Child health Flashcards
Measuring growth
Centile charts
- dots for height and weight, x for bone health
- MPH plotted at 20 years (mid +7 for boys -7 for girls)
- TPR ±10cms for males, ±8.5cms for females
Height velocity on chart
Monitor secondary sex characteristics with Tanner staging (absent=0): B1-5 (breast stage) P1-5 (pubic hair stage) G1-5 (penis and testicle development) A0-1 (axillary hair)
Key ages in growth
- age 0-2 – driven by nutrition mainly
- 2-puberty – driven by GH mainly
- Puberty-adulthood – driven by sex steroids and increased GH
- Menarche ~13
- Sexual precocity (if any signs of puberty developing before these ages, then urgent investigation needed)
In girls before 8
In boys before 9 - Peak height velocity
In girls, when breast stage 2-3 (early)
In boys, when 12-15mls testes (late)
Factors affecting height
Normal
- familial short stature
- intrauterine growth retardation
- constitutional delay in growth and puberty – not a disease – but many find it problematic (depends on parental ages of puberty)
Pathological
- hypothyroidism (congential hypothyroidism should be detected on screening at day 4 – but if central (low TSH) then won’t be detected)
- chronic disease – coeliac, crohn’s, cystic fibrosis
- excess corticosteroids (Cushings syndrome common, Cushings disease rare)
- parental neglect
- growth hormone deficiency
- diabetes mellitus (usually T1, so need short acting insulin in day + long acting at night, ~30% on insulin pumps, aim to maintain 2-4.0mmol, can use continuous blood sugar monitoring)
- coeliac disease
Investigating short stature
= height <3rd centile - record birth weight - record both parental final heights \+ calculate MPH and TPR - check feeding technique!
- measure height velocity, if poor…
- check bone age
- check FBC, U+Es, TFTs, coeliac screen
- karyotype in girls (Turner’s XO)
- MSU
- coeliac serology, U+E, glucose, LFT, calcium levels, proteins, CRP, TSH (hypothyroid common!), FBC
- sweat test
- stools (MC+S and sugar)
- CXR, renal or CNS USS
- skeletal study for dwarfism and abuse
- ECG/echo
1st – assume constitutional delay (likely parents were the same), so offer testosterone. If testosterone not improving height velocity…
- hypogonadothropic hypogonadism (small gonads due to pituitary problem – lack of gonadotrophs, test FSH / LH levels)
- Kleinfelter’s syndrome – XXY, test karyotype
Turner’s syndrome
XO
- can present with hand/foot lymphoedema, webbed neck, shield chest (nipples point out), cardiac/renal abnormalities, intellectual delay
- but often just detect in growth clinic as short stature (if mosaic, not complete)
- need oestrogen replacement therapy for life, and also give GH eg somatotrophin
Increased height
- thyrotoxicosis
- precocious puberty
- Marfan’s syndrome
- homocystinuria
Precocious puberty
If onset before 8 in girls, before 9 in boys (10x more common in girls)
Central PP - with genital changes
- due to abnormality in pituitary gland -> LH + FSH -> testes/ovaries
- can be idiopathic in females
- in males, is often due to tumours (craniopharyngioma), so always brain scan
Pseudo PP - only other SSCs, not gonadal enlargement
- due to sex steroids from adrenal glands - CAH or tumours
- congenital adrenal hyperplasia, autosomal recessive (usually 21-hydroxylase (on cholesterol)) affecting aldoesterone/cortisol pathways)
- GIRLS – most present with ambiguous genitalia as neonate, clitoromegaly (and can be so extreme that labia fuse and appears male. But can be partial CAH and present later (eg age 3) – further clitoral growth, and more ossification in bones, increased bone age – will end up being very short as androgens drive fusion of growth plates.
- BOYS – present around 4-6 weeks usually, with salt loss crisis – low Na, high K, acidosis, low glucose, shock. Needs emergency aldosterone or will die. Or can be partial CAH, and just get precocious puberty.
Advantages of breastfeeding
- mutual gaze, emotional input from mother, oxytocin surge
- sucking promotes uterine contractions, so avoiding some PPHs
- less insulin resistance, high BP, & obesity
- breast milk is free and clean!
- colostrum has endorphins: good for birth-associated stress
- IgA, macrophages, lymphocytes (with interferon), and lysozyme protect from infection, acids in breast milk promote growth of friendly lactobacilli in the baby’s bowel (less gastroenteritis)
- lower infant mortality, otitis media, pneumonia, & diarrhoea
- breast milk contains less Na+, K+, and Cl– than other milk, so aiding homeostasis - less risk dehydration and hyponatraemia
- future disease protection eg T1DM, RA, IBD, allergies etc
- natural contraceptive and weight loss for mother
- protection in premenopausal years against maternal breast cancer
Mastitis
Common reason to give up breastfeeding but easily treatable
- tender red hot area of breast ± fever
- treat with flucloxacillin 7-10days, ibuprofen, continue breastfeeding/expressing, check technique
Ages for feeding
- recommend exclusive breastfeeding until 6mo
- if bottle feeding, essential to sterilise
- start weaning around 6mo when showing signs of ready, starting with soft food then finger food, continuing with milk also until toddler!
Causes of undernutrition (growth faltering)
Reduced intake of food
- social/parental factors (insufficient diet, formula dilution / excessive juice, errors in food preparation, child/parent interaction problems, maternal depression/mental health problems, child abuse, neglect or emotional deprivation)
- feeding difficulties (breastfeeding difficulties, oromotor dysfunction – cerebral palsy, cleft palate, developmental delay, behavioural)
- medical problems eg recurrent vomiting (GI problems – reflux, intestinal obstruction, malrotation), neurological problems)
Malabsorption
- cystic fibrosis
- coeliac disease
- hepatobiliary disease
- food protein allergy/intolerance
- infection
- short gut syndrome
Increased metabolic demand
- chronic disease
- congenital infection – HIV, TORCHES
- syndromes
- malignancy
- metabolic disorders
- immunodeficiency/autoinflammatory
- endocrine – diabetes mellitus, diabetes insipidus, hyperthyroid
- complications of prematurity and IUGR
Childhood obesity
= BMI >98th centile (91st is overweight)
- due to diet, exercise, sleep deprivation, SES, genetics, medication, + hypothyroid, Cushing’s, GH deficiency, Prader-Willi syndrome
Medium and long term consequences… (insulin resistance, T2DM, sleep apnoea, orthopaedic problems, NAFLD, psychosocial, PCOS, Vit D deficiency) + (atherosclerosis, CVS disease, cancers, subfertility, hypertension)
Bronchiolitis
- <2 years, but most seen in <6 months
- bilateral wheeze and creps (is always the diagnosis if <1) – URTI, then cough, then development of respiratory distress over 3-4 day
- viral, due to RSV usually (diagnose with naso-pharyngeal aspirate)
- winter peaks
- self-limiting illness, supportive treatment – rare mortality, so look for signs of exhaustion (but salbutamol doesn’t work)
- breathing support (nothing -> oxygen (nasal) -> CPAP ->I + V)
- feeding support (little and often -> NG tube -> IV fluids)
- higher risk if bronchopulmonary dysplasia (preterm, BPD), congenital heart disease, or severe combined immunodeficiency (SCID) so given monthly passive antibody vaccination over winter season
Community acquired pneumonia
- creps/decreased air entry in just one area – lobar pneumonia
- birth-3 weeks
Bacterial – E. coli, GBS, monocytogenes - 3 weeks-3 months
Bacterial – Chlamydia trachomatis (with sticky eye), Pneumococcus
Viral – adeno, influenza, parainfluenza, human metapneumovirus, RSV - 4 months-5 years
Bacterial – Pneumococcus, Chlamydia pneumoniae, Mycoplasma pneumoniae, H influenza
Viral – adeno, influenza, parainfluenza, rhinovirus, RSV - 5 years-adolescence
Bacterial – Pneumococcus, C pneumoniae, M pneumoniae, H influenza
Stridor
- high-pitched inspiratory noise, from partial obstruction at the larynx or large airways
Causes
- congenital: laryngomalacia, web/stenosis, vascular rings
- inflammation: epiglottitis, croup, anaphylaxis, laryngitis
- tumours: haemangiomas or papillomas (usually disappear without treatment)
- trauma: thermal/chemical, or from intubation
- foreign body
Croup
- barking cough ± respiratory distress due to upper airway obstruction
- often worse at night (low cortisol)
- usually viral, eg parainfluenza
- give all children a single dose of dexamethasone, or inhaled adrenaline if emergency
- advise usually self-limiting and resolves within 48hrs (well-seeming, just lots of coughing)
Epiglottitis
- rapidly progressive inflammation of the epiglottis
- emergency! as respiratory arrest can occur abruptly due to airway obstruction
- 2–4 years old, present with a short history of fever, irritability, sore throat, pooling and drooling of saliva, and a muffled voice or cry, NO cough
- prefer to lean forward
- rare in children in the UK (Haemophilus influenzae type b vaccination)
- needs rapid intubation
DO NOT EXAMINE THROAT
Laryngomalacia
- congenital anomaly of the larynx, noticeable from birth (noisy breathing)
- excessive collapse and indrawing of the supraglottic airways during inspiration leading to stridor, breathing and feeding difficulties
- noise varies with alertness and with positioning
- usually not a problem, investigate if severe obstruction or failure to gain weight
Asthma vs viral associated wheeze
Viral associated wheeze
- common in first 2-3 years
- initially indistinguishable from early onset asthma
- majority lose symptoms by school age
- no evidence for need to use bronchodilators or steroids
Atopic asthma
- associated with eczema and rhinitis
- asymptomatic intervals, but wheeze on most days and night waking
Asthma drug therapy
- occasional B-agonists with spacer. If needed >3≈ per week, add step 2 (also if >5 yrs and many exacerbations, or asthma wakes from sleep >once/wk)
- inhaled steroid, eg beclometasone
- Review diagnosis; check inhaler use/concordance; eliminate triggers; monitor height
- if <5yrs: Add montelukast
- if >5yrs: LABA or montelukast - Refer to specialist (±CXR), increase steroid dose and consider theophylline
Acute asthma treatment
Severe asthma
- unable to complete sentences
- using accessory muscles of respiration
- O2 sats on air <92%
- peak expiratory flow <50% predicted
Life threatening asthma
- able to only say few words or unable to speak
- signs of exhaustion
- cyanosis
- silent chest
- PEF <33% predicted
A-E and giving oxygen throughout!
1st – 3,2,1 burst step – if this is working at 1 hour, maintain with hourly salbutamol (if needed) until they can have no treatment for 4 hours before discharge
- 3x salbutamol
- 2x Atrovent (ipratropium)
- 1x prednisolone
If needing more before an hour, IV bolus step
- MgSO4
- Salbutamol – look out for toxicity – vomiting and tremors
- Aminophylline
IV infusion step
- Aminophylline
- Salbutamol
Panic step
- Intubate and ventilate
Cystic fibrosis
- multiple episodes of bacterial infection, + pale bulky stools, + poor weight gain (= classical, but now really unusual presentation – newborn screening!)
- commonest autosomal recessive condition from CFTR mutations (usually dF508), affecting transmembrane chloride channels in lung, gut, sweat glands
- diagnose with genetics (+ sweat test)
- treatment - physiotherapy, antibiotics, mucolytics, nutritional support, small molecule therapy
Bacterial tracheitis
- barking cough
- bacterial cause
- toxic, NO drooling (unlike epiglottitis)
- croupy cough
- long onset history
- 80% need intubation
- treat with ceftriaxone and flucloxacillin
Causes of wheeze
If <1 year = bronchiolitis – salbutamol and other asthma meds don’t work!
1-5 years acute = viral induced wheeze (common)
1-5 years multiple episodes = multi-trigger wheeze
Over 5 years = asthma
Can also be caused by:
- respiratory infection (acute – bronchiolitis (common complication -> bacterial infection) or chronic – post-bronchiolitic wheezing, CF)
- aspiration pneumonitis (gastroesophageal reflux, abnormal airways (TOF))
Causes of cardiovascular disease by age
First few hours
- pulmonary/aortic critical stenosis
- hypoplastic heart syndrome
First few days
- transposition, tetralogy, large PDA in prematures
- co-arctation of the aorta
First few weeks
- aortic stenosis
- co-arctation of the aorta
First few months
- any left to right shunt as pulmonary resistance falls, eg VSD
(but most serious problems should present antenatally at 20 week scan!)
Cardiology presentations at birth
Murmur
- normal in most, don’t refer if Soft, Systolic, aSymptomatic, left Sternal edge (likely due to physiological tricuspid regurgitation or pulmonary artery flow), should disappear by day 2
Blue baby
Collapse
Left to right shunt
- breathless and pink from 2-3 weeks (signs of heart failure - breathless, sweaty, hepatomegaly, cold peripheries, failure to thrive)
- atrial septal defect (may present with chest infection from wet lungs)
- ventricular septal defect (most common ‘hole in the heart’, usually presents with asymptomatic murmur at 8 weeks, most close spontaneously)
- persistent arterial duct (allowed until gestational age reached, machinery murmur)
Right to left shunt
- present blue baby, cyanosed with sats <94% in first few days
- tetralogy of Fallot’s - subpulmonary stenosis, VSD, subaortic area overriding aorta, right ventricle hypertrophy (loud murmur, clubbed and cyanosed by 8 weeks, surgical repair at 6 months)
- transposition of the great arteries (collapse at days 2-5, severe cyanosis with death if duct closes this way - give prostaglandins until surgery)
Mixed shunt
- presents breathless and blue
- AVSD (usually due to Down’s syndrome, so automatic screening both ways), maybe + complex lesions. Give early surgery 3-4 months
Well + obstruction
- aortic stenosis (asymptomatic, carotid thrill and ejection systolic murmur louder on expiration, treat only when severe narrowing with balloon dilatation and then replace aortic valve as adult)
- pulmonary stenosis (asymptomatic, as above, louder on inspiration)
Sick + obstruction
- coarctation of the aorta (presents at 2 days as duct closes, no femoral pulses and severe acidosis, resuscitate with prostaglandins and ICU support, surgery ASAP)
- hypoplastic left heart syndrome (LV too small to maintain life, need multiple operations through life)
Signs of the seriously ill child
GRUNTING
Grunting, weak or continuous high-pitched cry, tachypnoea
Rib recession, retraction of sternomastoid, nasal flaring, wheeze, stridor
Unequal or unresponsive pupils, focal CNS signs, fits, marked hypotonia
Not using limbs/lying still, odd or rigid posture, decorticate (flexed arms, extended legs), de-cerebrate (arms + legs extended)
T° >38°c if <6 months or >39° especially if cold or shutdown peripheries
I have a bad feeling about this baby!
Neck rigidity, non-blanching rash, meningism, bulging fontanelle, etc
Green bile in vomit (≈GI obstruction, eg atresia, volvulus, intussusception).
Kawasaki disease
- medium artery vasculitis of unknown cause
- 1-5yo, more in winter, increasing incidence (rare)
- fever >5 days + one of RED signs (lymphadenopathy, rash, mucositis, conjunctivitis, red extremities) + irritability, abdominal pain, hepatitis
- diagnosis with bloods - high CRP and ESR, high WBC, low platelets
- rapid treatment - IV immunoglobulins, 6hrly aspirin, high dose IV steroids, ECG, echo, lifelong aspirin
Infective endocarditis
- fever, splenomegaly, clubbing, splinter haemorrhages, anaemia, rash, heart failure, microscopic haematuria, new murmur
- typical cause: Streps, staphs
- blood cultures (different times and different sites), echocardiogram
- blind treatment after 3 blood cultures: benzylpenicillin, gentamicin, get microbiological help
- at risk if VSD particularly (any known congenital heart defect) or lines in situ
Chest pain and collapse in children
Chest pain
- common presentation in teenagers
- if sharp pain when resting, almost never due to heart disease (likely GORD or pleuritic chest pain) so reassure if at rest
- if crushing pain comes on in fit child/teenager during exercise then needs referral – many rare causes
Faints/syncope
- almost never due to heart disease
- reassure and advise food and fluid, unless preceded by palpitations, not worrying
Causes of vomiting
Mechanical
- proximal valve defect
- over-filling of stomach
- distal obstruction
- GORD (especially in premature, cerebral palsy, chronic respiratory problems, treat by elevating cot, frequent feeds, feed thickener, antacids, pro-kinetics, surgery. Overmedicalised! Often doesn’t need treatment if just milk posset)
- pyloric stenosis (in 4-6 weeks old, mainly boys, with family history. Hypertrophy of pylorus muscle, get projectile vomiting after feed, hungry baby, constipated, palpable mass (difficult to feel), failure to gain weight, hypokalasemic, hypochloraemic alkalosis (vomiting loss). Treat with rehydration, and Ramstedt’s pyloromyotomy)
Local GI infection (should just be 1-2 days)
Intoxication
Systemic
- remote infection
- pyrexia
- raised ICP
- metabolic disease
Surgical emergency - bilious vomiting!
- duodenal atresia – see double bubble
- intussusception
- volvulus
- malrotation
- Hirschsprungs
Acute causes of diarrhoea
Gastroenteritis
- almost always (rotavirus) viral
- rarely need to investigate or treat with abx, just supportive + fluids
- BEWARE dysentry (blood/mucus in diarrhoea (need stool samples here) - bacacterial – shigella, campylobacter, salmonella, E.coli or amoebic. Risk from food poisoning, overseas travel, contact with infected animal)
- risk of Haemolytic Uraemic Syndrome (HUS), typically after E coli 0157 -> renal failure
Antibiotics
Toxins
Systemic infection
Chronic causes of diarrhoea
Non-pathological – thriving
- toddler diarrhoea (normal! Rapid bowel transit time, and especially in diet high in sugars, low fat, high fibre. Resolves with time – lower fibre and reduce especially citrus juices)
- constipation with overflow
Malabsorption – failing to thrive
- cystic fibrosis
- coeliac disease
- secondary lactose intolerance (to gastroenteritis)
Inflammation
- Crohns disease
- cow’s milk protein intolerance
- ulcerative colitis
Infection
- Giardia
Dehydration in children (following N+V)
See: dry mouth/tongue, decreased skin turgor, few/no tears, sunken cheeks/eyes, fontanelles, abdomen, reduced consciousness, less urine (most babies need 6-12 nappies per 24h period, parents will notice if they need to change less!)
Need: oral rehydration (little and often) -> NG fluids -> IV fluids
- IV if shock suspected, if red flag symptoms and deteriorating despite ORS, if persistently vomiting ORS despite trickle feed or NG
- 0.9% NaCl or 0.9% NaCl with 5% glucose – hypoglycaemia common!
- anti-emetics
Beware also risk of acid-base imbalance, electrolyte imbalance (hypernatraemic dehydration - jittery movement, increased muscle tone, hyperreflexia, convulsions, drowsiness)
Fluid management
Maintenance fluids
- 1st 10kg – 100ml/kg/day
- 2nd 10kg – 50ml/kg/day
- Anything above 20kg – 20mls/kg/day
Correct deficit
- % dehydration x weight x 10 = total fluid deficit
- replace this amount over 24-48 hours with maintenance fluids
Bolus fluids
- 20ml/kg 0.9% NaCl in most situations
- or 10ml/kg if DKA, trauma, or fluid overload
Constipation
- very common, rarely specific cause, mostly functional
- initial advice – fluid intake, dietary management, toileting routine, laxatives (movicol)
- can have psychosocial causes, can causes RAP
Red flags and concerns
- no meconium in first 24hr of life - Hirschsprung’s
- faltering growth - hypothyroid, coeliac
- gross distension - Hirshsprung’s or GI dysmotility
- abnormal lower limb deformity or neurology - lumbosacral pathology
- sacral dimple over natal cleft/spine, hairy/discoloured skin - spina bifida occulta
- abnormal appearance of anus
- perianal bruising or fissures - sexual abuse
Acute abdominal pain according to age
<1yr
- pyloric stenosis
- intussusception
- obstruction
1-4yr
- intussusception
(appendicitis)
5-11yr
- appendicitis
- testicular torsion
(intussusception)
12yr+
- appendicitis
- testicular torsion / ectopic pregnancy
+ also gastroenteritis, mesenteric adenitis, UTI, RAP, poisoning, DKA, sickle cell, constipation, referred pain (eg pneumonia)
Intussusception
- proximal bowel telescopes into distal segment, dragging along mesentery
- compression of mesenteric vessels and lymphatics -> oedema, ischaemia, mucosal bleeding, perforation, peritonitis
- causes episodic crampy abdominal pain as bowel tries to peristalsis, + pallor and irritability, ‘red currant jelly’ stools, (bilious) vomiting
- peak age 6-9 months, 4x more in males
- may feel mass on examination
Investigations
- abdominal XR -> distended proximal small bowel, absence of gas in distal colon/rectum
- USS -> halo sign (spiraling around)
Management
ABC
- surgical referral!
- IV access, fluids, NGT
- reduction by rectal air insufflation (air enema)
- or operative reduction if unsuccessful or already peritonitic
Appendicitis
- peak in adolescence, rare in younger children
- central pain, localising to RIF, + fever and vomiting
- maybe signs of peritonism – rebound guarding, tenderness (ask them to walk/cough/laugh)
Investigations
- bloods – WCC, CRP
- USS – check for mesenteric adenitis (enlarged mesenteric lymph nodes) which presents very similarly to appendicitis
Management
- initial stabilisation – fluids
- pain management
- laparoscopy if acute appendicitis suspected (if it were MA then would resolve on its own)
Recurrent abdominal pain
- very common in 10-15 age group!
- ?trigger factors, explore psychosocial
- often little to find on examination
- 90% no structural cause identified
- but could be GI, gynae, psychosocial, urinary tract, hepatobiliary
Testicular torsion
- never miss this… any boy presenting with acute pain from nipple level down, examine the testes!
- peak age 12-13 (never really <10)
- acute onset, examination shows one testis enlarged, red, elevated and tender, absent cremasteric reflex
- spermatic cord twists on itself and cuts of blood supply to testis
Management
- needs urgent surgical exploration (or will result in sub/infertility) and bilateral orchidopexy (if both viable, if not then will remove one)
- USS are not reliable enough, go straight to surgery based on clinical signs
Diabetic ketoacidosis
- present ~10yo after hx of polyuria and fatigue, then diffuse abdo pain and vomiting
- ++ ketones and glucose in urine
- needs admission under medical team for fluid resuscitation, manage electrolytes, correct glucose, prevent complications eg cerebral oedema and EDUCATION if first diagnosis of DM
Henoch
HSP
- short history of intermittent abdo and joint pain (especially knees and ankles), then develop non-blanching purpuric rash over legs and buttocks, haematuria
- usually self-limiting, but may relapse and may have long-term renal problems
Causes of abdominal distension
- always remember acute GI obstruction as a cause!
Air: faecal impaction, air swallowing, malabsorption
Ascites: nephrosis, hypoproteinuria, cirrhosis (CCF)
Solid masses: Wilm’s tumour, neuroblastoma, adrenal tumour
Cysts: polycystic kidney, pancreatic cyst, hepatic cyst
+ hepatomegaly from infection, malignancy, metabolic conditions
Coeliac disease
- malabsorption!
- diarrhoea, failure to thrive ± anaemia (low folate and ferritin), abdominal protrusion, everted umbilicus and wasted buttocks (if late-presenting)
- subclinical/latent forms also - anaemia, fatigue, IBS symptoms, diarrhoea, weight loss, arthralgia, eczema, short stature
- presents at any age - but may see deceleration on growth chart at weaning
- serology shows raised IgA anti-tissue transglutaminase and endomysial antibodies
- confirm by finding villous atrophy on small bowel biopsy via endoscopy (villi return to normal on the special diet)
- no gluten challenge test unless diagnosis is in doubt
GI malformations
Hirschsprung’s disease
- absence of ganglia in segment of colon -> functional GI obstruction, constipation, megacolon
- 3x more in males
Oesophageal atresia + tracheo-oesophageal fistula
- usually come together
- in utero see polyhydramnios
- at birth get cough, airway obstruction, blowing bubbles, distended abdomen, cyanosis, aspiration
- needs surgical repair
- 50% have other anomalies so scan
Inguinal hernias
- patent processus vaginalis (passage for testicle into scrotum)
- bulge lateral to pubic tubercle, worse when eg crying
- risk of incarceration, younger needs prompter fix
Hydroceles
- processus vaginalis patent at birth just allowing fluid down, closes in first year of life (only repair if persists)
Mid-gut malrotations -> bilious vomiting, immediate surgery
- volvulus
Anterior abdo wall defects
- gastroschisis (abdo contents extrusion without covering, diagnose in utero, quick surgery)
- omphalocele (herniation of abdo viscera with amnio sac, delayed closure)
Small bowel obstruction
- persistent (bilious) vomiting, abnormal/absent stool, abdominal distension
- lower obstruction presents later with more distension
Caused by:
- atresia or stenosis of duodenum (1/3 Downs syndrome)
- atresia or stenosis of jejunum or ileum
- malrotation with volvulus
- meconium ileus (in CF, so thick it becomes impacted)
- meconium plug (will pass spontaneously)
Causes of jaundice by age
<24hr
- haemolytic disorders - rhesus incompatibility, ABO incompatibility, G6PD deficiency, pyruvate kinase deficiency
- congenital infection
24hr-2 weeks
- physiological jaundice
- infection eg UTI
- haemolysis (as above)
- bruising
- polycythaemia
- Crigler-Najjar syndrome
> 2 weeks
- unconjugated - physiological, infection, hypothyroid, haemolytic anaemia, high GI obstruction (eg pyloric stenosis)
- conjugated - bile duct obstruction, neonatal hepatitis, hepatic dysfunction!
Urinary tract infections
- often non-specifically ill (infants collapse and septicaemia, toddlers vomiting, failure to thrive, colic, pyrexia)
- often abnormal urinary tract (vesico-ureteric reflux)
- common (more in girls)
- usually E coli (coloniser of bowel, and flagella allows swimming against urinary flow)
- if not E coli, may want to consider urinary tract abnormalities
- lower tract symptoms – not too concerning
- upper tract symptoms – risks of pyelonephritis
- urine dip – nitrites, leukocytes
- midstream sample is ideal but challenging
- bloods for CRP etc if concerned (can be very dangerous in young children especially)
- prompt abx treatment IV or PO amoxicillin
- advise drink plenty, avoid constipation, access to clean toilets, don’t delay voiding
Nephrotic syndrome
- breakdown of glomerular basement membrane
- loss of protein (albumin) - triad of proteinuria, hyperlipidaemia, hypoalbuminaemia
- presents with oedema (third spacing), tachycardia, slow cap refill
- primary (genetic/idiopathic) or secondary (SLE/HepB/C)
- steroid sensitive or not (or frequently relapsing/dependent)
Treatment
- give fluid bolus
- give steroids (80% due to minimal change nephrotic syndrome (MCD))
- don’t give furosemide!
- give antibiotics as losing immune response
Complications
- hyperlipidaemia
- thrombosis risk (liver overdrive)
- end stage renal failure (FSGS)
Nephritic syndrome
- presents with milder oedema, haematuria, hypertension
- loss of dark blood in urine (coca-cola)
- usually due to glomerular nephritis – post infectious (Group A beta haemolytic strep), HSP, IgA, SLP
- high risk AKI
- treat with diuretic
Acute kidney injury
- sudden rapid loss of renal function, usually reversible
Causes
- Pre-renal – congenital heart disease, hypovolaemia (most common cause in children), renal artery stenosis, hypoxia
- Renal – HUS (E coli 0157), acute GN, interstitial nephritis, infection
- Post-renal – stones, tumour, retroperitoneal fibrosis - always perform an USS to ensure no obstruction!
Consequences
- Hyperkalaemia – give calcium gluconate, give sodium bicarbonate, salbutamol neb
- Acid-base imbalance
- Fluid overload
- Hypertension
- Toxin excretion
Causes of haematuria
Nonglomerular
- infection (bacterial, viral, TB, schistosomiasis)
- trauma to genitalia, urinary tract or kidneys
- stones
- tumours
- sickle cell disease
- bleeding disorders / vasculitis eg HSP
- renal vein thrombosis
- hypercalcuria
Glomerular
- acute glomerulonephritis (with proteinuria)
- chronic glomerulonephritis (with proteinuria)
- IgA nephropathy
- familial nephritis
- all patients get urine MC+S, KUB USS, FBC, platelets, sickle cell and coagulation screen
Causes of proteinuria
- orthostatic proteinuria
- glomerular abnormalities - MCD, glomerulonephritis, abnormal glomerular basement membrane
- increased glomerular filtration pressure
- reduced renal mass in CKD
- hypertension
- tubular proteinuria
Chronic kidney disease
At stage 4-5, present with:
- anorexia, lethargy
- polydypsia, polyuria
- faltering growth
- bony deformities (renal rickets)
- hypertension
- acute on chronic renal failure (after dehydration or infection)
- incidental proteinuria finding
- unexplained normochromic normocytic anaemia
Management
- diet - calorie supplements, high protein, low potassium and phosphate
- calcium carbonate and vitamin D for renal osteodystrophy
- salt and water balance control - free access and supplements
- bicarbonate to prevent acidosis
- subcut EPO (for anaemia)
- recombinant growth hormone
- dialysis and transplantation
Enuresis
= regular bedwetting past age 5 in girls, age 6 in boys
- if clinical suspicion then test for UTI, diabetes, GU abnormality
- treat with reassurance, no caffeine, 4-7x per day to toilet, rewards for agreed behaviours (drinking water, using toilet before bed, taking medicines, changing sheets), maybe try alarms that awake when wet, desmopressin sublingually for eg school trips/sleepovers
- secondary enuresis = wetness after >6mo dryness - concerns about worries, illness, abuse
- persistence past age 15 rare, usually fhx
Hypertension
RFs - high salt intake, obesity, low birth weight
Causes
- renal parenchymal disease 80%
- renal vascular disease
- coarctation of aorta
- endocrine causes
- essential hypertension
- iatrogenic
Presentation
- non-specific in infant
- headaches, fatigue, blurred vision, epistaxis, Bell’s palsy, sleep-disordered breathing
Investigations
- urine for albumin and blood
- U+E, creatinine, FBC
- renal USS
- co-morbidities eg fasting lipids and glucose, sleep study
- ECG, echo, retinal screening for end organ damage
Hypertensive crisis
ICU!
- cerebral oedema, heart failure, seizures, pulmonary oedema, renal failure
- treat with nifedipine, labetolol, or sodium nitroprusside - slowly over several hours
Cryptorchidism
= undescended testes
- 5% UDT at birth, but may continue to descend until 1yo
- testes may be undescended, ectopic or impalpable (intra-abdominal or absent)
- consequence of UDT (if by 1yo) – so want to see in clinic only by age 7 months - infertility, tumours, torsion, cosmetic/psychological
Management
- palpable - orchidopexy (to fix in place)
- impalpable - laparoscopy, orchidopexy, staged procedure
- bilateral impalpable - ? female sex, disorders of sexual development
- if retractile (sometimes obvious if warm and relaxed), then monitor, no surgery
Cerebral palsy
= chronic disorders of posture and movement caused by non-progressive CNS lesions sustained before age 2, resulting in delayed motor development, CNS signs, learning disability (35%) and epilepsy
- see weakness, paralysis, delayed milestones, seizures, language/speech problems
- 4 types - spastic, dyskinetic, ataxic, mixed
- may use botulinum toxin to help with spasticity
Causes (much more common in premature)
- prenatal - APH (with hypoxia), Xrays, alcohol, CMV/rubella/HIV, toxoplasmosis, rhesus disease
- perinatal - birth trauma, fetal distress, hypoglycaemia, hyperbilirubinaemia
- postnatal - trauma/intraventricular haemorrhage, hypoxia, meningoencephalitis, cerebral vein thrombosis
Febrile convulsions
- single tonic–clonic, symmetrical generalized seizure lasting <15min, occurring as temp rises rapidly in a febrile illness (usually viral)
- typically in a normally developing child ½–6yrs old
- common, benign
- strong association to family history
- must be without recurrence in 24hrs (or same febrile illness)
- look for infection! confirm diagnosis.
- management - put in recovery position, give antipyretics
- if lasting >5min give buccal midazolam or PR diazepam
- parental education - benign illness, likely to happen again, give anti-pyretics early in future febrile illness
Epilepsy
Seizure = abnormal electrical discharge of neurones resulting in disruption of consciousness Epilepsy = tendency to recurrent unprovoked seizures
Types
- Tonic/clonic (grand mal): Limbs stiffen (the tonic phase) and then jerk force-fully (clonic phase), with loss of consciousness
- Absences (petit mal): Brief (eg 10sec) pauses (‘stops mid-sentence, and carries on where he left off ’); eyes may roll up; unaware of the attack, provoked by hyperventilation
- Infantile spasms/West syndrome: Peak age: 5 months. Clusters of head nodding (‘Salaam attack’) and arm jerks, every 3–30sec. IQ low in ~70%. EEG is characteristic (hypsarrythmia). Treatment: prednisolone 1st line; 2nd line vigabatrin (SE: visual fi eld defects); 517some specialists prefer ACTH
- Myoclonic seizures: 1–4yrs; eg ‘thrown’ suddenly to the ground. Treatment: valproate.
- Partial epilepsy: Signs from part of one hemisphere
Causes:
- none found
- infection (eg meningitis)
- hyponatraemia
- low glucose
- low Ca2+
- low Mg2+
- raised or lowered Na+
- toxins
- trauma
- metabolic defects
- tuberous sclerosis
- CNS tumour (<2%) or malformation
- triggers - flickering lights, exercise,
EEG limited use unless during seizure! MRI.
MLA (Modern Language Assoc.)
Andrew Baldwin, et al. Oxford Handbook of Clinical Specialties. Vol. Tenth edition, OUP Oxford, 2016.
APA (American Psychological Assoc.)
Andrew Baldwin, Nina Hjelde, Charlotte Goumalatsou, & Gil Myers. (2016). Oxford Handbook of Clinical Specialties: Vol. Tenth edition. OUP Oxford.
Status epilepticus management
- ABC, high-flow O2, check blood glucose, IV access
- 5mins - Lorazepam IV or buccal midazolam
- 15mins - repeat lorazepam, call for senior help, prepare phenytoin
- 20mins - Phenytoin IV, monitor ECG, Phenobarbital, call PICU & anaesthetist, prepare for intubation
- 40mins - Rapid sequence induction, transfer to PICU
Anti-epileptics
Choice depends on syndrome
Carbamazepine
- SE: rash, low platelets, agranulocytosis, aplasia (all rare).
Sodium valproate
- SE: vomiting, appetite increase, drowsiness, low platelets, rare hepatotoxicity can be fatal so monitor LFT, TETAROGENIC
Ethosuximide - absence seizures
- SE: D&V, rashes, erythema multiforme, lupus syndromes, agitation, headache.
Lamotrigine - absences and intractable epilepsy as an add-on
Vigabatrin
- SE: drowsiness, depression, psychosis, amnesia, diplopia, and field defects (test every year)
Diet - consider a high-fat ketogenic diet under specialist supervision if 2 drugs fail to work
Education - showers are safer than baths, avoid risky behaviours, emphasize compliance/concordance
Other causes of funny turns
Breath-holding attack
- eg after a tantrum – scream and cry until cry becomes soundless, breath is held in expiration, apnoea, short period of cyanosis, LOC, floppy, sometimes stiff/few jerks, rapid recovery
- common, 5% of children (usually not presenting to hospital), young children, age 1-2, usually resolve by 5
Vasovagal syncope / simple faint
- (May also shake/lose urinary continence)
- drop in bp
- common, females more than males, more in adolescents
- triggers – pain, fear, hunger, nausea, orthostatic stress, heat/cold
- often get aura – light-headed, visual disturbance (tunnel vision), hot and sweaty, nausea, ringing in ears
- rapid recovery
Reflex anoxic seizure
- 1% children, 6mo-2yr
- often after pain/knocking themselves, or sudden fear causes vagally mediated bradycardia/asystole
- limp, falls to ground, pale, maybe stiff/jerking of arms and legs
- lasts around 1 min, then rapid recovery
+ daydreaming, night terrors, tic disorder, psychological episodes
Acute vs chronic headache
Acute
- often concomitant viral or bacterial infection, with fever + signs, often URTI or meningitis
- tension type (constriction band)
- migraine without aura (bi or unilateral, pulsatile, GI disturbance, abdo pain, photophobia, relieved by sleep, dark and quiet)
- migraine with aura (visual sensory or motor)
- mixed-type
Chronic progressive
- severe, no return to normal baseline
- worse early in the morning, or wakes child from sleep
- ICP raised due to tumour, progressive hydrocephalus, intracerebral abscess, intracranial bleeding
+ vomiting, withdrawal, seizures, unsteadiness, squint, enlargement of head, 3rd/6th nerve palsy, papilloedema, ataxia, weakness and loss of reflexes, spasticity, torticollis (neck pain), ‘cracked pot’ sign
- worry about personality/behaviour changes – frontal lobe tumours not uncommon
Red flags for SOL headache
- worse lying down or with coughing and straining
- headache wakes from sleep (not on awakening)
- confusion
- morning or persistent N+V
- recent change in behaviour, personality or educational performance
- growth failure
- visual field defects (craniopharyngioma)
- squint
- CN abnormality
- cerebellar coordination
- torticollis (neck pain)
- UMN or cerebellar signs on gait
- papilloedema on fundi
- bradycardia
- cranial bruits
Meningitis
- suspect in any ill baby or child
- may be subtle symptoms - irritability, abnormal cry, lethargy, difficulty feeding, fever, seizures, apnoea, bulging fontanelle
- septic signs - raised temp, cold peripheries, limb/joint pain, abnormal skin colour, odd behaviour, rash, DIC, low bp, raised resp rate
- meningeal signs - later and less in young children - stiff neck, Kernig’s sign (knee raise on hip flex), photophobia, opisthotonus (hyperextension)
- IV CEFOTAXIME or CEFTRIAXOME ASAP, or IM benzylpenicillin. Dexamethasone to protect risk of deafness
- LP would show high pressure, high proteins, excess neutrophils. Any <3mo old with fever gets one!
- not if focal neurology, prolonged fit, GCS <13, coagulation disorder, abnormal pupils
Complications - secondary abscess, subdural effusion, hydrocephalus, ataxia, paralysis, deafness, lower IQ, epilepsy, brain abscess
Meningitis organisms
Neisseria meningitiis
- abrupt onset with rash (non-blanching purpuric classically, starting on legs)
- any age
- gram -ve cocci in pairs
- cefotaxime/ceftriaxone or benzylcnicillin
Haemophilus influenzae - rare if immunised
- <4 years
- gram -ve rods
- ceftriaxone + steroids
Strep pneumoniae
- any age
- following resp infection, skull fracture, meningocele, HIV
- grame +ve cocci
- ceftriaxone or benzylpenicillin
Escherichia coli
- neonates
Group B haemolytic streptococci
- via mother’s vagina, fall ill ~24hr old-1 mo
- benzylpenicillin
Listeria monocytogenes
- soon after birth, rare unless immunocompromise
TB
- long prodrome with lethargy and malaise, no classical photophobia or neck stiffness
Gross motor developmental delay
Maybe considering a diagnosis of cerebral palsy. Scoliosis risk if high or low muscle tone, especially in times of increased growth.
History
- pregnancy, foetal movement, labour, delivery
- acquisition of gross motor milestones (4-5 months rolling, 6 months sitting)
- other domains – fine motor/vision, speech/language, social/play
- family history
Examination
- function – observe locomotion eg Gower’s manouvre, muscle bulk, posture, tone, power, reflexes, head circumference (+ intelligence)
- structure - dysmorphism, disproportion of limbs, joints – general, hips, spine
Causes of gross motor delay/disorder:
Central
– maturation - global delay, developmental coordination disorder, visual impairment, systemic illness
– upper motor neurone - cerebral palsy, trauma, neurometabolic
Peripheral
- lower motor neurone - spina bifida
- muscle - Duchenne muscular dystrophy
Speech and language developmental delay
History
- pregnancy, labour, delivery
- acquisition of speech – understanding? Normal, delayed, disordered
- family history
- social history – watching TV/reading? Neglect? Other languages at home?
Examination
- look in mouth, ears and nose (eg for cleft palate)
Causes of speech and language delay or disorder
o Hearing loss – sensorineural/conductive
o Anatomical problems – cleft palate
o Functional – dysarthria
o Linguistic environment
o Autism spectrum disorder
o Part of global delay
o Part of developmental syndrome – Landau-Kleffner syndrome, dyspraxia
Social and play developmental delay
History
- pregnancy, labour, delivery
- age of development of social smile (by 6 weeks), shared attention, play skills
- family history
Examination
- observe play and interaction with carer/other children/self
Causes of social/play delay or disorder o Autism Spectrum Disorder o Sensory difficulties (hearing/vision) o Speech and language impairment o Global developmental delay o Genetic – eg Fragile X, Tuberous sclerosis (gives ASD like phenotype) o Lack of opportunity o Emotional attachment – eg selective mutism
Global developmental delay
Which domain most affected, and which others?
- pregnancy, family history, milestones etc
Causes of global developmental delay
- chromosomal disorders
Down’s syndrome (trisomy 21)
Angelman syndrome (on chromosome 15, segment has two copies from dad)
Prader-Willi syndrome (on chromosome 15, segment has two copies from mum)
- single-gene disorders
Rett syndrome
mucopolysaccharidoses - endocrine - hypothyroid
- antenatal exposure - fetal alcohol syndrome, congenital infection
Raised ICP
Causes
- meningoencephalitis
- head injury
- subdural/extradural bleeds
- hypoxia
- ketoacidosis
- tumours
- thrombosis
- Reye’s
Signs - listless, irritable, drowsy, headache, diplopia, vomiting, tense fontanelle, reduced consciousness, pupil changes, abnormal posturing, Cushin’s triad (slow pulse, raised BP, breathing pattern abnormalities), papilloedema and hydrocephalus if chronic
ABC management
- help venous drainage - head central at 25 degree
give O2 if temp >40
- treat hypoglycaemia
- control seizures
- NO LP until CT done and child intubated
- if severe, ITU - intubate, mannitol, dexamethasone, fluid restrict and diuresis
Spina bifida
Neural tube defect, forms between week 3-4 in utero - should diagnose on USS
- SB when incomplete vertebral arch
- commoner in young primips, lower SES, genetic risk (folic acid!)
- maybe neurological deficit, maybe not
- postnatal surgery
