate days for 4 weeks and then top. Urine should be protein free by ~11 days.
If steroid resistant, refer to paediatric nephrologist and manage oedema with diuretic therpay, salt restriction, ACE inhibitors.
AKI Ix and Mx
Overall, care is symptomatic and dependent on the cause
- USS to identify obstructive cause, see if it is chronic (small kidneys) or acute (large, bright kidneys with loss of corticomedullary differentiation).
- Use fluid balance charts to monitor intake
- If there is circulatory overload, restrict fluids and challenge with diuretic.
- Metabolic abnormality management:
1. HyperK-> SABA, Ca gluconate if ECG changes, Glucose
and insulin, dietry restriction
2. HyperP -> Calcium carbonate, dietary restriction
3. Met acidosis -> Sodium bicarbonate
4. HUS -> Anti-hypertensives, 50% of kids will need
dialysis
- Dialysis criteria: FISH. Failure (of conservative mx or multisystem failure); Increased bp or pul oedema; Severe (acidosis, hypo/hypernatraemia), Hyperkalaemia
- Post renal failure -> obstruction relief by nephrostomy or bladder catheterisation, surgery can be performed once stable
- If cause not known -> renal biopsy to rule out rapidly proressive glomerulonephritis (if +ve treat immediately with immunosuppressants)
Bacterial meningitis Mx
NICE:
<3 months with ?bacterial meningitis using IV cefotaxime plus amoxicillin or ampicillin
>3 mnths ^^^^ IV ceftriaxone
Treat ?meningococcal disease using IV ceftriaxone.
If has travel hx or prolonged/ multiple exposure to abx (within 3 mnth) with additional VANCOMYCIN.
Give DEXAMETHOSONE (0.15 mg/kg to a max dose of 10 mg, four times daily for 4 days) if LP reveals: purulent CSF, WCC > 1000/microlitre, raised WCC with protein concentration greater than 1 g/litre or bacteria on Gram stain. To prevent long term Cx such as deafness
meningitis & encephalitis causative organisms
BACTERIAL
< 3 months - GBS, Ecoli (and other coliforms), Listeria monocytogens
1 month - 6 years - Haemoph & Neisseria & Strep pneumoniae
> 6 years - Neisseria & Strep pneumoniae
VIRAL:
Enteroviruses, EBV, adenovirus and mumps
ENCEPHALITIS:
Enteroviruses, respiratory viruses and herpes viruses in UK, (worldwide mycoplasma, lyme disease).