Paediatric Notes
Paediatric History
 Presenting Complaint
 History of Presenting Complaint
 Systems Review
o General: fever, rash, weight loss
o CVS: sweating, cyanosis, pallor, SOB, faints
o Resp: runny nose, sore throat, earache, cough, SOB, snoring, exercise capacity
o GI: appetite, feeding, vomiting, stools, abdominal pain/distension
o GU: urine output, smell, colour
o Neuro: headaches, fits, hearing, vision, developmental milestones
o Musc: joint pain or swelling
 Past Medical History
o Chronic conditions
o Hospital admission
o Operations
 Medications & Allergies
 Immunisations
 Pregnancy & Birth
o Born at: ? wks in which country
o Mother’s health during pregnancy
o Delivery: normal, instrumental, elective C-section, emergency C-section
 Neonatal & Infant Development
o Admission to SCBU, oxygen required
o Breast-feeding
o Do they have red book?
o Has anyone been worried about the child’s development?
o Age when: smiled, sat unsupported, crawled, used 3-4 words, ate solids, talked, walked
 Family History
o Siblings
o Mother & Father age & occupation
o Parents blood related?
o Diseases that run in the family
 Social History
o Lives with: parents? siblings? adopted?
o Lived in the UK since? / Ethnic origin
o First language
o Accommodation: house/flat
o Pets / Travel
o Alcohol / Smoking / Drugs
o Schooling
 Which year
 Any problems/concerns
 Happy at school
Developmental Milestones
Gross Motor
Newborn
6 weeks
Fine Motor &
Vision
Limbs Flexed
Head Lag
Primitive reflexes
Raise Head (4mths)
Primitive reflexes
6 months
Sits without
support (9mths)
10 months
Crawls
Cruises
12 months
Unsteady braod
based gait
Steady walking
18 months
2 years
Fixes & follows
moving object
(3mths)
Reaches for toys
Palmar grasp
Transfers (8mths)
Pincer Grasp
3 block tower
6 block tower
Draws a straight
line
Hearing, Speech &
Language
Startles to noise
Social
Smiles
Responsively
Vocalises
Turns to sounds
out of sight
Parents can
discriminate
sounds
2-3 words
Puts food in mouth
Stranger
awareness
Waves bye-bye
Peek-a-boo
Drinks from cup
6-10 words
Uses a spoon to eat
2-3 word sentences Symbolic play and
potty trained
Primitive Reflexes
Reflex
Moro
Eliciting
Sudden head extension
Description
Symmetrical extension then flexion
of all 4 limbs
Grasp
Place object in palm of hand
Flexion of the fingers of the hand
around object
Rooting
Stimulus near mouth
Turning of head towards stimulus
Placing
Hold infant vertically and place Child steps with one foot then the
the dorsum of feet on a hard
other
surface
Positive Supporting reflex
Infant held vertically, feet on a Legs support body weight, may
surface
push up against gravity
Atonic Neck reflex
Head turned to one side whilst Fencing posture with arm
supine
outstretch in the direction of the
head
N/B - these reflexes should be gone by 6 months
Immunisation Schedule
Age
Birth
2 Months
3 Months
4 Months
12 Months
13 Months
Vaccnations
BCG & Hep B (to high risk Groups)
Diptheria, Tetanus, Pertusis, Polio, Hib,
Pneumococcal
Diptheria, Tetanus, Pertusis, Polio, Hib, Men C
Diptheria, Tetanus, Pertusis, Polio, Hib,
Pneumococcal, Men C
Hib, Men C
MMR, Pneumococcal
4 Years
12 – 13 Years
13 – 18 Years
Diptheria, Tetanus, Pertusis, Polio, MMR
HPV
Diptheria, Tetanus, Polio
NEONATES
 < 28 days old
 Full term preg is 37-42 weeks
 Pre-term preg is < 37wks.
 Post term > 42 wks.
 Low BW <2.5kg, V .low BW <1.5kg, extremely low BW <1kg
Infections of the newborn
 ↑ risk if PROM (>24h), chorioamnionitis, preterm
 Organisms: Group B Strep, Listeria Monocytogenes, Candida Albinans, HSV
Neonatal sepsis
 Temp instability - fever, hypothermia
 Poor feeding
 Abdo distension
 Vomiting
 Apnoea
 BC
 Resp distress







Pallor/mottled skin
Jaundice
Neutropenia
Hypo-perglycaemia
Shock
Irritability
Seizures
Ix/Rx:
 septic screen: FBC, blood culture, CRP, urine/CSF M,C,S + CXR
 IVABs:
o Penicillin/amoxicillin for group B strep, listeria
o Ceph for gram -ve bacteria.
Rubella
 Routine antenatal screening for rubella IgM.
 Live Vacine before birth if neg.
 Complications:
o <8/40: sensorineural deafness, congenital HD, cataracts/glaucoma, hepatosplenomegaly, dev
delay/IUGR.
o 13-16/40: impaired hearing (30%)
o >18/40: minimal risk
CMV
 Most common
 40% of infants infected in maternal infection
o 90%: normal at birth and development
o 5%: clinical features of infection at birth:
 IUGR
 HSmegaly
 Petechiae
 Pneumonitis
 Jaundice
 Deafness

Encephalitis/micro
encephaly/IC
calcification IQ
Malformations of the Neonate
Down’s syndrome (trisomy 21)
 1 in 1000 LBs
 Sx:
o Newborn: ++nuchal skin, hypotonia, sleepy
o Facial appearance: round face, epicanthic folds, protruding tongue, upslanting palpebral fissures,
small low set ears
o Other anomalies: flat occipital, single palmar creases, incurving 5th digit, saddle gap
 Complications:
o Learning diff
o Vision/hearing impairment
o Congenital HD
o Hypthyroid
o Duodenal atresia
o Leukaemia
o Recurrent resp inf
o Alzeheimers
Patau’s Syndrome (trisomy 13)
 1 in 14000 LBs
 Sx:
o Small head and eyes
o Absent corpus calloscum with single
ventricle
o Heart lesion
o Polycystic kidneys
o Cleft lip/palate
o Hands show flexion contractures +/polydactyl
Edward’s syndrome (trisomy 18)
 2nd commonest trisomy
 Female 2:1 male
 Sx:
o Rigid baby + limb flexion
o Odd low set ears
o Receding chin
o Proptosis (forward displacement of eyes)
o Rocker bottom feet
o Cleft lip/palate
o Umbilical/inguinal hernia
o Short sternum (therefore widely spaced
nipples)
o Mean survival 10/12
Turner’s syndrome (45X)
 >95% result in early miscarriage
 1 in 2500 LBs
 Females only
 Sx:
o Lymphoedema of hands and feet (neonate)
o Short stature; webbed neck
o Wide carrying angle (cubitus valgus)
o Widely spaced nipples
 Dx:
o Detect on USS - cystic hygroma and oedema
 Rx:
o GH and oestrogens
Klinefelter’s syndrome (47, XXY)
 1-2 in 1000 LBs
 Males only
o Congenital HD (esp coarctation of the
aorta)
o Ovarian dygenesis (infertility)
o Normal interlectual development
 Sx:
o Infertility (commonest presentation)
o Hypogonadism and small testes
o Gynaecomastia in adolescence
o Tall stature
o N intelligence but psychological probs
Microdeletion syndromes
 Cri du chat syndrome: High-pitch mewing cry in infancy, CVS abnorms, Microencephaly, Widely spaced
eyes, ‘moon’ face
 Di George: Congenital HD, cleft palate, thymus
 William’s: Usually sporadic, face - epicanthic folds, small ears, stellate eyes
 Angelman’s: Maternal deletion. ataxia, seizures, microencephaly
 Prader-willi: Hypotonia, obesity, hypogonad, dev delay
Preterm infants
Respiratory distress syndrome (RDS)
 Due to surfactant def
 Most babies <28/40 effected
 Rare at term
 Rx:
o Antenatal corticosteroids (need 24h to act)
o Exogenous surfactant: via ET tube, decreasing mortality by 40%
o CPAP: increases end exp press. Intubation + ventilation
Pneumothorax
 In RDS air from overdistended alveoliinterstitium
 Present in 20% of ventilated infants
 Sx:
o TV
o O2 requirement
 Rx:
o Chest drain
o breath sounds/exp
o Preventable by ventilating with low press
Apnoea and bradycardia
Temp control
 Large SA:vol ratio
 Little subcut fat
PDA
 May need inotrphic support.
 Rx with fluid restriction + indomethacin (prostaglandin synthase-I)
Hypotension
Nutrition
 high nutritional requirement for rapid growth (Suckling reflex develops at 34/40)
 NG tube, Pref breast milk
 Consider parentral nutrition
 Supplement with phosphate, Ca and Vit D (bone mineralization)
Anaemia of prems
 Fe transferred in last trimester
 Blood loss from blood samples + inadequate erythropoietin
Infection
 Increased risk (esp group B strep and coliforms)
Intracranial lesions
 Interventricular hemorrhage
o High risk if: asphyxia, RDS, pneumothorax
 Post-haemorrhage hydroencephalus
o Sutures separate, incraesed HC, bulging fontanelle
o Rx: LP/ventricular tap, shunt
 Periventricular leucomalacia
o Due to ischaemia
o High risk if: inf, hypoT, MZ twins sharing placenta
Renal
 Low renal flow in fetus.
 At 28/40 GFR=25% of term. Doubles in 1st 2/52 of life
Necrotizing enterocolitis (NEC)
 Bowel wall ischaemia (gut microorganisms to colonise bowel wall)
 Sx:
o No feeding
o Distended abdo
o Milk aspirations
o Blood in stool
o Vomiting (bile stained)
 Can cause shock if haemorrhagic colitis
 AXR: shows distended bowel + air in bowel wall/portal tract
 Rx: stop feeding, IVABs, ventilate/circ support, surgery (if perforated)
 Complications: strictures, short bowel syndrome (malabs)
Retinopathy of prematurity (ROP)
 Common (50%)
 Can cause retinal detachment, fibrosis, blindness (in 1%)
 Screen all v. low BW at 6-7/52 with opthalmoscopy
 Rx: Cryotherapy/laser Rx
GOR
Inguinal hernias
Metabolic
 Hypoglycaemia: maintain BM (>2.6mmol/L) to prevent neurodamage
 Hypocalcaemia
 Electrolyte imbalance: due to poor renal function and por resorption
 Osteopenia of prems: therefore give ca, phosphate, Vit D
Bronchopulmonary dysplasia/chronic lung disease
 If infant has prolonged O2 requirements (beyond 36/40)




Lung damage is from: press/vol trauma from ventilation, O2 toxicity, inf, ++lung secretion
CXR shows: areas of opacification + cystic change
Wean infants onto CPAP
Complications: inf, cor pulmonale
The consequences of traumatic delivery
 Injury occurs if baby:
o Malpositioned
o Too large for pelvic outlet
o Manual manoeuvres
o Forceps
o Ventouse
Soft tissue injuries
 Caput succedaneum - presents immediately, oedema of scalp, superficial to periosteum, resolves
spontaneously
 Cephalhaematoma - bleed below periosteum within skull sutures, fluctuant + slower to develop,
resolves over wks, may cause/contribute to jaundice
 Chignon - large caput from ventouse
 Bruising – face, genitalia/buttocks if breech, Prems bruise easily
 Abrasions - from scalp electrodes
 Subaponeurotic heamatoma – rare, ++blood loss between aponeurosis + periosteum
Nerve palsies
 Erb’s palsy - upper N root injury (C5 + C6). Straight arm, limp pronated hand.
 Lower roots injury - less often. Weak wrsit extensor and intrinsic muscles of hand.
Fractures
 Clavicles - from shoulder dystocia, may hear snap or see lump/callus
 Humerus/femur - usually mid shaft occurring in breech. Heal quickly if immobilised
Neonatal jaundice
 Yellow pigmentation of skin/whites of eyes, due to a high bilirubin in plasma
 Clinically jaundiced = >80-120mol/L
Jaundice <24h
 Rhesus haemolytic disease
 ABO incompatibility
 G6PD deficiency
Jaundice 24h - 2wks of age
 Physiological - UNCONJUGATED
 Breast milk jaundice - UNCONJUGATED
 Infection - UNCONJUGATED
 Other causes
Persistent jaundice (>2weeks)
UNCONJUGATED:
 Breast milk jaundice - 15%, disappears by 3-4/52
 Infection - UTI
 Congenital hypothyroidism
CONJUGATED (dark urine, pale stools):
 Neonatal hepititis syndrome
 Biliary atresia:
Management:
 Hydration
 Phototherapy
 Exchange transfusion
Respiratory distress
 Signs:
o Tachypnoea
o Laboured breathing
o Expiratory grunting
o TC
o Cyanosis
 Admit to SCBU
 Monitor: HR, RR, sats, circ
 CXR
 Causes
o Transient tachypnoea of the newborn
o Meconium aspiration
o Pneumonia
o Pneumothorax
o Milk aspiration
o Persistent pulmonary HT of the newborn
o Diaphragmatic hernia
The childhood exanthems
Measles
Cause:
RNA paramyoxovirus
Spread:
Droplets
Incubation:
7-21 days
Sx:
Prodrome (catarrh, wretchedness, conjunctivitis, fever)
Conjunctiuvae look glassy, then semilunar fold swells (Meyer’s sign).
Koplik spots are pathognomonic, often fade as the rash appears (starts behind ears
on day 3-5, then spreads down body becoming confluent).
Complications:
Febrile fits, otitis media, meningitis, D&V, keratoconjunctivitis, immunosuppression,
subacute sclerosing panencephalitis. Worst complication is encephalitis (headache,
lassitiude, fits coma), 15% may die.
Treatment:
Isolate in hospital. Ensure adequate nutrition. Treat 2º bacterial inf e.g. Amoxicillin
Immunisation:
MMR
Chickenpox (Varicella Zoster virus)
Presentation:
Crops of vesicles of diff ages on the skin, typically starting on back.
Incubation:
11-21 days
Infectivity:
4 days before the rash until all lesions have scabbed (1 wk)
Spread:
Droplet. Immunity is life-long.
Tests:
Fluorescent Ab tests and Tzanck smears rarely needed.
Course:
Treatment:
Complications:
Immunisation:
Fever, rash (2 days later). Macule, papule, vesicle
Keep cool, daily antiseptic for spots, trim nails, Flucloxacillin if bacterial inf. Anti-VZV
Igs + acyclovir if immunosuppressed or on steroids.
If spots blackish (purpura fulminans) or coalescing and bluish (necrotising fasciitis)
With live-attenuated vaccine if pre-cytotoxics/steroids.
Rubella (german measles)
Cause:
RNA virus
Incubation:
14-21 days
Infectivity:
5 days before and 5 days after rash starts
Signs:
Usually mild, macular rash, suboccipital lymphadenopathy
Treatment:
Symptomatic
Immunization:
Live virus
Complications:
small joint arthritis. Malformations in utero.
RESPIRATORY SYSTEM
Asthma
 Reversible airway obstruction with wheeze, dyspnoea or cough.
 RF:
o Male
o Atopy
o Past bronchopulmonary dysplasia
o BW
o Passive smoking
o Family Hx
o Bottle fed
 Presentation:
o Recurrent wheeze
o Nocturnal cough
o Cough and breathlessness
o Eosiniophilia and  serum IgE
 Diagnosis:
o Hyperinflation of chest (pectus carinatum and Harrison’s sulcus)
o Generalised exp wheeze with prolonged exp phase
o Signs of atopy
 Ix:
o Skin tests
o PEFR (in over 5yrs)
o CXR (hyperinflatio)
 Management:
o High-dose inhaled B2 bronchodialtor (Salbuatmol or Terbutaline)
o Ipratropium nebulised
o O2 if low sats
o IV aminophylline or salbutamol
o IV hydrocortisone
Cystic fibrosis
 Autosomal recessive disorder.
 Mutations in the CF transmenbrane conductance regulator gene (CFTR)
o Abnorm ion transport across epithelial cells of exocrine glands of resp tract and pancreas
 Clinical features:
o Malabs + FTT from birth + recurrent/persistent chest inf.
o Meconium ileusinspissated meconium causes intestinal obst + vomiting + abdo distension +
failure to pass meconium
o Malabs and steatorrheoa due to insufficiency of pancreatic
 Management:
o Genetic counselling
o Inhaled salbutamol for reversible airway
o Abs
obst
o Good nutrition
o Lung transplant?
o Pertussis, MMR and pneumococcal
o Synthetic Es (pancrex)
vaccination
o Cimetidine (H2-R antagonist)
o Physio 3xday
o Vit supplements
o High calorie/protein diet
Pertussis
 Specific and highly infectious form of bronchitis, caused by Bordetella pertussis.
 Signs:
o Bouts of coughing ending with vomiting (+/- cyanosis),
o Worse at night and after feeding
o Whoop (not always present) is caused by inspiration against a closed glottis.
 Peak age: 3yrs
 Incubation: 10-14days
 Complications:
o Prolonged illness
o Hernias
o Petechiae
o Bronchiecttasis
o Microhaem
 Rx:
o Erythromycin to exposed infants
o Live vaccine at 2 months
o Admit if <6/12 old
Bronchiolitis
 Typical cause: winter epidemics of RSV
 Signs:
o Coryza (coldlike Sx)
o Sharp, dry cough
o Low fever
o Tachypnoea
o Wheeze (high pitched exp>insp)
 Diagnosis:
o Immunoflourescence of nasopharyngeal aspirates
o CXR shows hyperinflation of the lungs
 Management:
o Admit if feeding diff
 Should recover in 2 weeks
 Prevention:
o Monoclonal AB to RSV given to at risk
Pneumonia
 Signs:
o Fever
o Malaise
o Feeding diff
o Tachypnoea
o
o
o
o
Apnoea
Intercostal recession +/- cyanosis
Hyperinflation of chest
Fine end-insp crackles
o Supportive care
o
o
o
o
Cyanosis
Grunting on exp.
Consolidation
CXR changes
 Management:
o Abs (oral or IV penicillin and erythromycin)
o May need O2
TB
 Signs:
o Anorexia
o Malaise
o Prolonged low fever
o Cough
o Failure to thrive
 Diagnosis:
o Screen with heaf test
o CXR: consolidation, cavities, miliary spread
o Diagnose with Mantoux test
 Treatment:
o 6/12 of triple therapy (Rifampicin, isoniazid and pyrazinamide)
o Dropped to Rifampicin & isoniazid after 2/12.
o BCG given to at risks at birth
Croup (laryngotracheobronchitis)
 >95% of laryngotracheal infections
 Parainfluenza viruses commonest cause, also RSV
 Peak age 2yrs
 Sx: start and worse at night.
 If severe can treat with oral dex, nebulised steroids and adrenaline
Acute Epiglottitis
 Med Emergency
 Caused by H. influenzae type B (incidence  due to Hib vaccine)
 Secure airway, take bloods for culture, start IV Abs (2nd or 3rd generation cephalosporins)
Common cold (coryza)
 Classsical features: clear or mucopurulent nasal discharge + nasal blackage
 Commonest pathogens = viruses: rhinoviruses, coronaviruses and RSV.
Sore throat (pharyngitis)
 Usually due to viral inf with respiratory viruses (adenovirus, enterovirus, rhinovirus)
 Pharynx and soft palate are inflammed + local lymph nodes are enlarged + tender
Tonsillitis
 Form of pharyngitis with intense inflammation and purulent exudate
 Common pathogens: group A -H. Strep and the EBV
 Marked constitutional disturbances e.g. headache, apathy, abdo pain
 ABs (penicillin or erythromycin)
 Avoid amoxicillin
Red Ear
 Otitis externa (swimmers ear): pain, discharge due to inflammation of the skin of the meatus.
Pseudomonas common organism. Aural toilet is the key to treatment.
 Otitis media: inflammation of the middle ear and classified on timing: acute, subacute and chronic.
o Rx: paracetamol and ABs (amoxycillin/augmentin)
o Complications: COM, mastoiditis, meningitis, cerebral abscess
 Foreign bodies.
CARDIOVASCULAR SYSTEM
Innocent murmur
Heard in up to 30% of all children
Ejection murmur
 Generated in ventricles, outflow tracts or great vessels on either side of heart by turbulent blood flow
 No structural abnormalities
 Soft blowing syst murmur, localised to L-sternal edge, no diastolic component, no radiation
Venous hum
 Turbulent blood flow in head and neck veins
 Disappears when lying flat or compressing ipsilateral jug V
Acyanotic congenital heart lesions
 VSD:
o Sx: asymptomatic, heart failure, recurrent chest inf, cyanosis, endocarditis
o Signs: parasternal thrill, harsh loud pansystolic ‘blowing murmur’, tachyop, tachycardia, enlarged
liver
o Ix: CXR=heart, pul A, pul vascular markings. ECG=ventricular hypertrophy, upright T wave=pul
HT.
o Course: 20% close in 9/12. Diuretics and ACE-Is. Surgery if pul HT as can cause pul vascular disease.
ABs to prevent bacterial endocarditis.

o
o
o
PDA:
Common in prem
Left to right shunt (aortapul A)
Signs: FTT, pneumonias, heart failure, collapsing pulse, thrill, S2, continuous murmur beneath Lclavicle
o Ix: CXR: vasc markings, enlarged aorta. ECG: usually N, LVH
o Rx: most close over time. Dex in preterm labour. If symptomatic, Rx with fluid restriction, diuretics,
indomethacin (a prostaglandin synthetase inhibitor). Surgical ligation or transvenous occlusion with
coil device.

o
o
o
ASD:
Special form of VSD, often seen in kids with Down’s syn.
Signs: widely split, fixed S2 and midsystolic murmur (2nd IC space of L sternal edge)
Ix: CXR: cardiomegaly, globular heart (primum defects). ECG: RVH +/- incomplete RBBB

o
o
o
o
o
Coarctation
Associated with other lesions e.g. bicuspid aortic valve and VSDs.
Neonates present with duct-dependent circ
Sx: circulatory collapse when duct closes, heart failure, murmur between shoulder blades.
Signs: diff in feeling femoral pulses, BP in arms, BP in legs, no foot pulses
Ix: CXR: rib notching (late), due to large collateral IC As running under ribs posteriorly to bypass
obstruction. ECG: RVH in neonate, LVH in older child
o Rx: surgical: resection and end to end anastomosis or balloon dilatation.
Cyanotic congenital heart lesions
 Tetralogy of Fallot
o 4 cardinal anatomical features:
 Large outlet VSD
 Overriding of the aorta with respect to the ventricular septum
 RV outflow tract obstruction (pul stenosis)
 RVH
o Signs: cyanosis as ductus closes, hypercyanotic spells, dyspnoea, faints, squatting at play, clubbing,
thrills, absent pulmonary part of S2, long, loud ejection systolic murmur at L sternal base.
o Ix: FBC: Hb CXR: small heart, uptitling apex (RVH), pulmonary artery ‘bay’. ECG: RVH and RAD (R
axis deviation)
 Transposition of the great arteries
o When there are 2 parallel circulations: no mixing is incompatible with life (ass. Anormalities)
o Sx: usually present day 1 or 2 of life with cyanosis
o Signs: cyanosis, clubbing, CCF +/- systolic murmur.
o Ix: CXR: narrow pedicle, ‘egg on side’, pul vasc markings. ECG: RVH. Echo: diagnostic
o Rx: prostaglandin infusion to keep ductus arteriosus open. Life-saving balloon atrial septostomy
NEUROLOGY
Epilepsy
 Tendency to intermittent, abnormal electrical brain activity
 Causes:
o 70-80% idiopathic,
o Cerebral tumour
o Neurodegenerative disorders
o 2to cerebral dysgenesis
o Neurocutaneous syndromes
o Cerebral damage
 Generalised epilepsies:
o Status epilepticus: multiple seizures, no recovery of consciousness in between
o Absence, tonic or tonic-clonic seizure disorders may remit; identification of the epilepsy syndrome
involved allows a more accurate prognosis
o Atonic and myoclonic seizures may accompany cerebral dysgenesis or a neurodegenerative
disorder and have a poor prognosis
 Localisation-related epilepsies (focal or partial):
o May arise from any of the 4 lobes
o Temporal lobe is most common: ‘complex phenomena’: conciousness, automatisms, deja vu,
jamais vu
o Frontal lobe involves motor cortex, patiel tonic, clonic movements
o Occipital lobe gives rise to distorted vision
o Parietal lobe contralateral dysaesthesias, vertigo + distorted body image
 Epilepsy syndromes
o Infantile spasms (west syndrome): between 4-6/12, violent flexor spasms of head, trunk, limbs
followed by extension of arms (‘salaam spasms’). Rx with vigabatrin or corticosteroids. Later learning
disability and/or epilepsy common.
o Typical (petit mal) absence seizures: 1-2% of childhood epilepsy. onset 4-12yrs. Induced by
hyperventilation. Good prognosis, 95% remission in teens
Meningitis
 Confirmed by inflammatory cells in the CSF
 Causes: viral are most common and are self-resolving. Bacterial may have severe consequences. Other
causes of meningitis inc: malignancy + autoimm diseases.
Bacterial Meningitis
 Usually follows bacteraemia.
 Host response to infection causes most damage.
 Inflam mediators, activated leucocytes & endothelial damage cause cerebral oedema, IC press and
cerebral blood flow.
 Organisms:
o < 3 Months: group B strep, E.coli, coliforms, Listeria monocytogenes
o < 6yrs: Neisseria meningitidis (meningococcus), strep pneumoniae, H. influenzae
o >6yrs: Neisseria meningitidis, strep pneumoniae
 Presentation:
o Meningeal signs: stiff neck, photophobia, opisthotonos
o IC press: irritable, high-pitch cry, drowsy, vomiting, fontanelle tense (late sign)
o Septic signs: fever, arthritis, odd behaviour, purpuric rash (in meningococcus), cyanosis, DIC, ++WCC
o Shock: tachycardic, hypotensive, poor capillary refill time, oliguria
 Ix: CSF (confirms Dx, identifies organism + AB sensitivity). Bloods, throat swab, rash scraping
 Rx:
o 3rd generation cephlosporin (cephotaxime or ceftriaxone).
o Ampicillin in <3/12 olds
o Dexamethasone reduces long-term complications
 Complications:
o Hearing loss
o Hydroencephalus
o Ataxia
o Subdural effusions
o Brain abscess
o Mental retardation
o Disseminated disease
o Paralysis
o Epilepsy
Cerebral Palsy
 Comprises a range of chronic disorders of posture and movement caused by non-progressive CNS lesion
sustained before 2 yrs old, resulting in delayed motor development, evolving CNS signs +/- learning
disability +/- epilepsy.
 Causes:
o Antenatal (80%): cerebral dysgenesis + malfornation, congen inf -rubella, tox, CMV
o Intrapartum (10%): birth asphyxia/trauma
o Postnatal: IVH, meningitis, trauma.
 Clinical presentation:
o Abnormal tone and posture
o Feeding difficulties
o Delayed motor milestones
o Abnormal gait once walking
o Developmental delay (language and social skills)
Spastic (70%)
 Damage to upper motor neurone (pyramidal or corticospinal) pathway
  limb tone (spasticity), deep tendon reflexes + extensor plantar response
 distribution of signs:
o Hemiplegia
o Diplegia
o Quadreplegia
Ataxic hypotonic (10%)
 Signs usually symmetrical
 Early hypotonia, poor balance, delayed motor development
 Later incoordination movements and intention tremor (cerebellum dysfunction)
Dyskinetic (10%)
 Leading to constant involuntary movements and poor postural control
 Intellect may be relatively unimpaired
 Damage to basal ganglia and associated pathways (extrapyramidal)
Intracranial neoplasms
 IC press with focal signs +/- false localising signs
 Sx of ICP:
o Headache (worse on lying down)
o Vomiting
o Papilloedema
o Squint (due to VIth N palsy)
o Nystagmus
o Ataxia
o Behaviour change
Myopathies
The muscular dystrophies
 Duchenne’s muscular dystrophy:
o X-linked recessive disorder
o Peak age of Dx = 5.5yrs
o Waddling gait, climb stairs one by one, ‘Gower’s sign’ + pes cavus
o Progressive, in wheel chair at 10-14yrs, death ensues late teens, early 20s.
 Becker’s muscular dystrophy:
o Some functional dystrophin is produced
o Slower progression. Dx at 11yrs, wheel chair late 20s, death 40s
 Congenital muscular dystrophies:
o Present with muscle weakness at birth/ early infancy
The inflammatory myopathies
 Benign acute myositis: follows URTI, self-limiting course, pain and weakness.
 Dermatomyositis: gradual onset, ascending muscle weakness. Heliotrope rash. Post-exercise aches and
pains
Myotonic disorders
 Dystrophia myotonia: inherited. Hypotonic baby, but classically presents in school age with learning
diff, expressionless face, distal wasting and myotonia.
Metabolic myopathies
 Present as floppy infant or in older child with muscle weakness + cramps on exercise
Congenital myopathies
 Presenting at birth or in infancy with generalised hypotonia and muscle weakness
 Categorised according to appearance of muscle Bx
Headache
 Causes of acute headache include:
o Febrile illness
o Head injury
o Migraine
o Benign intracranial HT
o Stress
o Drugs inc alcohol
o Acute sinusitis
o Subarachnoid/intercerebral haemorrhage
o Meningitis/encephalitis
o Temperomandibular pain
 Causes of recurrent headaches:
o Tension headache: symmetrical, gradual onset, tightness (band), frequent
o Migraine: sudden onset, unilateral, visual and GI disturbances
o ICP: headache worse when lying down, vomiting in a.m.
 Ix: CT/MRI if ICP suspected.
 Rx: advice, reduce stress. Mild analgesics, anti-emetics if vomiting. Prophylaxis for migraine
ENDOCRINOLOGY
IDDM
 Genetic predisposition and environmental precipitants
 AI process which damages -cells in pancreas leading to absolute I def
 Associated with other AI disease e.g. hypothyroidism
 Dx: symptomatic child with raised random blood glucose (>11.1mmol/L) or fasting blood glucose of
>7.8mmol/L and raised HbA1c
 Presentation
o Most common: polydipsia, polyuria, wt loss
o Less common: enuresis, skin sepsis, candida and other infections
DKA
 Insulin def
 Aetiology: poor control, poor adherence, illness (inf), initial presentation
  I causes:
o Hyperglycaemia: hepatic production, uptake, proetolysis
o Osmotic diuresis: loss of water and electrolytes
o Dehydration: due to osmotic diuresis. Dehydration causes: CCA,cortisol,GH,AVP
o Ketosis: due to lypolysisFFsketone production
o Acidosis: due to ketones. Therefore metabolic acidosis +/- resp compensation
 Presentation
o Acetone on the breathe
o Hyperventilation (kussmaul breathing)
o Vomiting
o Hypovolaemic shock
o Dehydration
o Drowsiness
o Abdo pain
o Coma
Hypothyroidism
Congenital hypothyroidism
 Common and Rxable (i.e. preventable cause of learning diff).
 Causes:
o Maldescent of thyroid and athyrosis
o Dyshormonogenesis
o Iodine def:
o Hypothyroidism due to TSH def:
 Clinical features:
o FTT
o Pale, cold, mottled skin
o Feeding probs
o Coarse facies
o Prolonged jaundice
o Large tongue
o Constipation
o Hoarse cry
 Rx: lifelong oral thyroxine, titrating dose to maintain N growth, TSH and T4
Juvenile hypothyroisism
 Usually caused by AI thyroiditis
 More common in girls
 Clinical features:
o Short stature/growth
failure
o Cold intolerance
o Dry skin
o Cold peripheries
o Bradycardia
 Rx: thyroxine
o
o
o
o
o
o
Thin,dry hair
Pale, puffy face
Goitre
Slow relaxing reflexes
Constipation
Delayed puberty
o Goitre (occasionally)
o Umbilical hernia
o Developmental delay
o Obesity
o Slipped upper
epiphysis
o Deterioration in school
work
o Learning diff
CAH
 AR disorder. More common in consanguineous marriages
 Abnormal adrenal steroid biosynthesis.
 Cortisol defACTHadrenal hyperplasia + androgens
 Presentation
o Female virilisation: clitoral hypertrophy, variable fusion of labia
o Male: enlarged penis. If a non-salt loser may present with tall stature, PP
o Salt-losing adrenal crisis in males presents in 1-3weeks with vomiting, wt loss, floppiness and circ
collapse
 Dx:
o  metabolic precursor 17 OH-progesterone
o Salt losers (pNa, pK, metabolic acidosis, hypoglycaemia in crisis)
 Mx:
o Corrective Sx
o Hydrocortisone, saline + dextrose in salt-losing crisis in males
GASTROINTESTINAL SYSTEM
Gastroenteritis
 Infective diarrhoea and vomiting
 Rotavirus (60%)
 Bacterial causes are suggested when blood in stools
 Rx:
o Fluid replacement
 Complications:
o Dehydration
o Temporary sugar intolerance
o Malnutrition
 Tests: stools
 Prevention: hygiene, water and food, education, fly control.
Secretory diarrhoea
 Causes: bacteria (campylobacter, staphylococcus, E coli, salmonella, shigella and vibro cholerae),
giardiasis, rotavirus, amoebiasis, cryptosporidium. IBD.
Constipation
 Painful passage of hard, infrequent stools
 Causes:
o Infant: organic cause most likely
o Older child: non-organic/functional cause most likely
 Ix: growth, general and anorectal, faeces palpable per abdomen. Bloods (exclude systemic cause). Plain
abdo X-ray may show faecal loading +/- megacolon.
 Rx:
o Treat underlying organic cause.
o dietary fluids and fibre
o Stool softeners (lactulose) and stimulants (senna)
o Evacuate overloaded rectum (enema or manual evacuation)
o Maintenance: stools should be kept soft for 3-6/12. Encourage daily sits on loo.
o Parallel psychological help: encouragement by family and health team
Hirchsprung’s disease
 Absence of ganglionic cells in largenarrow, contracted segment from rectum proximally ending in
normally innervated dilated colon.
 Presentation: usually as neonate with intestinal obstruction (failure to pass meconium in 1st 24habdo
distension + bile stained vomitus). Can present in 1st few weeks with Hirshsprung’s enterocolitis (C. diff
infection), or in later childhood with chronic, profound constipation + abdo distension - soiling.
 Ix: DRE: may reveal narrow segment + withdrawing finger causes gush of liquid stool and flatus. Rectal
Bx: diagnostic, showing aganglionic cells
 Management: colostomy then anastamosing normal bowel to anus.
FTT
 Ix:
o Hx: mid-parental hts, pregnancy Hx, feeding Hx
o Exam: Ht, Wt, head circ, full exam, urinalysis, signs of abuse + neglect
o Ix: serial measurements of wt, all bloods, stools, CXR, renal + CNS US, skeletal survey, ECG/echo,
endomysial + antigliadin Abs (coeloiac), sweat test
 Causes:
o Inadequate intake
o Iatrogenic (corticosteroids)
o Psychosocial deprivation
o Systemic disease
o Familial short stature
o Endocrine
o Small-for-date
o Chromosomal (Down’s)
o Malabsorption
o Metabolic
o Mental retardation
 Rx: of non-organic cause is multidisciplinary in 1care e.g. HV, dietician
Faecal soiling
 Abnormal after the age of 4yrs
 With loaded rectum or without loaded rectum
 Faeces in the rectum is always an abnormal finding
Loaded rectum
o Poor coodination with anal sphincter relaxation
o Following febrile illness
o Inhibition for fear of punishment if incontinent
o Anxieities about using toilet facilities
 Rx as you would for constipation + star charts + explain to child and parents about retention and how it
leads to incontinence.
Empty rectum
 Urgency of defecation and can’t hold it in
 Neuropathic bowel
 Diarrhoea
 General learning disability
 Child may defecate intentionally to spite
parents
Gastro-oesophageal reflux (GOR)
 Physiological, asymptomatic reflux may occur in any child/adult but is infrequent
 Measurements of lower oesophageal pH show that acidity for <4% of 24h is normal
 More than this results from functional immaturity of LOS
 Common in under 1yrs, then spontaneously resolves
 A sliding hiatus hernia is present in some symptomatic infants
 Severe reflux is uncommon but may be in potentially serious complications:
o Cerebral palsy
o Bronchopulmonary dysplasia (chronic lung disease of prematurity)
o Following surgery for oesophageal atresia or diaphragmatic hernia
 Presentation:
o Regurg
o Apnoea
o FTT + anaemia
o Distress after feeds
o pneumonia
 Ix: 24h oesophageal pH monitoring. Barium swallow. Endoscopy and Bx
 Rx:
o Reassurance
o Thickening agents to feeds (Carobel)
o Avoid over feeding
o Antacids (gaviscon)
o Lie on front
 Drugs
o Enhance gastric emptying e.g. domperidone
o H2-antagonists e.g. ranitidine to reduce oesophagitis
 Surgery: fundoplication, oesophageal stricture, recurrent aspiration
Inflammatory bowel disease (IBD)
 Crohn’s disease
o Present with: abdo pain, diarrhoea + growth failure with pubertal delay
o May also present with: oral/perianal ulcers, fever, arthritis, uveitis, erythema nodosum
o Diagnosis: barium and colonscopy, ESR and CRP.
 Ulcerative colitis
o Presents with: rectal bleeding, diarrhoea, colicky pain, wt loss
o Also: erythema nodosum, pyoderma gangrenosum (acute ulcerating skin), arthritis, spondylitis
(inflammation of synovial joint of backbone)
Coeliac disease
 Gliadin fraction of gluten provokes a damaging immune response in proximal small intestine
 Lymphocytic infiltration and villous atrophy
 Presents in 1st 2yrs of life following introduction of gluten in cereals with:
o FTT
o Abnorm stools
o General irritability
o Abdo distension
o Buttock wasting
o Presents in later life with anaemia +
growth failure
Pyloric stenosis
 Hypertrophy of pylorus causing gastric outflow obstruction
 2-7wks of age, boys 4:1
 Presents with:
o Projectile vomiting after feeds
o Hypochloraemic alkalosis
o Constant hunger
o Wt loss and poor Wt gain
 Diagnosis:
o Visible gastric peristalsis
o Pyloric ‘olive’ palpable in RUQ
Intussusception
 Invagination of proximal bowel into distal
 Commonest cause of intestinal obstruction in infants, usually 2 months to 2 yrs.
 Presentation:
o Acute, severe colicky pain and pallor
o Passage of red currant jelly stools
o Sausage shaped mass in abdomen
o Abdo distension and shock
 X-ray shows distended small bowel + absent gas in distal colon and rectum
 Rx: fluid resus and air enema. Surgical reduction if this fails.
GENITOURINARY SYSTEM
Nephrotic suyndrome (nephrosis)
 ++proteinuria   albumin + oedema + hypoproteinaemia + hypercholestrolaemia
 Sx:
o Anorexia,
o Oedema (periorbital, genital),
o GI disturb,
o Ascites,
o Infections,
o Oliguria,
o Irritability
o Breathlessness
 Ix: urine (frothy, +++albumin and casts, Na , blood (albumin, urea and creatinine normal). Renal
biopsy in older kids.
 Rx:
o Low sodium diet limits oedema
o Consider furosamide IV + spironolactone PO
o Prednisolone (course of 3-7/12)
 Complications:
o Hypovolaemia
o Infection
o Thrombosis
o Hypercholesterolemia
Urinary tract infection
 Presentation:
o Newborn Sx non-specific and may develop rapidly into septicaemia.
o Toddlers: present as ‘gastro-enteritis’, FTT, colic, PUO
o Older child: dysuria without fever due to vulvitis in girls and balanitis in boys
 Collection of sample:
o ‘clean catch’ in to sterile pot
o Adhesive bag applied to perineum, after careful washing
o Suprapubic aspiration (SPA) in severely ill child
 Diagnosis: culture
 Causes:
o Infecting organism: E. Coli, Proteus, Pseudomonas
o Incomplete bladder opening: infrequent voiding therefore large bladder, vulvitis, hurried
micturition, obstruction from loaded rectum, neuropathic bladder.
o Vesicoureteric reflux: developmental anomaly of vesicoureteric junctions therefore urine goes
bladderureters.
 Management:
o Oral AB (co-amoxiclav) or IV AB (cefotaxime or ampicillin
o Preventative: avoid constipation, oral fluids, encourage full voiding
Glomerulonephritis
 Haematuria + oliguria (+/- HT + ureamia) produced by immune mechanism in kidney
 Peak age 7yrs
 Causes:
o Malignancies

Strep sore throat or skin infection
o Infection (viruses, SBE, syphilis)
o HSP
o Renal vein thrombosis
o Toxins (heavy metals)
o Berger’s disease
 Presentation:
o Haematuria
o Periorbital oedema
o Loin pain
o Oliguria
o Fever
o GI dist
o BP

Ix:
o MSU: RBCs, WBCs, red cell casts
o Renal US, renal Bx
o Bloods: urea, ESR, acidosis, C3 titre

Rx:
o Restrict protein in oliguric phase
o Monitor BP, treat severe HT.
o Penicillin IV and then PO for strep
infection
Wilm’s neuroblastoma

Malignant tumour composed of embryonic nerve cells

Commonest intra-abdominal tumour in children

Originates from embryonic renal tissue

Rarely seen after 10yrs

Presentation:
o Abdo mass
o Fever
o Flank pain
o Haematuria

Ix: US or CT show intrinsic renal mass, mixed tissue densities

Rx: avoid Bx. Nephrectomy and 4/52 chemo. Radiotherapy may help
Enuresis

Most children are psychologically and physically normal

Different types
o 1 nocturnal enuresis: common. FHx of delay in acquiring sphincter competence.
o Day time enuresis: nocturnal enuresis usually also present. Common causes are lack of sensation
(behavioural prob), detrusor instability (uncoordinated bladder contraction), bladder neck
weakness, UTI, constipation, neurogenic
o 2 enuresis: is the loss of previously achieved urinary continence, may be due to emotional upset
(commonest cause), UTI, polyuria


Ix: -MSU, -US, -x-ray (may show vertebral abnorm), MRI (spinal roots)
Rx:
o Avoid acrimonous blame, and reassurance
o Enuresis alarm
o Fluid restriction before bed
o Desmopressin (Short term relief)
o Star chart
o Anticholinergic or adrenergic drugs
HAEMATOLOGY
Anaemia

Hb below normal range for child’s age and gender.

Clinical features:
o Asymptomatic
o Tiredness
o Pallor

Management:
o IDA: dietary advice and oral Fe therapy
o Aplastic anaemias: stem cell or BM transplant, immunosuppressive therapy, ABs
Sickle cell disease

Inherited disorders of Hb structure or its production.
Sickle cell (HbS), homozygous state (SS)
 a.a substitution on codon 6
 Hb molecule becomes deformed in low O2, dehydration, cold  thrombosis and ischaemia
 Management:
o Hydration
o Blood and BM transplant
o Warmth
o Penicillin
o Analgesia
o Pneumococcal vaccine
o Blood transfusion
o Folic acid
Sickle cell trait (AS)
 Usually asymptomatic except under v.v.low O2 tensions
Sickle cell-Hb C (SC) disease
 Nearly normal Hb levels, few painful crisis, but may develop proliferative retinopathy
Thalassaemia
 Syndromes are due to inherited defects of globin chain synthesis
  or absent chain  excess of other type  precipitates in RBC membrane  cell death in BM and
premature removal from the circ by the spleen
-thalassaemia

-thalassaemia major
o Severe anaemia and jaundice from 6/12 + FTT + hepatosplenomegaly
o Extramedullary haemopoesis  BM expansion  classical faces (maxillary overgrowth and skull
bossing)
o Rx: reg blood transfusion and chelating therapy. BM transplant is curative.

-thalassaemia intermedia
o Clinical manifestations are more variable


o Anaemia is moderate
o Blood transfusion sometimes required
-thalassaemia minor
o Asymptomatic
o onfused with mild IDA and lead to unnecessary Fe therapy
-thalassaemia
o More common in Asians
o 4 gene del: fetal hydrops and death in utero.
o 3 gene del: moderate chronic haemolysis.
o 1-2 gene del: no clinical Sx
Leukaemia
Presentation:

o Malaise
o Abnormal bruising
o Bone pain
o Infections
o Hepatosplenomegaly
o Pallor
o Lymphadenopathy

Ix: low Hb. leukaemic blast cells on film. BM aspirate needed for diagnosis. CSF

Treatment
o Remission induction: correct any aneamia, infection, then 4/52 combo chemo
o Intensification: blocks of intensive rx given to maintain remission
o CNS Rx: by intrathecal chemo, cranial irradiation, high dose methotrexate
o Continuing therapy: modest intensity for long time 3 yrs.
o Treatment for relapse: high dose chemo with total body irradiation, BM transplant.
DERMATOLOGY
Eczema

Atopic (commonest), allergic (type VI hypersensitivity) or caused by irritants or venous stasis.

Diagnosis: clinically + IgE + specific allergens identified with skin prick and (RAST).

Clinically:
o Itch
o Dry skin,
o Classic distribution,
o Lichenification

Management:
o Avoid irritants
o Antihistamines: H1 histamine antagonists
o Emollients
o Dietary elimination
o Topical corticosteroids
o Psychosocial support: National Eczema
o Occlusive bandages
Society
o ABs and antivirals
Psoriasis

Rare before the age of 2

Guttate type:
o Most common in children
o Follows strep/viral sore throat or ear infection
o Lesions small, rain-drop shaped, round/oval scaly patches on trunk and upper limbs
o Resolves in 3-4/12
o Rx: bland ointments. Coal tar preparations. Dithranol for chronic plaques

Pityruasis Rosea:
o Acute benign, self-limiting of viral origin
o single round scaly macule (2-5cm) in a few days numbers of smaller dull pink macules on trunk,
upper arms and thighsrash spreads in line with ribs posteriorly ‘fir tree pattern’.
o Sometimes itchy
o No Rx required resolves in 4-6wks
MUSCULOSKELETAL SYSTEM
Variations of normal posture

Bow legs (genu varum)
o Bowing of the tibiae causing knee to be wide apart
o Common in 0-3yrs, no need for Rx

Knock-knees (genu valgum)
o Feet are wide apart when knees held together. Seen in 2-7yrs, usually resolves.

Flat feet (pes planus)
o Toddlers learning to walk have flat feet, due to flat medial longitudinal arch + fat pad
o Marked flat feet can be a presentation of a collagen disorder e.g. Ehlers-Danlos syn
o Rx with exercises, arch support in shoes, surgery for symptomatic adolescent

In-toeing
o 3 main causes:
 Metatarsus varus: an adduction deformity of a highly mobile forefoot
 Medial tibial torsion: at lower leg when tibia is laterally rotated less than normal
 Persitent anteversion of the femoral neck: at the hip when femoral neck is twisted forward
more than normal

Out-toeing
o Uncommon, but may occur in infants between 6-12 months
o When bilateral it is due to lateral rotation of the hips and resolves spontaneously

Toe walking
o Common in 1-3yrs. If persisting: CP, tight Achilles tendons, Duchenne’s Muscular Dystrophy
DDH (Developmental Dysplasia of the Hip)

At risk babies:
o Breech
o Caesarean for breech
o BW
o Older mother

Diagnosis: examine hips at day 1 and at 6 wks.
o click test of Ortolani:
o Barlow manoeuvre

US: image of choice.

Rx:
o Positioning device in abduction (Craig splint)
o Restraining device (Pavlik harness)
o
o
o
o
+ve FHx
Postmaturity
Other malformations
Oligohydramnios
Club foot (talipes equinovarus)

Positional talipes from intrauterine compression is common. Foot is normal size, deformity is mild and
can be corrected to the neutral position with manipulation.

Talipes equinovarus is a complex abnormality.
1. Inversion
2. Adduction of forefoot relative to hindfoot
3. Equinus (plantar flexion)
o 2x more common in males
o Rx: start in 1st wk with foot manipulation, strapping and splinting. If Rx not worked after 3 months
operative reduction is carried out.
Juvenile chronic arthritis

Now called Juvenile idiopathic arthritis = a group of conditions where arthritis for > 6wks in kids under
16yrs.
Systemic arthritis (‘Still’s disease’)
 Affects young children
 Sx:
o Acute illness/malaise
o Arthralgia/myalgia
o High, spiking fever
o Hepatosplenomegaly
o Anorexia, wt loss
o Hb, neutrophil + platelets + acute
o Salmon pink rash when fever high
phase reactants
 Some recover without getting chronic arthritis, others develop polyarthritis
Polyarticular
 All ages. Girls > boys.
 Usually symmetrical involvement of wrists, hands, knees and ankles
 Polyarticular disease + rheumatoid factor = ‘juvenile rheumatoid arthritis’
Pauciarticular/oligoarthritis
 Usually in young children.
 Usually knees, sometimes ankles and wrists.
 risk of eye disease, especially girls with antinuclear Abs (ANA)
 ‘Extended oligoarthritis’ when further larger joints are involved after 6 months
Enthesitis-related arthritis
 Affects older boys. Large lower limb joints affected and a ‘sausage finger’
 May have HLA-B27 tissue type and FHx.
 Acute iritis common.
Juvenile psoriatic arthritis
 Involes interphalangeal jts therefore ‘sausage fingers’ + skin lesions + nail pitting
Hip diseases in childhood

Transient synovitis (TS, irritable hip)
o Most common cause of acute hip pain
o Occurs at 2-12yrs. Follows viral in
o FBC, blood cultures and x-ray usually normal. Joint effusion on US. No pain at rest
o Rx: bed rest and skin traction. Usually better in few days.

Perthes disease
o Ischaemia of femoral epiphysisavascular necrosisrevascularisation + reossification.
o Age 5-10yrs.
o Male:female 5:1. Bilateral in 10-15%
o Onset insidious, limp, hip pain
o Ix: X-ray shows density in femoral heads. Bone scan and MRI
o Rx: bed rest and traction. In more severe disease maintain hip in abd with plaster

Slipped upper femoral epiphysis
o Displacement of epiphysis of femoral head postero-inferiorly. Bilateral in 20%
o Most common in 10-15yrs, during adolescent growth esp obese boys
o Presentation: may be acute after minor trauma
o Sx: limp, hip, groin pain (referred to knee), limited movements.
o Ix: diagnosis by X-ray
o Rx: surgical (pin fixation in situ)
Osteomyelitis

Infection in the metaphysis of long bone.

Common sites distal femur + prox tibia.

Causes: Staph aureus, strep, H. influenzae, TB

Presentation: painful, immobile limb, fever, swelling, tenderness, red, warm over affected area

Ix: blood culture +ve, WBCs and acute-phase reactants. Bone scan identifies site of infection.
Rx: IV ABs for several weeks, then oral. Surgical drainage if not responding quickly to ABs. Limb rested
in splint then mobilised.