paeds Flashcards
signs of moderate resp distress
Tachypnoea, Tachycardia, Nasal flaring, Use of accessory respiratory muscles, Intercostal and subcostal recession, Head retraction, Inability to feed
signs of severe resp distress
Cyanosis, Tiring because of increased work of breathing, Reduced conscious level, Oxygen saturation <92% despite oxygen therapy
stridor
= predominantly inspiratory = from extrathoracic airway obstruction in the trachea and larynx
causes of stridor
Commonly caused by croup, also epiglottitis, inhaled foreign body
wheeze
predominantly expiratory = from intrathoracic airway narrowing.
causes of wheeze
Bronchiolitis, asthma
causes of coryza
Causes: rhinoviruses, coronaviruses and RSV
sx coryza
Nasal discharge, nasal blocking, cough
pharyngitis
= pharynx and soft palate are inflamed, and local lymph nodes are enlarged and tender
causes pharyngitis
adenoviruses, enteroviruses, rhinoviruses, In older children = group A -haemolytic streptococcus is common.
tonsilitis
is a form of pharyngitis which includes intense inflammation of the tonsils, often with a purulent exudate
causes tonsilitis
= group A -haem strep and the Epstein-Barr virus.
features tonsilitis
Headache, apathy, abdo pain, white tonsillar exudate and cervical lymphadenopathy are more common with bacterial infection. It is not possible to clinically distinguish between viral and bacterial tonsillitis.
mx tonsilitis
Antibiotics e.g. penicillin V or erythromycin (if penicillin allergy) are often prescribed for severe pharyngitis and tonsillitis even though only 1/3 are caused by bacteria (10 days).
fever pain criteria
Fever in past 24 hours
Absence of cough or coryza
Symptom onset ≤3 days
Purulent tonsils
Severe tonsil inflammation
fever pain score interpretation
A score of 0-1 =No antibiotics recommended.
A score of 2=Delayed antibiotic may be appropriate.
A score of 3 =Delayed antibiotic may be appropriate.
A score of 4 or more = Consider antibiotics if symptoms are severe or a short delayed prescribing strategy may be appropriate (48 hours)
what is fever pain score for
determining if bacterial or viral pharyngitis/tonsilits
what is centor criteria for?
Estimates probability that pharyngitis is streptococcal
centor critieria
Tonsillar exudate.
Tender anterior cervical lymphadenopathy or lymphadenitis.
History of fever (over 38°C).
Absence of cough
interpreting centor score
A score of 0, 1 or 2 is thought to be associated with a 3-17% likelihood of isolating streptococcus. A score of 3 or 4 is thought to be associated with a 32-56% likelihood of isolating streptococcus.
cause whooping cough
bordatella pertussis
features whooping cough
After a week of coryza, child develops spasmodic cough followed by a characteristic inspiratory whoop. Often worse at night and may lead to vomiting. During heavy coughing, child may go blue or red in the face, and mucus flows from the nose and mouth.
diagnosing whooping cough
culture of organism on pernasal swab, marked lymphocytosis on blood film (>15x109/L)
mx whooping cough
Clarithromycin if present within 21d
cause pneumonia
Newborn = group B streptococcus, gram -ve enterocci and bacilli. Infants and young children=. RSV, Strep pneumoniae or H. influenzae. Children >5 yrs- Mycoplasma pneumoniae, Strep pneumoniae, Chlamydia pneumoniae
features pneumpnia
Fever, cough, rapid breathing, Preceded by URTI, lethargy, poor feeding, ‘unwell’ child.
Examination: Tachypnoea , Nasal flaring, Chest indrawing, May be end-inspiratory coarse crackles
diagnosing pneumonia
CXR, A nasopharyngeal aspirate
when to admit to hospital with pneumonia
xygen sats <92%, Recurrent apnoea, Grunting, Inability to maintain adequate feed/fluid.
mx pneumonia
oxygen for hypoxia and analgesia for pain, IV fluids if necessary. Newborns = broad spectrum antibiotics. Older infants = oral amoxicillin, with broader spectrum e.g. co-amoxiclav reserved for complicated cases, >5 years = amoxicillin or oral macrolide e.g. erythromycin.
bronchiectasis
permanent dilatation of the bronchi. May be generalised or restricted to a lobe of the lung.
causes bronchiectassi
Generalised may be due to cystic fibrosis, primary ciliary dyskinesia, immunodeficiency or chronic aspiration.
Focal is due to previous severe pneumonia, congenital lung abnormality, or obstruction by a foreign body.
ix bronchiectasis
CT
cause croup
Parainfluenza, rhinovirus, RSV and influenza,
typically occurs from 6 months to 6 years of age the peak incidence is the 2nd year of life, in autumn.
features croup
are coryza and fever, followed by: Hoarseness ,A barking cough, Harsh stridor. The symptoms often start, and are worse, at night
mx croup
1st line treatment = oral dexamethasone, oral prednisolone, or nebulized steroids (budesonide). These reduce the severity and duration of croup and are first line for croup causing recession at rest. They have been shows to reduce the need for hospitalisation. If severe: nebulised epinephrine (adrenaline) with oxygen by face mask provides rapid but transient improvement.
what is bacterial tracheitis
pseudomembranous croup)
features bacteria tracheitis
High fever appears very ill, rapidly progressive airways obstruction with copious thick airway secretions. caused by staph aureus.
mx bacterial tracheitis
IV abx and intubation and ventilation if required
cause acute epiglottitis
H. influenzae type b (Hib), Most common aged 1-6 years but affects all age groups.
features acute epiglottitis
Onset of epiglottitis is usually very acute, with: High fever in a very ill, toxic-looking child, An intensely painful throat that prevents the child from speaking or swallowing; saliva drools down the chin, Soft inspiratory stridor,The child sitting immobile, upright, with an open mouth to optimise the airway, cough minimal or absent
what not to do in acute epiglottitis
DO NOT lie the child down or examine the throat with a spatula or perform a lateral neck X-ray must not be undertaken as they can precipitate total airway obstruction + death.
mx acute epiglottitis
Senior anaesthetist, paediatrician, ENT surgeon should be involved. Intubation. Once airway is secured, blood should be taken for culture and abx started e.g. cefuroxime. Tracheal tube removed after 24hrs, abx 3-5 days. Prophylaxis rifampicin is offered to close household contacts (H.influenzae infection).
cause bronchiolitis
RSV is the main cause (80%), but it can also be cause by parainfluenza virus, rhinovirus, adenovirus, human metapneumovirus or influenza virus.
features brochiolitis
Coryzal symptoms may precede a dry cough and increasing breathlessness.
Examination:Tachypnoea and tachycardia, Subcostal and intercostal recession, Hyperinflation of the chest, Sternum prominent, Fine end-respiratory crackles, High-pitched wheezes – expiratory > inspiratory
ix brobchiolitis
Pulse oximetry, CXR and blood gases only indicated if resp. failure is suspected.
when to admit with bronchiolitis
Sleep apnoea, Persistent oxygen sats <90% in air, Inadequate oral fluid intake (50-75% of usual volume), Severe respiratory distress – grunting, marked chest recession, or a resp. rate over 70 breaths/minute.
mx bronchiolitis
Humidified oxygen via nasal cannula or a head box, assisted ventilation – CPAP (continuous positive airway pressure
prevention bronchiolitis
A monoclonal antibody to RSV (palivizumab)
inheritance CF
Autosomal recessive, carrier rate 1 in 25. Defective protein called the CF transmembrane conductance regulator (CFTR). The gene for CFTR is located on chromosome 7.
pathophysiology CF
abnormal ion transport across epithelial cells. In the airway, this leads to reduction in the airway surface liquid and consequent impaired ciliary function and retention of mucopurulent secretions. Defective CFTR also causes dysregulation of inflammation and defence against infection. The pancreatic duct becomes blocked by thick secretions, leading to pancreatic enzyme deficiency and malabsorption.
features CF in children
Newborn= Diagnosed through newborn screening, Meconium ileus. Infancy= Prolonged neonatal jaundice, Growth faltering, Recurrent chest infections, Malabsorption, steatorrhea. Young child = Bronchiectasis, Rectal prolapse, Nasal polyp, Sinusitis. Older child and adolescent= Allergic bronchopulmonary aspergillosis, Diabetes mellitus , Cirrhosis and portal hypertension, Distal intestinal obstruction (meconium ileus equivalent), Pneumothorax or recurrent haemoptysis, Sterility in males
On examination: Persistent, wet cough, productive of purulent sputum, Hyperinflation of the chest – air trapping, Coarse inspiratory crepitations, Expiratory wheeze, Finger clubbing
diagnosis CF
THE SWEAT TEST = concentration of chloride in sweat is markedly elevated. Cl 60-125mmol/L in CF, compared to 10-40mmol/L (normal).
mx CF
Children should have physiotherapy at least twice a day, aiming to clear the airways of secretions. Medication: Continuous prophylactic oral abx (flucloxacillin) are recommended, with additional rescue abx for any flare ups, Daily nebulised antipseudomonal abx = slow decline of lung function caused by chronic Pseudomonas infection. Bilateral sequential lung transplantation is the only therapeutic option for end-stage CF lung disease
:, Due to increasing chest infections, CF patients are segregated and advised not to socialise with other people with the disease,
CF in teenagers and adults
CF in teenagers and adults: Diabetes mellitus – decreasing pancreatic endocrine function, Evidence of liver disease with hepatomegaly on palpation, abnormal LFTs or an abnormal US, Distal intestinal obstruction syndrome (meconium ileus equivalent) is usually cleared by a combination of oral laxative agents, Due to increasing chest infections, CF patients are segregated and advised not to socialise with other people with the disease, Males are virtually always infertile due to absence of the vas deferens.
features viral induced wheeze
only wheezes when has a viral upper respiratory tract infection (URTI) and is symptom free inbetween episodes
mx viral induced wheeze
Tx when symptoms, no prophylaxis. first-line is treatment with short acting beta 2 agonists (e.g. salbutamol) or anticholinergic via a spacer, next step is intermittent leukotriene receptor antagonist (montelukast), intermittent inhaled corticosteroids
features moderate acute asthma
able to talk
oxygen sat s>92
peak flow >50%
RR: </= 40 for 2-5y, </=30 for 5-12 yr, </= 25 for 12-18y
HR: </= 140 for 2-5y, </= 125 for 5-12 yr, </= 110 for 12-18y
features severe asthms
too breathless to talk
oxygen sats <92
peak flow 33-50%
RR: > 40 for 2-5y, >30 for 5-12 yr, > 25 for 12-18y
HR: > 140 for 2-5y, > 125 for 5-12 yr, > 110 for 12-18y
features life threatening asthma
silent chest, cyanosis
poor resp effort
exhasution
arrhythmia, hypotension
altered consciousness
agitation, confusion
oxygen sats <92
mx moderate acute asthma
calm and reassure
SABA via spacer + face mask <3 2-4 puffs increaseing by 2 puffs every 2mins until 10 puffs if needed
oral pred 1-2mg/kg max 40mg
monitor response for 15-30min
mx severe acute asthma
high flow oxygen
SABA via spacer, 10 puffs or nebulised (2.5mg salbutamol <8, 5mg >8)
oral pred or IV hydrocortisonw
consider; inhaled ipratropium, IV B agonist (salbutamol) or aminophylline or magnesium
mx life threatening acute asthma
high flow oxygen
SABA via spacer, 10 puffs or nebulised (2.5mg salbutamol <8, 5mg >8)
oral pred or IV hydrocortisonw
nebulised ipratropium
consider; inhaled ipratropium, IV B agonist (salbutamol) or aminophylline or magnesium
discuss with PICU
next steps if respondin tto tx in acutr asthma
responding: bronchodilators 1-4hr prn, discharge with 3-7d oral pred when on 4hrly
at discharge: rev medication and inhaler techique, personalsied action plan, arrange follow up
steps if not responding to tx in acute asthma
transfer to HDU
senior rev
consider IV therapies not used (magnesium, aminophylline, B2agonist)
CXR and blood gas
consider mechanical venitaltion
patterns of wheezing in asthma
Viral episodic wheezing – wheeze only in response to viral infections. Multiple trigger wheeze – in response to multiple triggers and which is more likely to develop into asthma over time, Asthma
multiple trigger wheeze and asthma
Frequent wheeze can be triggered by many stimuli, such as: Viruses, Cold air, Dust, Animal dander, Exercise. Atopic asthma is strongly associated with other atopic diseases such as eczema, rhinoconjunctivitis and food allergy
causes of persistent childhood wheeze
Viral episodic wheeze, Multiple trigger wheeze, Asthma , Recurrent anaphylaxis (e.g. in food allergy), Chronic aspiration, Cystic fibrosis, Bronchopulmonary dysplasia, Bronchiolitis obliterans, Trachea-bronchomalacia
pathophysiology asthma
Atopy
Bronchial inflammation – oedema, excessive mucus production, infiltration with cells
Genetic predisposition
Environmental triggers e.g. URTIs, allergens, smoking, cold air, chemical irritants, emotional upset/anxiety, exercise
Bronchial hyperresponsiveness – exaggerated twitchiness to inhaled stimuli
Airway narrowing – reversible airflow obstruction (e.g. peak flow variability)
Symptoms – wheeze, cough, breathlessness, chest tightness
features asthma
Clinical features: Asthmatic wheeze is a polyphonic, Symptoms worse at night and in the early morning, Symptoms that have non-viral triggers, Interval symptoms, i.e. symptoms between acute exacerbations, Personal or family history of an atopic disease, Positive response to asthma therapy
On examination: Long standing asthma – hyperinflation, generalised polyphonic expiratory wheeze with a prolonged expiratory phase. Onset of asthma in early childhood may result in Harrison’s sulci
ix asthma
Younger children – asthma usually diagnosed from history and exam alone. Skin-prick testing for common allergens may be performed to aid the diagnosis of atopy and to identify allergens. Peak expiratory flow rate (PEFR) may be measured or spirometry performed - Poorly controlled asthma leads to increased variability in peak flow, with both diurnal and day-to-day variation.
mx chronic asthma 5-16
- SABA, 2. SABA + ICS, 3. SABA + ICS + LTRA, 4. SABA + MART, 5. SABA and MART with moderate dose ICS, 6. Asthma specialist: MART with high dose ICS or additional drug e.g. theophylline
mx chronic asthma <5
- SABA, 2. 8wk trial moderate dose ICS + SABA, 3. If sx recur within 4wk stopping ICS start low dose ICS, if after 4wk then redo trial, 4. ICS + LTRA + SABA, 5. stop LTRA and refer
cause acute otitis media
Most common at 6-12 months of age. Infants + young children prone to it = Eustachian tubes are short, horizontal and function poorly.
Pathogens include viruses (esp. RSV and rhinovirus), bacteria incl. pneumococcus, H. influenzae and Moraxella catarrhalis
sx acute otitis media
Pain in the ear + fever.
complications acute otitis media
mastoiditis and meningitis (uncommon)
mx acute otitis media
: analgesia. Most cases resolve spontaneously. Antibiotics reduce duration of pain, give if unwell still after 2-3d – amoxicillin usually
glue ear
acute otitis media with effusion
cause glue ear
Recurrent ear infections
features glue ear
Usually asymptomatic apart from possible decreased hearing.
The eardrum is seen to be dull and retracted, often with a fluid level visible.
mx glue ear
Conservation – do nothing, Eustachian tube auto inflation (Otovent balloon), In children that develop conductive hearing loss due to this, insertion of grommets (ventilation tubes) is performed, but benefits only last 12 months
sensorineural hearing loss
caused by a lesion in the cochlea or auditory nerve and is usually present at birth
conductive hearing loss
from abnormalities of the ear canal of the middle ear, most often from otitis media with effusion
causes sensorineural hearing loss
Causes: Genetic (the majority). Antenatal and perinatal: Congenital infection, preterm, Hypoxic-ischaemic encephalopathy, Hyperbilirubinaemia. Postnatal: Meningitis/ encephalitis, Head injury, Drugs e.g. aminoglycosides, furosemide, Neurodegenerative disorders
mx sensorienural hearin gloss
severe bilateral sensorineural hearing impairment will need early amplification with hearing aids for optimal speech and language development.
Children with microtia and meatal atresia can be helped with bone conduction hearing aids
Cochlear implants may be required where hearing aids give insufficient amplification
Gesture, visual context and lip movement will also allow children to develop language concepts.
Specialist teaching and support service in preschool and school years is provided by peripatetic teachers for children with hearing impairment.
causes conducitve eharing loss
It is much more common than sensorineural hearing loss. In association with URTI, many children have episodes of hearing loss, which are usually self-limiting. In some cases of chronic otitis media with effusion, the hearing loss may last months or years.
Children with Down syndrome, cleft palate and atopy are particularly prone to hearing loss from middle ear disease.
diagnosis conductive hearin g;oss
Impedance auditory tests, which measure the air pressure within the middle ear and the compliance of the tympanic membrane
mx conductive hearin gloss
t: If the condition does not improve spontaneously, medical treatment (decongestant or a long course of abx or treatment of nasal allergy) can be given. If that fails, surgery is considered, with insertion of tympanostomy tubes (grommets) with or without the removal of adenoids.
nystagmus
= A repetitive, involuntary, rhythmical eye movement.
causes nystagmus
May be found in association with a structural eye problem (sensory defect nystagmus) but can also be a consequence of a problem at the cortical level.
If no structural eye or brain problem is found = idiopathic nystagmus.
squint
strabismus) = Misalignment of the visual axes.
causes strabismus
common underlying cause is refractive error, but cataracts, retinoblastoma, and other intraocular causes must be excluded. Higher incidence of strabismus in infants with cerebral palsy
esotropia
One eye looks straight ahead; another eye looks towards the nose (convergent)
exotropia
One eye looks straight ahead; another eye looks outwards (divergent)
hypertropia
One eye looks straight ahead; another eye looks upwards (vertical)
hypotropia
One eye looks straight ahead; another eye looks downwards (vertical)
concomitant squint
non-paralytic, common) – usually due to a refractive error in one or both eyes. Correction of the refractive error with glasses often corrects the squint. The squinting eye most often turns inwards (convergent) but there can be outward (divergent), or vertical deviation
paralytic squint
(rare) – varies with gaze direction due to paralysis of the motor nerves. This can be sinister because of the possibility of an underlying space-occupying lesion such as a brain tumour.
ix squint
corneal light reflex, cover test
mx squint
Conservative=Optical - glasses/ CL, Prisms, Orthoptic exercises. Surgery. Botulinum toxin injection
causes severe visual impairment
Cataract, Albinism, Retinal dystrophy, Retinoblastoma, Congenital infection
Retinopathy of prematurity, Hypoxic-ischaemic encephalopathy, Cerebral abnormality/ damage, Optic nerve hypoplasia , Trauma, Infection , Juvenile idiopathic arthritis
hypermetropia
(long sight): Can be corrected with convex (plus) lenses. These make the eye look bigger.
myopia
Myopia (short sight): This is relatively uncommon in young children, presenting usually in adolescence. Can be corrected with concave (minus) lenses. These make the eye look smaller
astigmatism
abnormal corneal curvature)
amblyopia
clear image. Types: strabismic amblyopia, anisometropia amblyopia, ametropic amblyopia, meridional amblyopia, stimulus deprivation amblyopia
tx refractive visual error
underlying condition, together with patching of the ‘good’ eye for specific periods of the day to force the ‘lazy’ eye to work and develop better vision
sx preseptal cellulitis
: erythema and oedema around one eye but normal visual acuity and eye movements
sx orbital celluliits
erythema and oedema around one eye, fever, reduced visual acuity, and painful eye movements – visual symptoms and limited eye movements
mx orbital cellulitis
Need CT scan and IV abx
sx bacterial conjunctivitis
itchy, irritated eyes with purulent discharge
when does squint become abnormal
> 3m
atrial septal defect
L to R shunt
Secundum ASD (80%)
Defect in the centre of the atrial septum involving the foramen ovale
Partial AVSD (common in trisomy 21)
Defect of the atrioventricular septum
features atrial septal defect
Recurrent chest infections, arrhythmias, Ejection systolic murmur at the upper left sternal edge
CXR: Cardiomegaly, enlarged pulmonary arteries, increased pulmonary vascular markings
ECG: Secundum – RBBB, right axis deviation
Partial – superior QRS axis
mx atrial septal defect
Secundum – cardiac catherisation with insertion of occlusion device
Partial – surgical correction
VSD
L to R shunt
Small – smaller than the aortic valve
Large – same size/larger than the aortic valve
features VSD
Small – loud pansystolic murmur, quiet P2
Large – soft panstolic murmur, thrill, loud P2
Heart failure, breathlessness, faltering growth, recurrent chest infections
CXR: Cardiomegaly, enlarged pulmonary arteries, increased pulmonary vascular markings, pulmonary oedema
ECG: Biventricular hypertrophy
mx VSD
Surgery at 3-6 months to prevent Eisenmenger’s
PDA
L to R shunt
Presents in pre-term, flow of blood is from aorta to pulmonary artery
features PDA
Continuous murmur, collapsing pulse, left subclavicular thrill, heaving apex bear, wide pulse pressure
Hepatomegaly, oedema
mx PDA
Cardiac catherisation + insertion of occlusion device 1 yrs. Indomethacin to neonate
tetralogy of fallot
R to L shunt
Large ventricular septal defect, aorta overriding the VSD, pulmonary stenosis, right ventricular hypertrophy
sx and signs tetralogy of fallot
Ejection systolic murmur at the left sternal edge, clubbing, central cyanosis
Dyspnoea on exertion, delayed puberty, low growth, cyanosis within first wk
CXR: Boot shaped heart
ECG: RVH
mx tetralogy of fallot
Surgery in first 2 years of life – closure of the VSD and correction of the pulmonary stenosis
transposition of the great ateries
R to L shunt
Aorta is connected to the right ventricle and pulmonary artery is connected to the left ventricle. Blue blood returned to body; pink blood to lungs
featuers transposition of the great arteries
Cyanosis by day 2 of life, loud/single S2, no murmur
CXR: Narrow upper mediastinum with an ‘egg on side’ appearance of the cardiac shadow
ECG: Biventricular hypertrophy
mx transposition of the great arteries
Maintain ductal patency with prostaglandin infusion.
Balloon atrial septostomy
AVSD
Seen in Down’s syndrome. A defect in the middle of the heart with a single five-leaflet valve between the atria and the ventricles. Stretches across the whole AV junction. Tends to leak
features AVSD
Cyanosis at birth OR heart failure 2-3 weeks of life
mx AVSD
Surgical repair 3-6 months of age
aortic stenosis
Aortic valve leaflets are partly fused together, giving a restrictive exit from the left ventricle
features aortic stenosis
Carotid thrill, ejection systolic murmur radiating to the neck, Only if severe stenosis – reduced exercise tolerance, chest pain on exertion, syncope
CXR: Prominent left ventricle with post stenotic dilatation of the ascending aorta
ECG: LVH
mx aortic stenosis
Balloon valvotomy, aortic valve replacement
pulmonary stenosis
Pulmonary valve leaflets are partly fused together, giving a restrictive exit from the right ventricle
eatures pulmonary stenossi
Ejection systolic murmur, ejection click at upper left sternal edge. If severe – heave (right ventricle). Asymptomatic
CXR: Post stenotic dilatation of the pulmonary artery
ECG: RVH
mx pulmonary stenossi
Transcatheter balloon diltation
coarctation of the aorta
Congenital narrowing of the descending aorta - Excessive blood flow is diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body 🡪 stronger perfusion to the upper body than the lower
features coarctation of the aorta
Radio-femoral delay, weak femoral pulse, systolic murmur, discrepancy between upper/lower limb BP. Heart failure
Can lead to infective endocarditis
CXR: cardiomegaly, irregularities of the inferior margins of the posteriorribs
mx coarctation of the aorta
ABCs, prostaglandins, balloon dilation and surgery
circulatory changes at birth
1.In the foetus, the left atrial pressure is low, as relatively little blood returns from the lungs.
2.The pressure in the right atrium is higher than in the left, as it receives all the systemic venous return including blood from the placenta.
3.The flap valve if the foramen ovale is held open, blood flows across the atrial septum into the left atrium, and then into the left ventricle, which in turn pumps it to the upper body.
4.With the first breaths, resistance to pulmonary blood flow falls and the volume of blood flowing through the lungs increases six-fold.
5.This results in a rise in the left atrial pressure. Meanwhile, the volume of blood returning to the right atrium falls as the placenta is excluded from the circulation.
6.The change in the pressure difference causes the flap valve of the foramen ovale to be closed.
7.The ductus arteriosus, which connects the pulmonary artery to the aorta in foetal life, will normally close within the first few hours or days.
causes dilated cardimyopathy
inherited, secondary to metabolic disease of a result of direct viral infection of the myocardium
features cardiomyopathy
an enlarged heart and heart failure who was previously fit and well
diagnosis cardio,yopathy
echo
mx cardiomyopathy
diuretics and ACEi and carvedilol, a a-adrenoceptor blocking agent. Usually improves spontaneously, but some children may require heart transplants
who is at increased risk infective endocarditis
VSD, coarctation of the aorta and PDA or if prosthetic material has been inserted at surgery
features IE
Clinical features: Fever, Anaemia and pallor, Splinter haemorrhages in nailbed, Clubbing (late), Necrotic skin lesions, Changing cardiac signs, Splenomegaly, Neurological signs from cerebral infarction, Retinal infarcts, Arthritis/ arthralgia, Haematuria (microscopic
diagnosis IE
Blood cultures. Echo. Acute-phase reactants are raised
cause IE
= B-haemolytic streptococcus
mx IE
Bacterial endocarditis is usually treated with high-dose penicillin in combination with an aminoglycoside (6 weeks IV therapy). Infected prosthetic material may require surgical removal
features HF
Symptoms: Breathlessness (particularly on feeding or exertion), Sweating poor feeding, Recurrent chest infections
Signs: Poor weight fain or faltering growth, Tachypnoea, Tachycardia, Heart murmur, gallop rhythm, Enlarged heart, Hepatomegaly, Cool peripheries
cause HF
In the first week of life, heart failure usually results from left heart obstruction, e.g. coarctation of the aorta. (Right-to-left shunt)
After the first week, progressive heart failure is most likely due to a left-to-right shunt.
eisenmenger syndrome
If a left-to-right shunt is left untreated, these children will develop Eisenmenger syndrome, which is irreversibly raised pulmonary vascular resistance resulting from chronically raised pulmonary arterial pressure and flow. Now the shunt is right-to-left, and the teenager is blue
mx eisenmenger syndrome
heart lung transplant
features rheumatic fever
Latent interval of 2-6 weeks following a pharyngeal or skin infection, polyarthritis, mild fever and malaise develop.
diagnosing rheumatic fever
two major, or one major and two minor criteria plus supportive evidence of preceding group A streptococcal infection
major jones criteria
carditis (endocarditis-significant murmur or valvular dysfunction, myocarditis-may lead to HF, pericarditis-pericardial friction rub, pericardial effusion, tamponade), migratory arthritis (ankles/knees/wrists tender, red, swollen), Sydenham chorea, erythema marginatum, subcutaneous nodules
minor jones criteria
fever, polyarthralgia, raised ESR/CRP/leucocytes, prolonged PR on ECG
mx rheumatic fever
Acute rheumatic fever = bed rest and anti-inflammatory agents. Corticosteroids may be required if fever and inflammation not resolving. Symptomatic heart failure is treated with diuretics and ACEi. Significant pericardial effusions will require pericardiocentesis
Effective prophylaxis = monthly injections of benzathine penicillin.
Prophylaxis is for 10 years/ until the age of 21 (which is longer).
supraventricular tachycardia
Most common child arrhythmia
250-300beats/min
presentation supraventicualr tachycardiq
Poor cardiac output, pulmonary oedema, hydrops fetalis/intrauterine death
ECG supraventrivcualr tachcyardi
re-entry tachcyardia
narrow complex
250-300bpm
mx supraventricualr tachcyardia
Restore sinus rhythm 🡪 IV adenosine
Maintenance therapy 🡪 flecainide/ sotalol
congenital heart block
Related to maternal anti-ro/anti-La antibodies
Prevents normal development of the electrical conduction system in the developing heart 🡪 Atrophy and fibrosis of the atrioventricular node
presentation congenital heart block
Presyncope / syncope
Death in utero/heart failure in neonates
ECG congenital heart block
P and QRS are dissociated
mx congenital heart block
an endocardial pacemaker
long QT syndrome
Autosomal dominant
Assess if family hx of sudden death / syncope
presentation lock QT syndrome
Sudden LOC during exercise/stress
mx long QT syndrome
Bblockers, pacemaker
ductus venosus role and remnant
allows blood from the placenta to bypass the highly demanding, but relatively inactive liver -> ligamentum venosum
ductus arteriosus role and remnant
allowing blood to pass straight from the right ventricle into the aorta and bypass the inactive lungs ->ligamentum arteriosum
forament ovale role and remnant
creates a shunt between the right atrium and the left atrium so oxygenated blood from the placenta can move to the left atrium -> fossa ovalis
causes of acute dairrhoea
Infective gastroenteritis, Non-enteric infections e.g. respiratory tract, Food hypersensitivity reactions, NEC, Drugs e.g. antibiotics, Henoch-Schonlein purpura, Intussusception (<4yrs), Haemolytic-uremic syndrome, Pseudomembranous enterocolitis
mx acute diarrhoea
Assess hydration and vital signs, pallor (blood loss), abdominal tenderness
mx mild/moderate dehydration
Replace fluid and electrolyte losses with oral glucose-electrolyte based rehydration fluid e.g. Dioralyte
mx severe dehydration/shock
U&E, creatinine, FBC, blood gas, stool M,C&S/virology, tests for specific disease + IV fluid and electrolyte replacement
causes of chronic diarrhoea <2y
Malabsorption e.g. post-infective gastroenteritis syndrome, lactose intolerance, cystic fibrosis, coeliac disease, Food hypersensitivity e.g. to cow’s milk protein, Chronic non-specific diarrhoea (toddler diarrhoea): child is usually thriving, Excessive fluid intake, Protracted infectious gastroenteritis, Immuno-deficiencies, Hirschsprung’s disease, Tumours (secretory diarrhoea), Fabricated induced illne s
causes of chronic dirahhoea in older children
IBD, Constipation (spurious diarrhoea), Malabsorption, IBS, Chronic infections, including giardiasis, bacterial overgrowth and pseudomembranous colitis, Laxative abuse (EDs), Excessive fluid intake, Fabricated induced illness
ix chronic dirahhoea
Stool microscopy, Blood: U&E, FBC, increased CRP/ESR. Radiology: AXR, US, barium meal and follow through
causes acute vomiting
infection, GI obstruction (congenital or acquired e.g. pyloric stenosis), adverse food reaction, poisoning, raised ICP, DKA
causes chronic vomiting
eptic ulcers, GORD, chronic infection, gastritis, gastroparesis, food allergy, psychogenic, bulimia, pregnancy. Cyclic: idiopathic, CNS disease, abdominal migraine, endocrine, metabolic, intermittent GI obstruction, fabricated illness
consequences of vomiting
Metabolic = Potassium deficiency, Alkalosis, Sodium depletion.
Nutritional .
Mechanical injuries to oesophagus and stomach: Mallory-Weiss, Boerhaave’s syndrome, Tears of the short gastric arteries resulting in shock and hemopritoneum.
Dental: erosions and caries.
Oesophageal stricture, Barrett’s metaplasia, broncho-pulmonary aspiration, FTT, anaemia
causes of constipation
= Low fibre diet, Lack of mobility and exercise, Poor colonic motility. Gastrointestinal: Hirschsprung’s disease, Anal disease (infection, stenosis, ectopic, fissure, hypertonic sphincter), Partial intestinal obstruction, Food hypersensitivity, Coeliac disease. Non-gastrointestinal: Hypothyroidism, Hypercalcaemia, Neurological disease e.g. spinal disease, Chronic dehydration e.g. diabetes insipidus, Drugs e.g. opiates and anticholinergics, Sexual abuse
ix in constipation
Investigations: If an organic cause is suspected consider: FBC – coeliac antibody screen, thyroid function tests, RAST testing. AXR, rectal biopsy (Hirschsprung’s disease).
mx constipation
tx cause. Dietary: increased oral fluid and fibre intake, natural laxatives, e.g. fruit juice. Behavioural measures: toilet footrests, regular 5min toilet time after meals, star charts and rewards for child passing stool. Regular oral faecal softeners e.g. Movicol, lactulose, or sodium docusate, will aid disimpaction. Oral stimulant laxatives, e.g. Senna, sodium picosulphate, may be required
abdo pain alarm feature
nvoluntary weight loss, Deceleration of linear growth, GI blood loss (visible or occult), Significant vomiting (incl. bilious, protracted, cyclical), Chronic severe diarrhoea, Persistent right upper or lower quadrant pain, Unexplained fever, Family Hx IBD, Abnormal or unexplained physical findings
presentation chronic non specific diarrhoea
toddlers diraahoea
6m-5y
Presents with colicky intestinal pain, increased flatus, abdominal distension, loose stools with undigested food . Child is otherwise well and thriving
GORD
reflux is repeated and severe enough to cause harm.
Reflux is very common in infancy and is associated with slow gastric emptying, liquid diet (milk), horizontal posture, and low resting lower oesophageal sphincter (LOS) pressure.
GORD presentation
Regurgitation, Non-specific irritability, Rumination , Oesophagitis (heartburn, difficult feeding with crying, painful swallowing, haematemesis), Faltering growth (calorie deficiency due to profuse reflux of ingested calories), Apnoea, Hoarseness, Cough, Stridor, Lower respiratory disease – aspiration, pneumonia, asthma
complications GORD
Oesophageal stricture (dysphagia), Barrett’s oesophagus (premalignant intestinal metaplasia), Faltering growth, Anaemia (chronic blood loss), Lower respiratory disease
ix GORD
Only appropriate when diagnosis uncertain, and there is poor response to treatment, Upper GI endoscopy, Oesophageal biopsy , 24hr oesophageal pH probe
mx GORD
Positioning, thickened milk feeds (infants), small frequent meals, avoid food before sleep, fatty foods, citrus juices, caffeine and carbonated drinks, gastric acid reducing drugs e.g. H2 receptor antagonists (ranitidine) or omeprazole (if oesophagitis) or Gaviscon. Surgery: only indicated if failure of intense medical treatment.
causes viral gastroenteritis
Rotavirus (most common), Small round structural virus e.g. winter vomiting disease caused by ‘Norwalk agent’, Enteric adenovirus, Astrovirus, CMV (in immune-comprised patients)
presentation viral gastroenteritis
Water diarrhoea (rarely bloody), Vomiting, Cramping abdominal pain, Fever, Dehydration, Electrolyte disturbance, Upper respiratory tract signs common with rotavirus, Vomiting predominates with Norwalk virus
mx viral gastroenteritis
Give supportive rehydration orally or with a nasogastric tube, or IV glucose and electrolyte solution
causes bacterial gastroenteritis
Salmonella, Campylobacter jejuni, Shigella, Yersinia enterocolitica, Escherichia coli, Clostridium difficile, Bacillus cereus, Vibrio cholerae
Sources of infection include contaminated water, poor food hygiene (meat, fresh produce, chicken, eggs, previously cooked rice), faecal-oral route.
presentation bacterial gastroenteritis
As for viral gastroenteritis plus: Malaise, Dysentery (bloody and mucous diarrhoea), Abdominal pain may mimic appendicitis or IBD, Tenesmus (feeling as though you need to pass stools even though your bowel is empty)
complications bacterial gastroenteritis
Bacteraemia, Secondary infections (particularly Salmonella, Campylobacter), e.g. pneumonia, osteomyelitis, meningitis, Reiter’s syndrome (Shigella, Campylobacter)
ix bacterial gastroenteritis
Stool +/- blood culture (some organisms need specific culture medium), Stool Clostridium difficile toxin, Sigmoidoscopy if IBD or colitis
mx bacterial gastroenteritis
Rehydration as for viral gastroenteritis. Consider: Erythromycin if Campylobacte, Oral vancomycin or metronidazole if Clostridium difficile (causes pseudomembranous colitis).
dehydration classification
Dehydration in children is classified as mild (<5%), moderate (5-10%) and severe (>10%).
presentation dehydration
: Children with mild dehydration appear completely normal on examination. Children with moderate dehydration appear well, but have reduced urine output and dry mucous membranes in the absence of other red flag features. Children with severe dehydration have red flag features including a pale, mottled appearance, cool extremities, tachycardia, tachypnoea and/or hypotension, delayed capillary refill, or a change in consciousness.
features crohns disease
Symptoms: Diarrhoea , Abdominal pain, Weight loss/failure to thrive, Systemic symptoms: fatigue, fever, malaise, anorexia
GI Signs: Aphthous ulcers , Abdominal tenderness/mass, Perianal abscess/fistulae/skin tags, Anal strictures, Abdominal distension (UC>CD), RIF mass
Non-GI signs and associations: Fever, Finger clubbing, Anaemia, Skin: erythema nodosum, pyoderma gangrenosum. Joints: arthritis, ankylosing spondylitis. Eyes: iritis, conjunctivitis, episcleritis. Poor growth, Delayed puberty, Sclerosing cholangitis, Renal stones, Nutritional deficiencies e.g. vitamin B12
complication crohsn disease
Small bowel obstruction, Toxic dilatation , Abscess formation, Fistulae , Malnutrition
ix crohns disease
Colonoscopy and biopsy=Crypt abscesses, granulomas, transmural inflammation. Radiology=Mucosal ‘cobblestone’ appearance, ulceration, dilatation, narrowed segments, fistula, ‘skip lesions
mx crohns disease
Mild-moderate = Oral 5-aminosalicylic acid (ASA) dimers, e.g. mesalazine. Moderate to severe = Induce remission with oral prednisolone or IV methylprednisolone, 1-2mg/kg/day until condition improved (<2wks) then wean over 6-8wks.. Antibiotics: e.g. ciprofloxacin or metronidazole, may also be useful. Maintenance treatment: immunomodifiers e.g. azathioprine, ciclosporin, tacrolimus, methotrexate, or infliximab (anti-TNF antibody). Surgery: local surgical resection for severe localised disease e.g. strictures, fistula, may be indicated, but there is a high re-operation rate as inflammation recurrence is universal.
features ulcerative colitis
Symptoms: Episodic or chronic diarrhoea, Crampy abdominal discomfort, Bowel frequency relates to severity, Urgency/tenesmus – proctitis, Systemic symptoms: fever, malaise, anorexia, weight loss
Signs: Acute, severe UC – fever, tachycardia, tender distended abdomen. Extra-intestinal signs: Clubbing, Aphthous oral ulcers, Conjunctivitis
ix UC
Endoscopy: UC histology – crypt abscesses, mucosal inflammation only, goblet cell depletion. Radiology: Mucosal ulceration, haustration loss, colonic narrowing +/- shortening
mx UC
: Mild UC = Mesalamine is the mainstay for remission-induction/maintenance. Moderate UC=Induce remission oral prednisolone. Surgery: total colectomy and ileostomy, and later pouch creation and anal anastomosis, cures UC.
pathology coeliac disease
: T-cell responses to gluten in the small bowel causes villous atrophy and malabsorption.
resentation coeliac disease
Pallor, Diarrhoea, Pale, bulky floating stools, Anorexia, FTT, Irritability. Later: Apathy, Gross motor developmental delay, Ascites, Peripheral oedema, Anaemia, Delayed puberty, Arthralgia, Hypotonia, muscle wasting, Specific nutritional disorders
ix coeliac disease
Low Hb, B12 and ferritin. Antibodies: anti-transglutaminase is single preferred test – check IgA levels, Serum tissue transglutaminase IgA antibody (TTG). Endoscopy small bowel biopsy of the third part of the duodenum shows diffuse, subtotal villous atrophy, increased intraepithelial lymphocytes, and crypt hyperplasia
IBS
A mixed group of abdominal symptoms for which no organic cause can be found. Most are probably due to disorders of intestinal motility, enhanced visceral perception or microbial dysbiosis.
presentation IBS
: Urgency, Abdominal bloating/distension, Worsening of symptoms after food, Symptoms are chronic >6 months and often exacerbated by stress, menstruation or gastroenteritis.
ix IBS
: FBC, CRP, ESR, U&E, Coeliac screen, Faecal calprotectin
Only diagnose IBS if recurrent abdominal pain associated with at least 2 of: Relief by defecation, Altered stool form, Altered bowel frequency (constipation/diarrhoea)
mx IBS
Should focus on controlling symptoms, initially using lifestyle/dietary measures, then cognitive therapy or pharmacotherapy if required. Constipation: ensure adequate water and fibre intake and promote physical activity. Diarrhoea: avoid sorbitol sweeteners, alcohol and caffeine. Reduce dietary fibre content, encourage patients to identify their own trigger foods. Colic/bloating: oral antispasmodics e.g. buscopan. Combination probiotics in sufficient doses may help flatulence or bloating. Less alcohol intake. Psychological symptoms/visceral hypersensitivity: emphasize the positive. Sinister pathology has been excluded and symptoms tend to improve over time. Consider CBT and hypnosis.
causes poor feeding
Premature birth – most common, Traumatic birth injuries that lead to neurological disorders, such as cerebral palsy, Cleft lip and/or cleft palate, Autism, Neck and head abnormalities, Low birth weight, Respiratory problems, Heart disease.
features of poor feeding
Arching the back andbodywhilefeeding, Fussinessor lack of alertness whilefeeding, Refusing to eat and drink food andliquids, Excessively long feeding times, Hoarse, or breathy voice quality, Frequent spitting up and/or vomiting, Recurring pneumonia or respiratory infections, Poorweight gain or growt
mx poor feeding
Medications, Food temperature and texture changes, Postural or positioning changes, Mouth exercises to make the mouth muscles stronger
failure to threive
Weight is the most sensitive indicator in infants and young children, whilst height is better in the older child.
Definition: Fall across 2 centiles on growth chart
causes FTT
not enough food being offered or taken, socioeconomic difficulty, emotional deprivation, unskilled feeding , Decreased appetite e.g. psychological or secondary to chronic illness, Inability to ingest, e.g. GI structural or neurological problems, Excessive food loss, e.g. severe vomiting (GORD, pyloric stenosis, dysmotility), diabetes mellitus (urine), Malabsorption, Increased energy requirements e.g. congenital heart disease, CF, malignancy, sepsis, Impaired utilisation (various syndromes)
mx FTT
If it resolves in a few weeks, give positive reinforcement and supervise, subsequent growth as an outpatient. If it persists, admit to hospital and observe under supervised adequate dietary input. Adequate growth suggests a non-organic cause
kwashiorkor
Kwashiorkoris a form of severe protein malnutrition characterized by oedema and an enlarged liver with fatty infiltrates. It is caused by sufficient calorie intake, but with insufficient protein consumption, which distinguishes it from marasmus.
features kwashiorkor
Growth retardation, Diarrhoea, Apathy, Anorexia, Oedema, Skin/hair depigmentation , Abdominal distension with fatty live
ix kwashiorkor
Bloods = hypoalbuminaemia, normo- and microcytic anaemia, low calcium, magnesium, phosphate, and glucose
mx kwashiorkor
Correct dehydration and electrolyte imbalance, Treat underlying infection and/or parasitic infections, Treat concurrent/causative disease and nutrient deficiencie
marasmus
inadequate energy intake in all forms, including protein.
features marasmus
Height is relatively preserved compared to weight, Wasted appearance, Muscle atrophy, Listless, Diarrhoea, Constipation
ix marasmus
Low serum albumin, Hb, U&Es, calcium, magnesium, phosphate and glucose, stool MC&S for intestinal ova, cysts and parasites
mx marasmus
: Correct dehydration and electrolyte imbalance, Treat underlying infection and/or parasitic infections, Treat concurrent/causative disease and nutrient deficiencies
presentation pyloric stenosis
M>F, may be a fhx, projectile non bile stained vomit first 4-6w life, hypochloraemic, hypokalaemic metabolic alkalosis
ix pyloric stenosis
Test feed or USS
my pyloric stenosis
Correct alkalosis, Ramstedt pyloromyotomy
presentation acute appendicitis
Uncommon <3y, Pain is aggravated by movement – right iliac fossa, Child may prefer to lie still with knees flexed, Mild fever, Peritoneal irritation results in involuntary spasm in the muscles of the abdominal wall (guarding).
ix acute appendicitis
USS
mx acute appendicitis
appendicectomy
presentation mesenteric adenitis
central abdo pain and urti
mx mesenteric adenitis
conservative
presentation intussusception
Telescoping bowel proximal to or at level of ileocaecal valve. 6-9m, colicky pain, diarrhoea, vomiting, sausage shaped mass, red jelly stool, drawing up of legs
ix intussusception
USS-target sign, AXR-small bowel obstruction
mx intussusception
Reduction and air inflation
presentation intestinal malrotation
High caecum at midline. Features in examphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia. May be complicated by volvulus (bile stained vomiting)
ix intestinal malrotation
Upper GI contrast study and USS
x intestinal malrotation
Laparotomy , if volvulus = ladds procedure
presentation hirschsprungs
Absence of ganglion cells from myenteric and submucosal plexuses. Delayed passage of meconium and abdo distension
ix hirschsprungs
ful thickness rectal biopsy
mx hirschsprungs
Rectal washouts then anorectal pull
resentation oesophageal atresia
Associated with trachea-oesophageal fistula and polyhydramnios. Choking, cyanotic spells following aspiration
presentation meconium ileus
Delayed passage meconium and abdo distension. Associated with CF
ix meconium ileus
AXR = bubbly, will not show fluid level.
mx meconium ileus
PR contrast and NG N-acetyl cysteine, Gastrograffin enema, surgery
presentation biliary atresia
Jaundice >14d, increased conjugated bilirubin, wt loss, swollen abdo
ix biliary atresia
Liver biopsy
my biliary atresia
Kasai procedure
presentation necrotising enterocolitis
RF=prematurity. Abdo distension and passage of bloody stools
ix necrotising enterocolitis
XR=pneumatosis intestinalis and free air
mx necrotising enterocolitis
TPN, if perforates laparotomy
presentation meckels diverticulum
presence of the embryonic vitelline duct that normally involutes during late foetal development.GI bleeding, obstruction, inflammation, umbilical discharge.
ix meckels diverticulum
Technetium 99 scan.
mx meckels diverticulum
Laparotomy and resection
causes chronic liver failure
Chronic hepatitis (After viral hepatitis B or C), Biliary tree disease e.g. biliary atresia, Toxin-induced e.g. paracetamol, alcohol, Alpha1-antitrypsin deficiency, Autoimmune hepatitis, Wilson’s disease (age >3yrs), Cystic fibrosis, Alagille syndrome or non-syndromic paucity of bile ducts, Tyrosinemia , Primary sclerosing cholangitis, PN-induced, Budd-Chiari syndrome
presentation chronic liver failure
Jaundice (not always), GI haemorrhage (portal hypertension and variceal bleeding), Pruritus , FTT, Anaemia, Enlarged hard liver (though liver often small in cirrhosis), Non-tender splenomegaly, Hepatic stigmata e.g. spider naevi, Peripheral oedema and/or ascites, Nutritional disorders e.g. rickets, Developmental delay or deterioration in school performance, Chronic encephalopathy
mx chronic liver failure
Treat the underlying cause and give nutritional support - Lower protein, increased energy, higher carbohydrate diet, Vitamin supplementation, particularly fat soluble vitamins A,D,E,K. involve a paediatric dietitian. Drug therapy: Prednisolone +/- azathioprine for autoimmune hepatitis, Interferon-alpha +/- ribavirin for chronic viral hepatitis, Penicillamine for Wilson’s disease, Colestyramine may be useful to control severe pruritus, Vitamin K1 if significant coagulopathy or bleeding. Treat symptoms: Oesophageal varices – endoscopy, Ascites – fluid restriction and spironolactone, Encephalopathy – reduce GI ammonia absorption using oral lactulose, Liver transplant
presentation alpha 1 antitrypsin deficiency
Cholestasis in infancy, may progress to liver failure, Cirrhosis can occur in late childhood to adult. Chronic liver disease affects 25% of patients in late adulthood. Pulmonary emphysema is the commonest presentation in adulthood
mx alpha 1 antitrypsin deficincy
Treatment: Supportive treatment of liver complications, Liver transplant for end-stage liver failure
nheritance wilson
autosomal recessive disorder
presentation wilsons
Kayser-Fleischer rings (copper deposition in Descemet’s membrane in the eye) often present and are pathognomonic. May require slit-lamp examination to visualise. Hepatic problems usually present in childhood (hepatitis, cirrhosis, fulminant hepatic failure). Adolescents/ young adults usually present with neurological disease
ix wilsons
Serum copper and ceruloplasmin low, 24hr urinary copper excretion >100microgram (normal <40), Molecular genetic testing – Wilson’s gene (ATP7B) mutation
mx wilsons
Lifelong chelation therapy with penicillamine (reverses pre-cirrhotic liver disease, but not neurological damage), Liver transplantation if end-stage hepatic failure
colic
when an infant who isn’t sick or hungry cries for more than 3 hours a day, more than 3 days a week, for more than 3 weeks.
presentation colic
likely to start around 2 weeks of age if your infant is full-term, or later if they were born prematurely.
Features: It’s hard to soothe or settle your baby, They clench their fists, They go red in the face, They bring their knees up to their tummy or arch their back, Their tummy rumbles or they’re very windy
inguinal hernia features
More common in boys, More common on the right side, usually asymptomatic, a reducible swelling in groin
mx inguinal hernia
Surgical herniotomy. Infants should be repaired within a few weeks of diagnosis because the risk of incarceration is high.
incarcerated hernia: results in an intestinal obstruction
mx umbilical hernia
Most will close spontaneously during the first few years of life, regardless of size
If the hernia fails to close surgical repair can be performed at around 5yrs of age
presentation congenital diaphragmatic hernia
Respiratory distress – tachypnoea, cyanosis, grunting. Scaphoid abdomen (because bowel in chest), Apparent dextrocardia (mediastinum displaced into right thorax, Bowel sounds may be audible in chest (uncommon)
mx congenital diaphragmatic hernia
Initial management consists of sedation, paralysis, endotracheal intubation, and mechanical ventilation with 100% O2, repair of the diaphragmatic defect is undertaken after a few days either by primary suture or insertion of a prosthetic patch
hiatus hernia
herniation of the stomach into the chest through the oesophageal hiatus in the diaphragm. The lower oesophageal sphincter also moves and becomes incompetent
Two types of hiatus hernia are recognised: Sliding (common), Rolling or paraesophageal (rare)
mx hiatus hernia
Diagnosis is made radiologically by barium meal. Surgery is reserved for children who fail to respond to medication, complicated reflux (e.g. peptic strictures), and paraesophageal hernias
presentration cows milk allergy
Symptoms depend on where the allergic inflammation is: Upper GI tract – vomiting, feeding aversion, pain. Small intestine – diarrhoea, abdominal pain, protein-losing enteropathy, FTT. Large intestine – diarrhoea, acute colitis with blood and mucus in stools, rarely chronic constipation
mx cows milk allergy
, first treat by limiting cow’s milk protein intake (and commonly soy protein). In exclusively breast-fed infants, this is achieved by a maternal exclusion diet to these proteins. In formula fed infants feed with a hydrolysed formula (short peptides)
presentation UTI
: Vomiting, poor feeding, with or without abdominal pain or tenderness, Lethargy or irritability, Urinary frequency or dysuria, Haematuria
ix UTI
> 10,5 organisms/mL in pure growth from a carefully collected urine sample (midstream urine, clean catch urine, or bag urine).
Investigations: Dipstick test in the urine. ‘Leucocytes’ and ‘nitrites’ strongly suggests UTI. Urine should be sent for microscopy, culture, and sensitivity,
mx UTI
Antibiotics should be started after urine collection e.g. Trimethoprim, Co-amoxiclav. Infants less than 3 months old should be referred immediately to a paediatrician. Children aged more than 3 months old with an upper UTI should be considered for admission to hospital. If not admitted oral antibiotics such as cephalosporin or co-amoxiclav should be given for 7-10 days. Children aged more than 3 months old with a lower UTI should be treated with oral antibiotics for 3 days according to local guidelines, usually trimethoprim, nitrofurantoin, cephalosporin or amoxicillin. Parents should be asked to bring the children back if they remain unwell after 24-48 hours
primary nocturnal enuresis
Majority of cases have no underlying organic cause and it is thought to be due to delayed maturation of bladder control mechanisms.
secondary nocturnal enuresis
UTI, spina bifida, diabetes mellitus, diabetes insipidus, Behavioural problems, Abuse
nocnturnal enuresis
Encourage regular drinks (water), but restrict in last hour before bed, Give drinking/ voiding chart, Enuresis alarm, >7 years: desmopressin can be considered
pre renal causes AKI
Hypovolaemia e.g. gastroenteritis, haemorrhage, DKA, nephrotic syndrome, Peripheral vasodilatation e.g. sepsis, Impaired cardiac output e.g. congestive cardiac failure, Drugs e.g. ACE inhibitors
renal causes AKI
Acute tubular necrosis, Interstitial nephritis, Glomerulonephritis, Haemolytic-uraemic syndrome, Cortical necrosis, Bilateral pyelonephritis, Nephrotoxic drugs e.g. aminoglycoside, IV contrast, NSAIDs, Myoglobinuria, haemoglobinuria, Tumour lysis syndrome, Renal artery/ vein thrombosis
post renal causes AKI
Obstruction, Post-urethral valves, Neurogenic bladder , Calculi, Tumours (rhabdomyosarcoma in infancy)
mx AKI
Treat electrolyte imbalances and shock. Fluids management: pre-renal – fluid bolus and furosemide. Otherwise restrict insensible losses + urine output.
Indications for dialysis: Severe hyperkalaemia, Symptomatic uraemia with vomiting/encephalopathy , Rapidly rising urea and creatinine, Symptomatic fluid overload, especially cardiac failure or pericardial effusion, Uncontrollable hypertension, Symptomatic electrolyte problems or acidosis, Encephalopathy or seizures, Prolonged oliguria: conservative regimen controls ARF, but causes nutritional failure, Removal exogenous toxins or metabolites (inborn error)
presentation CKD
Failure to thrive, Polyuria and polydipsia, Lethargy, lack of energy, poor school concentration, Other abnormalities such as ricket
auses CKD
Congenital =Renal dysplasia, Obstructive uropathies, Vesicoureteric reflux nephropathy. Hereditary =PKD, Hereditary nephritis, Cystinosis, Oxalosis . Glomerulopathies= Focal segmental glomerulosclerosis. Multisystem disorders=SLE, HSP, Haemolytic-uraemic syndrome. Others=Wilms’ tumour, Renal vascular disease, Unknown
hypospadias
A birth defect in which the opening of the urethra is on the underside of the penis instead of at the tip.
consequences hypospadias
difficulty urinating while standing and a cosmetic appearance Sexual function is not affected unless chordee, which may cause painful erections, is present
mx hypospadias
do not circumcise, surgery
vesicoureteral reflux
retrograde flow of urine from the bladder into the upper urinary tract.
Grade of VUR: I-V
diagnosis vesicoureteral reflux
Micturating cystourethrogram – requires catheter, Indirect cystogram
mx vesicoureteral reflux
Prophylactic antibiotics against UTI, surgery
features haemolytic uraemic syndrome
A group of blood disorders characterized by low red blood cells, acute kidney failure, and low platelets.
Initial symptoms typically include bloody diarrhoea, fever, vomiting, and weakness. Kidney problems and low platelets then occur as the diarrhoea is improving.
Microangiopathic haemolytic anaemia, Thrombocytopenia, Acute kidney failure
cause HUS
e.coli
phimosis
tigh foreskin
nephrotic syndrome
Defined as a combination of: Heavy proteinuria (urinary protein to creatinine ratio >200mg/mmol), Hypoalbuminemia (albumin <25g/L), Oedema, Hyperlipidaemia
causes nephrotic syndrome
Primary =Congenital,Infantile. Secondary =Minimal change disease (MCD): commonest, Focal segmental glomerulosclerosis, Membranoproliferative glomerulonephritis, Membranous glomerulonephritis
mx nephrotc syndrome
: fluid restriction and prevention of hypovolaemia , Trial of oral steroid therapy to induce remission is also started, Prophylaxis against bacterial infection (particularly pneumococcal)
complications nephrotic syndrome
Predisposition to infection is due to decreased IgG levels, Thrombosis, Hypovolaemia
minimal change disease
most common cause of nephrotic syndrome in children (~70%) and is characterised by minimal histological changes in the kidney structure
presentation minnimal change disease
facial swelling and are most commonly 1-8 years old. May be asymptomatic
mx minimal change disease
Fluid restriction and reduced salt intake, Corticosteroid therapy: prednisolone, Human albumin and furosemide
complications minimal change diseas
Spontaneous peritonitis, Thrombosis, Recurrent minimal change disease, Hypertension
nephritic syndrome
Haematuria, Oedema (to a lesser extent compared to nephrotic syndrome), Reduced urine output, Uraemic symptoms (e.g. reduced appetite, fatigue, pruritus, nausea), HTN, mild proteinuria
causes neohritic syndrome
Post-infectious = Bacterial: streptococcal commonest, Staphylococcus aureus, Mycoplasma pneumoniae, Salmonella, Virus: herpes viruses (EBV, varicella, CMV), Fungi: candida, aspergillus,Parasites: toxoplasma, malaria, schistosomiasis . Others (less common) = MPGN (membranoproliferative glomerulonephritis), IgA nephropathy, SLE, Subacute bacterial endocarditis, Shunt nephritis
mx nephritic syndrome
fluid balance and restrict salt, mx HTN with alpha blocker or CCB
features post strep glomerulonephritis
Usually presents 1-2weeks after a URTI and sore throat, treat with antibiotics (penicillin)
