Loading presentation...

Present Remotely

Send the link below via email or IM


Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.



No description

André Almeida

on 25 June 2013

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of Paediatrics

Fetal medicine
Child Abuse
Risk factors: parents with a hx of alcoholism or drug use; children with mental retardation or a handicap
Infants: can present as apnoea, seizures, feeding intolerance, excessive irritability, somnolence, or failure to thrive.
Retinal Haemorrhages
Conditions that mimic abuse:
Mongolian spots - bruises
Osteogenesis imperfecta - fractures
Bullous impetigo - cigarette burns
Shaken Baby Syndrome - Retinal Haemorrhages or subdural haematoma
A - Appearance
B - Behaviour
C - Cognition
D - Delusions
M - Mood
S - Speech
H - Hallucinations
I - Insight
T - Thoughts

Cyanotic Heart Defects: 5 T's
T1 - Truncus Arteriosus
T2 - Transposition of the great vessels
T3 - Tricuspid atresia
T4 - Tetralogy of Falot
T5 - Total Anomalous Pulmonary Venous Drainage
Holes - Acyanotic "pink" babies
VSD - 32%
Common in Down's Syndrome, Fetal Alcohol Syndrome, TORCH (Toxoplasmosis, other agents, rubella, CMV, HSV)
Left to Right shunt; Pansystolic (Holosystolic) murmur best heard at the left sternal edge.

Large defect can present with frequent respiratory infections, dyspnoea, FTT, and CHF. Murmur is softer but can be accompanied by a systolic thrill, crackles, hepatomegaly and a mid-diastolic murmur.

Diagnosis: Echo is diagnostic, ECG can show biventricular hypertrophy and CXR can show cardiomegaly and increases pulmonary vascular markings

Management: HF - Diuretics and ACEI (captopril) ; Surgery between 3-6 months of age - before developing Eisenmenger syndrome
ASD - 10%
Common in fetal alcohol syndrome and Down's Syndrome

Left to Right shunt. Frequently asymptomatic.

Two types:
Primum - detected early in childhood with a murmur or fatigue on exertion
Secundum (80%) - present late childhood or early adulthood

Ejection systolic murmur best heard at the left upper sternal edge - increased flow through pulmonary valve; wide and fixed split S2

Echo is diagnostic; ECG may show RVH and right atrial enlargment (plus PR prolongation); CXR reveals cardiomegaly and increased pulmonary vascular markings

90% of ASD close spontaneously; Catheter closure is indicated in patients with CHF
PDA - 12%
Risk factors include first-trimester rubella infection, prematurity, and female gender.

Acyanotic left to right shunt from the aorta to the pulmonary artery
Continuous machinery murmur at the second left intercostal space at the sternal border, a loud S2, wide pulse pressure and bounding peripheral pulses.

In large PDAs, heart failure and pulmonary hypertension can occur

Doppler is diagnostic. In large PDAs echo shows left atrial and left ventricular enlargement

Indomethacin or surgery.
Outflow obstruction
Aortic Stenosis
Pulmonary Stenosis
Coarctation of the Aorta
Can be association with mitral valve stenosis
and coarctation of the aorta
Severe: reduced exercise intolerance
chest pain on exertion and syncope
Carotid Thrill
Ejection systolic murmur (Upper Right Sternal Edge
radiates to the neck)
Apical ejection click
ECG: Downgoing T waves
Maybe LVH
Mx: Balloon Valvotomy
Neonates with severe PS have duct-dependent
pulmonary circulation - present with cyanosis
Ejection systolic murmur (Upper left sternal edge)
ECG: Upright T wave in V1
Transcatheter balloon dilation when
98% below the left subclavian artery
Associated with Turner's Sysndrome,
berry aneurysms and male gender.
>2/3rds have a BICUSPID aortic valve
Asymptomatic HTN
Upper extremity HTN (R arm)
Murmur - back, between scapulae
Weak femoral pulses
Radiofemoral delay
Older kids: LVH on ECG, "3" sign on CXR - pre- and postdilatation of the coarction segment and rib notching - collateral circulation through the intercostals
Severe coarctation in infants: keep ductus arteriosus open with PGE1
Cyanotic "Blue" Babies
Right-to-Left Shunts
Tetralogy of Fallot
1. Infundibular PS
2. Overriding Aorta
3. RVH
4. VSD
Risk factors: maternal PKU (phenylketonuria) and DiGeorge Syndrome
Dyspnoea and Fatigability
Cyanosis develops in the first 2 years of life
Degree of cyanosis reflects extent of PS
Children squat for relief during hypoxemic/hypercyanotic spells
Ejection systolic murmur at left upper sternal border
Clubbing of fingers and toes develops in older children
Echo and cath - diagnostic
CXR: boot-shaped heart with reduced pulmonary vascular markings
ECG: R-axis deviation and RVH
PGE1 - if severe PS
Hypercyanotic spells - O2, propanolol, phenylephrine
the knee-chest position, fluids, bicarbonate and morphine
Temporary palliation - ballon atrial septostomy
Definitive surgery at 6 months
Transposition of the great arteries
Aorta is connected to the right ventricle
Pulmonary arteries connected to the left ventricle
Associated anomalies: ASD, VSD and PSD
Presents at day 2 of life with cyanosis - duct closure
CXR: narrow mediastinum and 'egg on the side'
appearance and increased pulmonary vascular markings
Echo - diagnostic
Protaglandin infusion - keep duct open
Balloon atrial septostomy (required in 20%)
Eisenmenger Syndrome: increased resistance in the
pulmonary circulation leading to reversal of a left to right
shunt. Occurs between 10-15 years of age and presents with cyanosis.
Arioventricular Septal
Defect (AVSD)
Commonly seen in children with Down's
Large defects results in Pulmonary HTN
Cyanosis at birt or HF at 2-3 weeks
Superior axis on ECG
Treat HF medically
Surgical repair at 3-6 months of age
Tricuspic Atresia
Only left ventricule is effective
Right ventricule is small and non-functional
Presents with cyanosis in the newborn period
Or cyanosis and breathlessness later
Blalock-Taussig shunt insertion (between the subclavin and pulmonary artery) - in severely cyanosed children
Fontan operation - link between the IVC and the pulmonary artery
Rheumatic Fever
Infective Endocarditis
Kawasaki disease


Common Cold
Local lymph nodes are enlarged and tender
Normaly viral (adeno, entero
and rhinoviruses)
Group A Beta-Haemolytic Streptococcus
Form of pharyngitis
Inflammation of the tonsils
with purulent exudate
Group A Beta-Hameolytic Strep
EBV (infectious mononucleosis)
Abdominal pain
Tonsillar exudate
Cervical lymphadenopathy
Abx in severe cases
Avoid amoxicillin
Acute otitis media
6-12 months of age
Pain and fever
Tympanic membrane: bright read and bulging with loss of normal light reflection
Virus (RSV, rhino)
Bacteria (Pneumococcus, H. influenza
Moraxella catarrhalis)
Complications (uncommon)
mastoiditis and meningitis
ABx (Amoxicillin)
Reccurent infections can lead
to otitis media with effusion
(glue ear or serous om)
Grommet insertion
May occur with viral URTIs
Secondary bacterial infection causes:
pain, swelling, tenderness over the cheek
Acute: abx and analgesia + topical decongestants
Laryngeal and tracheal infections
Bacterial tracheitis
Acute epiglottitis
Stridor, heard predominantly on inspiration
Barking cough
95% of laryngotracheal
infections is viral croup
Parainfluenza virus (commonest)
Barking cough
Harsh stridor
Preceded by fever and coryza
Oral dexamethasone, oral prednisolone
and nebulised steroids (budenoside) reduce
severity and duration of croup and the
need for hospitalisation
If severe: nebulised adrenaline with O2
by facemask
Rare dangerous condition
Staphylococcus aureus
Similar to severe croup
High fever and copious thick secretions
IV abx and intubation and ventilation
if required
Life-threatening emergency
High risk of respiratory obstruction
H. influenza type b
Decrease in incidence after
introduction of Hib vaccine
Intense swelling of the epiglottis
Associated with septicaemia
Often very acute onset:
high fever in an ill child
painful throat - no speaking or swallowing
soft stridor and respiratory difficulty
sat upright, immobile, mouth open
No cough
Intubation under GA
Bloods for culture
Abx (cefuroxime)
In children - acute
Inflammation of the bronchi
Wheeze and coarse crackles
Cough and fever
Whooping cough (pertussis)
Highly contagious - Bordatella Pertussis
First - coryza
Second - characteristic paroxysmal or spasmodic cough followed by inspiratory whoop
Worse at night
May result in vomit
Infants who have not completed their primary vaccination at 4 months are particularly susceptible
Marked lymphocytosis on blood count
In infants whoop is uncommon
Cough is followed by apnoea (potentially dangerous)
Commonest serious respiratory infection of infancy
90% are aged between 1-9 months
80% of cases caused by RSV
Dry cough
Increasing SOB
Difficulty feeding with increasing dyspnoea
Sharp dry cough
Subcostal intercostal recession
Hyperinflation of the chest:
(Prominent sternum + liver displaced downwards)
Fine end-inspiratory crackles
High-pitched wheezes
Cyanosis or pallor
Supportive Mx
Humidified O2 via nasal cannulae
Fluids (NG tube or IV)
Some require CPAP or full ventilation
High-risk preterms - palivizumab
Viruses - younger children
Bacteria - older children
Newborn - Group B Strep, Gram-negative enterococci
Infants/young child - RSV
Child over 5 - Mycoplasma pneumoniae, Strep pneumoniae and chlamydia pneumoniae
All ages - M. tuberculosis
Fever + difficulty breathing
Preceded by URTI
Tachypnoea (KEY)
Nasal flaring
Chest indrawing
Classic signs of consolidation are often absent
Indications for admission include: sats <93%, severe tachypnoea, difficulty breathing, grunting, apnoea, not feeding or family unable to provide appropriate care
Supportive care : O2, analgesia, fluids
Newborn -Broad spectrum abx
Older infants - amox
Complicated - co-amoxiclav
>5 years - amox or eryhromycin
Cystic Fibrosis
Recurrent wheeze associated with allergy to one or more inhaled allergens - 'atopic asthma'
Associated with eczema, rhinoconjunctivitis and food allergy
Symptoms worse at night
Trigger causes symptoms

Symptoms between acute exacerbations
MHx or FHx of atopy
Good response to ashtma Rx
exercise, pets, dust, cold air, emotions..
Long-standing: hyperinflation, polyphonic expiratory wheeze and prolonged expiration
Response to Rx is useful investigation
PEFR should increase by 10-15% after bronchodilator
SA-B2 agonists - salbutamol, terbutaline
Rapid onset, lasts for 2-4h
LA-B2 agonists - salmeterol, formoterol
Effective for 12h, not prescribed without inhaled steroid, useful in exercise-induce asthma
Ipratropium bromide - anticholinergic
Inhaled corticosteroids - prophylactic therapy
Used in conjunction with LABA
SE in high doses: impaired growth, adrenal supression and altered bone metabolism
Oral prednisolone on alternative days if other Rx fails
Leukotriene receptor antagonist - Montelukast
Anti Ig-E therapy (omalizumab)
Acute Asthma
Rx already given
Course of previous attacks
Wheeze and tachypnoea
>50 in children 2-5
>30 in children >5
Increasing tachycardia***
>130 bpm children 2-5
>120 bpm children >5
(not a good guide to severity)
Accessory muscles and chest recession
Late signs: cyanosis, fatigue and drowsiness + silent chest = life-threatening asthma
O2 sats <92% =severe or life-threatening
Moderate: SABA via spacer up to 10 puffs; consider oral pred: reassess within 1 h
Severe: O2; SABA via spacer or nebulised;
Oral pred or IV hydrocortisone; Ipratropium nebs if poor response; repeat bronchodilators every 20-30 mins
Life-threatening: O2, SABA + Ipratropium nebs; IV hydrocortisone; PICU or paediatrician, repeat bronchodilators every 20-30 min
Not responding
Transfer to HDU or PICU
CXR and blood gas
IV salbutamol or aminophyline
Bolus IV Mg sulphate
Chronic Lung Infection
Persistent 'wet' (productive) cough
Primary ciliary dyskinesia
Chronic aspiration
1:2500 live births
1:25 carriers
Cystic fibrosis transmembrane conductance regulator (CFTR)
Cl channel
Autosomal recessive chromosome 7
Retention of mucopurulent secretions
Chronic endobronchial infection with Pseudomonas aeruginosa
10-20 % have meconium ileus (bilious vomiting in newborn)
Pancreatic enzyme deficiency and malabsorption
High [Cl] and [Na] in sweat
Initial infection with Staph aureus and H. influenza
Then with pseudomonas or burkholderia species
Bronchietasis and abscess formation
Persistent, loose cough, productive of purulent sputum
Hyperinflation of the chest, coarse inspiratory crepitations and/or a wheeze
Finger clubbing
Clinical Features
Pancreatic exocrine insufficiency
maldigestion and malabsorption
Untreated : FTT and steatorrhoea
Dx: Sweat Test - High chloride
Genetic testing
Regular lung function test by spirometry
FEV1 expressed as a % predicted for age, sex and height, is an indicator of clinical severity and declines with disease progression
Twice a day physiotherapy
Airway clearance with chest percussion and postural drainage
Prophylactic abx (flucloxacillin) + rescue abx if symptoms arise.
Persistent sympotms - IV abx for 14 days
Nebulised DNAse or hypertonic saline - decrease viscosity of sputum and reduce exacerbations
Oral enteric-coated pancreatic replacement therapy taken with all meals and snacks
High calorie diet - 150% of normal
Overnight feeding via gastrostomy tube - more common
Fat soluble vitamin supplements
Teenagers and Adults
Develop diabetes mellitus
Liver disease : hepatomegaly and abnormal LFTs
Ursodeoxycholic acid - improves bile flow
Distal Intestinal Obstruction Syndrome (Meconium ileus equivalent)
Pneumothorax and haemoptysis
Bronchodilators and corticosteroids
May be associated with infection outside GI tract, urinary tract of CNS
Projectile at 2-7 weeks - pyloric stenosis
Bile stained - obstruction e.g. intussusception, malrotation and strangulated inguinal hernia
Very common in infancy
Nearly all symptomatic reflux resolves spontaneously by 12 months
Severe reflux is common in children with cerebral palsy or other neurodevelopmental disorders; preterm infants or after surgery for oesophageal atresia diaphragmatic hernia
Complications: FTT, oesophagitis, recurrent aspiration (pneumonia).
Add inert thickening agents to feeds + positioning in a 30 degree head-up prone position after feeds
Significant disease: ranitidine, omeprazole
No response to medical Rx - Surgery (fundoplication)
Pyloric Stenosis
Gastric outlet obstruction
Presents between 2-7 weeks
M:F 4:1
Maternal FHx
Vomiting which increases in frequency and forcefulness, ultimately becoming projectile
Dehydration leads to loss of interest in feeding
Weight loss if delayed presentation
Hypochloraemic metabolic alkalosis with hyponatraemia and hypokalaemia
Test Feed
Correct fluid and electrolyte disturbance with IV fluids
(0.45% saline and 5% dextrose with potassium supplements)
Visible gastric peristalsis
Palpable abdominal olive shaped mass
Baby's response to hunger and discomfort
'Always crying' - potential or actual non-accidental injury
Infant 'colic'
Paroxysmal, inconsolable crying or screaming often accompanied by drawing up of the knees and passage of excessive flatus several times a day, particularly in the evening
40% of babies
Resolves by 4 months
Can be due to GORD or cow's milk protein allergy
Acute abdominal pain
Acute appendicitis
Commonest surgical abdomen in children
Very uncommon in <3 year olds
Anorexia, vomiting
Abdominal pain, initially central and colicky but then localising to the RIF - agravated by movement
Flushed face, oral fetor
Low grade fever (37.2-38º C)
Persistent tenderness in RIF (McBurney's point)
1/3 of the distance between the ASIS and the umbilicus
Review every few hours - progressive condition
US may support the clinical diagnosis
Complicated appendicitis: appendix mass, an abscess or perforation
With perforation (generalised guarding) IV fluids and IV abx are given before laparotomy
NSAP & Mesenteric adenitis
Resolves in 24-48h
Less severe pain than in appencitis
Variable RIF tenderness
Accompanied by URTI with cervical lymphadenopathy
Definite diagnosis is made if large mesenteric nodes are seen at laparotomy or laparoscopy
Invagination of proximal bowel into a distal segment
Commonly involves the ileum passing into the caecum through the ileocaecal valve
Commonest cause of intestinal obstruction after the neonatal period
Peak age between 3 months - 2 years
Serious complications: stretching and constriction of the mesentery - venous obstruction, engorgement and bleeding from the bowel mucosa, fluid loss - perforation, peritonitis and gut necrosis.
Paroxysmal severe colicky pain and pallor
Draws up legs during painful episodes
Feed refusal + vomiting (maybe bile stained)
Sausage-shaped abdominal mass
***Redcurrant jelly stool (blood stained mucus)***
Abdominal distension and shock
Fluid resuscitation and AXR
If no peritonitis - rectal air insufflation (radiologist)
75% success, 25% surgical reduction, 5% recur...
Meckel diverticulum
2% of individuals have one
Contains ectopic gastric mucosa or pancreatic tissue
If symptomatic - several rectal bleeding - neither bright red nor true melaena
Can present as intussusception, volvulus around a band or diverticulitis which mimics appendicitis.
Rx: Surgical resection
Can present as:
Obstruction with a compromised blood supply
Common presentation in the first few days of life with obstruction with bilious vomiting
Child with dark green vomit - contrast study
Signs of vascular compromise - urgent laparotomy
Plus: abdominal pain and tenderness from peritonitis or ischaemic bowel
10% of children under 5 yo present with gastroenteritis
60% caused by rotavirus in children <2 yo
Campylobacter jejuni is the commonest baterial cause - severe abdominal pain
Shigella and salmonella - blood and pus in the stool, pain and tenesmus
Loose or watery diarrhoea and vomiting
Contact with someone with diarrhoea or travel abroad
Can cause dehydration - shock
At risk:
Under 6 months or with low birthweight
6 or more diarrhoeal stools in 24h
Vomited 3 or more times in 24h
Not taken fluids
Children with malnutrition
Weight loss is useful but hard to assess
Degree of dehydration:
No clinical signs (<5% of loss of body weight)
Clinical dehydration (5-10%)
Shock (>10%)
Isonatraemic and hyponatraemic dehydration
Equal loss of water and sodium
If children drink a lot of hypotonic solutions - decrease in plasma sodium - water moves from extra to intracellular space - raised brain volume - convulsions + greater degree of shock --- common in developing countries.
Hypernatraemic dehydration
Water moves from intra to extracellular space
Signs of ECS fluid loss are clinically less obvious (esp. in obese children)
Cerebral shrinkage - jittery movements, increased muscle tone with hyperreflexia, altered consciousness, seizures and multiple, small cerebral haemorrhages.
In hypernatraemic dehydration fluid replacement should be done over 48h to prevent cerebral oedema (rate of <0.5 mmol/L per h)
No place for anti-diarrhoeals or antiemetics!!!
Abx only indicated in:
suspected or confirmed sepsis
extra-intestinal spread of bacterial infection
salmonella if <6 months
malnourish or immunocompromised
5% dehydrated - 50ml/kg
10% dehydrated - 100ml/kg
+ maintenance fluids
Abnormal stools
FTT or poor growth in most but not all cases
Specific nutrient deficiencies
Stool - difficult to flush and smelly
Acrodermatitis enteropathica - Zinf deficiency
Coeliac disease
Gliadin fraction of gluten provokes a damaging immunological response in the proximal small intestine
Results in flat mucosa
1:3000 in Europe (classical coeliac)
Classic presentation:
8-24 months after introduction of wheat-containing foods
Abdominal distension
Buttock wasting abnormal stools
General irritability
(Uncommon presentation now - present later in childhood)
Screened in children at risk: type 1 DM, autoimmune thyroid disease and Down syndrome
Diagnosis: small intestine (jejunal) biopsy ***
Removal of all products containing wheat, rye and barley from diet
Incidence of small bowel malignancy is increased in coeliac disease - gluten free diet probably reduces the risk
Inflammatory bowel disease
Incidence has increased in the last two decades
IBD results from environmental triggers in a genetically predisposed individual
Crohn's disease
Ulcerative colitis
Classical presentation: abdominal pain, diarrhoea and weight loss
Can be mistaken for psychological problems or anorexia nervosa
Growth failure, puberty delayed
General ill health (fever, lethargy, WL)
Extra-intestinal: oral lesions or perianal skin tags, uveitis, arthralgia and erythema nodosum
High ESR, CRP, platelets; iron deficiency anaemia and low serum albumin may help diagnose
Transmural disease - commonly affects distal ileum and the proximal colon
Inflamed thickened bowel - strictures and fistulae
Diagnosis: endoscopy and histology
Nutrional therapy - whole protein modular feeds for 6-8 weeks
effective in 75% of cases
systemic steroids required if ineffective
Relapse is common - immunosuppressant medication (azathioprine, mercaptopurine or methotrexate)
Anti-TNF agents (infliximab and adalimumab) if conventional treatment fails
Surgery is need for complications of Crohn's - obstruction, fistulae, abscess formation or severe localised diseased
Presents with rectal bleeding, diarrhoea and colicky pain
Can also include weight loss and growth failure
Extra-intestinal: erythema nodosum and arthritis
Diagnosis: endoscopy and histology
90% of children have pancolitis (in contrast with adults where the distal colon is usually affected
Mild disease - aminosalicylates (balsalazide and mesalazine)
Aggressive and extensive disease - systemic steroids for acute exacerbations and immunomodulatory therapy (azothioprine) to maintaing remission alone or with combination with low dose steroid
Severe fulminating disease - IV fluids and steroids
If this fails - ciclosporin
Increased incidence of adenocarcinoma of the colon in adults (1:200 risk for each year of disease between 10 and 20 years)
Colectomy with an ileostomy or ileorectal pouch
Infrequent passage of dry, hardened faeces often accompanied by straining or pain
In long-standing cases, can lead to overflow incontinence - soiling
Polyethylene glycol and electrolytes (Movicol paediatric plain)
Or stimulant laxative senna or sodium picosulphate
Polyethylene glycol with or without stimulant
Maintenance treatment:
Hirschsprung disease
Absence of ganglion cells from the myenteric and submucosal plexuses of part of the large bowel (rectum and part of colon)
Narrow, contracted bowel segment
75% - confined to rectosigmoid
10% - entire colon
Presents in neonatal period with intestinal obstruction
failure to pass meconium in first 24h
Abdominal distension and bile stained vomit
Later childhood - presents with chronic constipation, abdominal distension but no soiling
Diagnosis: suction rectal biopsy
Initial colostomy followed by anastomosing normally innervated bowel to the anus
Congenital Abnormalities
1:200-400 births
Antenatal US screening
Absence of both kidneys (renal agenesis)
Severe oligohydramnios, fatal
Multicystic dysplastic kidney (MCDK)
Kidney replaced by fluid-filled cysts + ureteric atresia
Potter syndrome
Potter syndrome if bilateral
*Potter Syndrome*
Compression of fetus from oligohydramnios
Caused by lack of fetal urine
Characteristic facies, lung hypoplasia, postural deformities
Autosomal recessive and autosomal dominant polycystic kidney disease
Bilateral cysts, some preserved function
Horseshoe kidney
Lower poles fused
Predisposed to infection or obstruction
Pelviureteric junction - unilateral hydronephrosis
Vesicoureteric junction - unilateral
Posterior urethra (valve) - bilateral
Postnatal prophylactic abx
Surgery if required
Urinary tract infection
Up to 1/2 of patients have a structural abnormality
Infection can damage the growing kidney predisposing to HTN and chronic renal failure
Infants - nonspecific symptoms
Fever (not always)
Septicaemia (can develop rapidly)
Symptoms of dysuria, frequency and loin pain become more common with increasing age
Urine microscopy and culture should be done
Dipstick testing
Nitrites - positive indicates high likelihood of UTI
Leucocytes - maybe positive or negative (unspecific - +ve in febrile ilness, balanitis and vulvovaginitis)
Test urine in all infants with unexplained fever >38
E. coli (most common)
Klebsiella Proteus
Vesicoureteric reflux presdisposes to UTI
Can result in reflux nephropathy
Atypical UTI:
Seriously ill or septicaemia
Poor urine flow
Raised creatinine
Infection with non E. coli
MCUG - Micturating Cystourethrogram
Infants <3 months - hospital and IV cefotaxime

Infants >3 months & actue pyeolonephritis/upper UTI - oral co-amoxiclav or IV cefotaxime for 2-4d and oral co-amoxiclav for 7-10d

Cystitis or lower UTI - oral abx for 3 days
(Nephrotic Syndrome)

If persistent, should be quantified by measuring the urine protein/creatinine ratio in an early morning sample (<20mg of protein/mmol of creatinine
In nephrotic symdrome - heavy proteinuria results in low plasma albumin and oedema
Unknown cause
Can be secondary to Henoch-Schonlein purpura and SLE, infections (malaria) or allergens
Clinical signs
Periorbital oedema (earliest sign)
Scrotal or vulval, leg and ankle oedema
Breathlessness due to pleural effusions and abdominal distension
Steroid sensitive NS
85-90% of children get better with corticosteroids
No progression to renal failure
Boys>girls; Asian>Caucasians
Often precipitated by respiratory infections
Features of SSNS
Age 1-10
No macroscopic haematuria
Normal BP, renal function, complement levels
Steroid therapy
4 weeks of oral 60mg/m2 of prednisolone
4 weeks of oral 40mg/m2 of pred on alternate days
Renal biopsy - usually minimal change disease
Hypovolaemia - depletion of intravascular space, abdominal pain and feeling faint - low urine sodium and high haematocrit - give IV albumin to prevent thrombosis and shock (be careful with colloid and diuretics)
Thrombosis - urinary loss of antithrombin, hypercoagulable state, exacerbated by steroid therapy and raised blood viscocity. Affects brain, limbs and splanchnic circulation
Infection - children in relapse are at risk of infection with pneumococcus - SBP can happen
SSNS patients
1/3 resolve directly
1/3 infrequent relapses
1/3 frequent relapses - steroid dependent
Steroid sparing agents
levamisole, cyclophosphamide, tacrolimus and mycophenilate mofetil
Steroid resistant NS
Refer to paediatric nephrologist
Management of oedema: diuretics, salt restriction, ACE inhibitors and sometimes NSAIDs
Focal segmental glomerulosclerosis - most common
Mesangiocapillary glomerulonephritis - common in older kids
Membranous nephropathy - Hep B, may precede SLE
Glomerular Haematuria: brown urine, deformed RBCs and casts. Accompanied with proteinuria
Lower urinary tract haematuria: red urine, not accompanied by proteinuria, unsual in children
UTI is the most common cause
Biopsy if:
significant persistent proteinuria
recurrent macroscopic haematuria
abnormal renal function
C levels persistently abnormal
Acute nephritis
low urine output and volume overload
hypertension (can cause seizures)
oedema, especially around the eyes
haematuria and proteinuria
Post-streptococcal nephritis
Follows streptococcal sore throat or skin infection
Common in developing countries, has become uncommon in developed ones
Good long term prognosis
Henoch-Schonlein Purpura
Type of vasculitis
characteristic skin rash - 1st clinical sign
arthralgia - joint pain, 2/3 of patients
periarticular oedema
abdominal pain - colicky
glomerulonephritis - common,
2:1 (Boys:girls)
3-10 year of age
Peaks in the winter months and often preceded by URTI
Children often present with fever and maculopapular purpuric rash (most obvious feature)
Symmetrical rash, over buttocks, extensor surfaces of limbs and over the ankles
IgA nephropathy
Macroscopic haematuria
Association with URTI
Familial nephritis
Alport Syndrome
X-linked recessive
Systemic Lupus Erythematosus
Adolescent girls and young women
Asians=Afro-Caribbeans >> Caucasians
dsDNA antibodies
Haematuria and proteinuria are indications for renal biopsy
Management: fluid and electrolyte balance, diuretics, monitor renal function
Acute kidney injury
Sudden, potentially reversible, reduction in renal function
Oliguria is usually present (< 0.5 ml/kg per h)
commonest cause in children
suggested by hypovolaemia
correction of hypovolaemia with fluid replacement
avoid acute tubular necrosis
Salt and water retention
Urine: blood, protein and casts
If fluid overloaded
Restrict fluids
Diuretic challenge
=may improve urine output
Commonest causes in children: Haemolytic uraemic syndrome and acute tubular necrosis
Acute tubular necrosis
Happens in multisystem failure in the intensive care unit
Correct metabolic abnormalities
metabolic acidosis - sodium bicarbonate
hyperphosphataemia - calcium carbonate, dietary restriction
hyperkalaemia - calcium gluconate (if ECG changes), salbutamol (nebs or IV), calcium exchange resin, glucose and insulin, dietary restriction and dialysis
Urinary obstruction
Assessment of the site of obstruction
Relief by nephrostomy or bladder catheterisation
Surgery after fluid and electrolyte abnormalities have been corrected
Dialysis indicated if
failure of conservative management
severe hypo- or hypernatraemia
pulmonary oedema or hypertension
severe acidosis
mulisystem failure
Haemolytic uraemic syndrome
Triad of:
1) acute renal failure
2) microangiopathic haemolytic anaemia
3) thrombocytopaenia
Typically secondary to GI infection with verocytotoxin producing E. coli or less often shigella
Supportive therapy including dialysis - good prognosis
Follow-up to check for persistent proteinuria, development of hypertension and declining renal function
Chronic Kidney Disease
Less common in children than in adults
Congenital and familial causes >> Acquired causes
Structural malformations
Presents with:
Anorexia and lethargia
Polydipsia and polyuria
Bony deformities from renal dystrophy
Acute-on-chronic renal failure (infection or dehydration)
Incidental proteinuria
Unexplained normochromic normocytic anaemia
Calorie supplements and nasogastric or gastrostomy feeding
Renal dystrophy - phosphate restriction (milk products), calcium carbonate and activated vitamin D
Salt supplements and free access to water
Bicarbonate - prevent acidosis
Dialysis and Renal Transplant
Erythropoietin and growth hormone
Musculoskeletal disorders
Abnormal posture
Developmental dysplasia of the hip
Ranges from dysplasia to subluxation through dislocation
Screening is done as part of routine examination of the newborn
Check if hip can be dislocated posteriorly and relocated on abduction
Presents with a limp or abnormal gait
6-10 per 1000 live births
Increased risk - family history, breech presentation
Lateral curvature in the frontal plane of the spine
Idiopathic - most common, often in girls during pubertal growth spurt (10-14 years)
Congenital - hemivertebra, spina bifida
Secondary - related to cerebral palsy, muscular dystrophy, Marfan's syndrome
Acute-onset limb pain
Infection of metaphysis of long bones
Distal femur and proximal tibia
Staphylococcus aureus
Markedly painful, immobile limb in a child with acute febrile illness
Affected site: swollen, very tender and may be red and warm
Pain on movement
WCC and acute-phase reactants are raised
X-rays - 7-10 days to show subperiosteal new bone formation and localised bone rarefaction
Several weeks - IV antiobiotics
Aspiration or surgical decompression - atypical presentation or immunodeficiency
Malignant disease
Acute lymphoblastic leukaemia (ALL) may present with bone pain and arthritis
Bone tumours
Osteogenic sarcoma
Ewing tumour
Pain, swelling and a pathological fracture
Osteoid osteoma - benign
adolescent boys
femur, tibia or spine
Transient synovitis "irritable hip"
Perthes disease
Slipped capital femoral epiphysis
Most common cause of acute hip pain
2-12 years old
Follows or accompanied by a viral infection
No pain at rest
decreased range of movement
May be difficult to distinguish between transient synovitis and ealy septic arthritis
Bed rest
Avascular necrosis of the capital femoral epiphysis of the femoral head
M:F = 5:1
Age 5-10 years old
Knee or hip pain
Bilateral in 10-20%
Early, <1/2 the femoral head affected:
Bed rest and traction
Late, severe disease:
Maintain hip in abduction with plaster or calipers
Femoral or pelvic osteotomy
Good prognosis esp <6 years old
Older children - deformity of femoral head and metaphyseal damage
Potential for subsequent degenerative arthritis
Displacement of epiphysis of the femoral head postero-inferiorly
Requires prompt treatment to prevent avascular necrosis
Common at 10-15 years of age during adolescent growth spurt
Obese boys
Bilateral in 20%
Associated with hypothyroidism and hypogonadism
Presents with:
limp or hip pain
can be referred to the knee
Examination - restricted abduction and internal rotation of the hip
X-ray is diagnostic
Surgical management - pin fixation in situ
Pain, swelling, heat, redness and restricted movement in a joint
Acute monoarthritis - unwell, fever
Reactive arthritis
Most common form in childhood
Transient joint swelling (<6 weeks)
Often ankles and knees
Enteric bacteria (salmonella, shigella, campylobacter and yersinia) are often the cause
Others: STIs, mycoplasma
Low-grade fever
Acute-phase reactants are normal or midly elevated
X-ray is normal
No treatment or NSAIDs
Septic arthritis
Serious infection of the joint space
Can lead to bone destruction
Most common <2 years old
Usually only one joint is affected
Haematogenous spread (or puncture wound)
Beyond neonatal period - Staphylococcus aureus
Predisposing illnesses - immunodeficiency or sickle cell disease
Erythematous, warm, acutely tender joint with a reduced range of movement in an acutely unwell, febrile child
Septic arthritis of the hip
Tenderness of head of femur
Leg held flexed, abducted, externally rotated
No spontaneous movement (pseudoparalysis)
High wcc and acute-phase reactants
X-rays - initially normal with widening of joint space and soft tissue swelling
IV antibiotics
Juvenile idiopathic arthritis
Defined as persistent join swelling (of >6 weeks) before 16 years in the absence of infection or any other defined cause
Polyarthritis >4 joints
Oligoarthritis ≤4 joints
Systemic - fever and rash
Gelling (stiffness after periods of rest)
Morning joint stiffness and pain
Or intermittent limp
If chronic - thickening of the synovium and swelling of the periarticular soft tissues
Chronic anterior uveitis
Flexion contractures of the joints
Growth failure
Induce remission as soon as possible
NSAIDs and analgesics - relieves symptoms during flares
Joint injections (US guidance) - esp in oligoarticular JIA
Methotrexate - early use reduced joint damage, effective in 70% with polyarthritis. Weekly dose - blood monitoring for abnormal LFTs and bone-marrow suppression. Nausea is common
Systemic corticosteroids - avoided if possible, to minimise risk of growth suppression and osteoporosis; pulsed IV for severe polyarthritis. Life saving for severe systemic arthritis
Cytokine modulators and other immunotherapies - anti-TNF, IL-1, CTLA-4 or IL-6
Down's syndrome
Incidence without ante-natal screening 1:650
flat occiput
single palmar crease
incurved 5th finger
wide sandal gap
Clinical features
30 - 40% have a congenital heart defect (AVSD)
Increased risk of
impairment of vision and hearing
atlanto-axial instability
Other anomalies: Hirschsprung disease, duodenal atresia
Late medical problems
Delayed motor milestones
Moderate to severe learning difficulties
Small stature
Hearing impairment from secretory otitis media
Visual impairment from cataracts, squints, myopia
Increased risk of leukaemia and solid tumours
Increased risk of hypothyroidism and coeliac disease
Alzheimer's disease
Meiotic non-disjuction (94%)
Translocation (5%)
Mosaicism (1%)
Edwards and Patau syndrome
Most affected babies die in infancy
Trisomy 21
Recurrence risk is low
Edwards - trisomy 18
Patau - trisomy 13
Edwards - clinical features
Low birthweight
Prominent occiput
Small mouth and chin
Short sternum
Flexed overlapping fingers
Rocker-bottom feet
Cardiac and renal malformations
Patau - clincal features
Structural defect of brain
Scalp defects
Small eyes (microphthalmia and other eye defects)
Cleft lip and palate
Cardiac and renal malformations
Turner syndrome
45, XO
95% results in early miscarriage
Detected antenatally by US when a fetal oedema of the neck, hands and feet or a cystic hygroma is identified
Short stature may be the only clinical abnormality in children
Clinical Features
Spoon-shaped nails
Short stature **
Neck webbing
Cubitus valgus
Widely spaced nipples
Coarctation of the aorta
Delayed puberty
Ovarian dysgenesis (infertility)
Renal anomalies
Recurrent otitis media
Normal intellectual function
Growth hormone therapy
Oestrogen replacement for development of secondary sexual characteristics
Klinefelter syndrome
47, XXY
Recurrence risk is low
Clinical Features
Infertility - most common presentation
Hypogonadism with small testes
Pubertal development may be normal
Gynaecomastia in adolescence
Tall stature
Intelligence in the normal range, some have educational and psychological problems
Noonan syndrome
Williams syndrome
Autosomal dominant congenital disorder
M:F 1:1
Clinical Features
Occasional mild learning diffuclties
Short webbed neck with trident hair line
Pectus excavatum
Short stature
Pulmonary stenosis
Flat nasal bridge
Widely set eyes
Low set ears
Deletion chromosome 7
Clinical features
Short stature
Elfin facial features
Cheerful demeanor
Transient neonatal hypercalcaemia
Supravalvular aortic stenosis
Mild to moderate learning diffuclties
Prader-Willi syndrome
Deletion in chromosome 15
Facial features
Narrow temples
Elongated face
Thin upper lip
Prominent nose
Clinical Features
Neonatal feeding difficulties
FTT in infancy
Obesity later in childhood
Developmental delay
Learning difficulties
Perinatal medicine
Glucocorticoid therapy
before preterm delivery
accelerates lung maturity and surfactant production
Decreases the incidence of respiratory distress syndrome, of intraventricular haemorrhage and neonatal mortality
Digoxin and flecanide - to mother to treat fetal supraventricular tachycardia
Rhesus isoimmunisation
Anaemia in the fetus causes hydrops fetalis with oedema and ascites; Doppler velocimetry of the fetal MCA detects anaemia; Fetal blood transfusion through the umbilical vein from 20w gestation may be needed
Anti-D lowered the incidence of rhesus haemolytic disease
Perinatal isoimmune thrombocytopenia
Like rhesus isoimmunisation
Anti-platelet antibodies cause thrombocytopenia
Intracranial haemorrhage in 25%
Prenatal IV Ig or fetal platelet transfusions
Fetal Surgery
Catheter shunts (pleuro-amniotic shunts) under US guidance - pleural effusions - chylothorax or cystic adenomatous malformation of the lung
Laser therapy to ablate placental anastomsoses - twin-twin transfusion syndrome
Shunting for obstruction to urinary outflow as with posterior urethral valves
Dilatation of stenotic heart valves
Congenital infections
Serological diagnosis
Before 8 weeks - deafness, congenital heart disease and cataracts in 80%
13-16 weeks - 30% get impaired hearing
Beyond 18 weeks - minimal risk to the fetus
Extremely rare because of MMR vaccination
Most common congenital infection
3-4/1000 live births
Of infected infants:
90% - normal
5% - hepatosplenomegaly and petechiae at birth and most will develop sensorineural hearing loss, cerebral palsy, epilepsy and cognitive impairment
5% - develop problems later in life - sensorineural hearing loss
RCTs with ganciclovir
No screening for CMV
No or unspecific symptoms in the mother
Infection with Toxoplasma gondii, protozoan parasite
Source: raw or uncooked meat or contact with the faeces of recently infected cats
0.1:1000 live births
Most infected infants are asymptomatic - still at risk of developing chorioretinitis in adulthood
In 10% - Clinical manifestations
Retinopathy, an acute chorioretinitis - sometimes interferes with vision
Cerebral calcification
Long-term neurological disabilities
1 year of pyrimethamine and sulfadiazine
Varicella zoster
Usually the fetus is unafected
in the first 1/2 of pregnancy (20 weeks); <2% risk of developing scarring of the skin and possibly ocular and neurological damage and digital dysplasia
within 5 days before or 2 days after delivery (unprotected by maternal antibodies); 25% develop vesicular rash; mortality is as high as 30%
Exposed susceptible mothers - protected with varicella Ig and treated with aciclovir
Infants born in high risk period -VZ Ig and aciclovir prophylaxis
Rash on soles of the feet and hands
If mothers treated 1 month before delivery - infant has good prognosis and doesn't require treatment
In doubt -penicillin
Bone lesions
Neonatal medicine
Hypoxic-ischaemic encephalopathy
Perinatal asphyxia - compromised or ceased gas exchange - cardiorespiratory depression
Result: hypoxia, hypercarbia, metabolic acidosis
Low cardiac output - poor tissue perfusion = hypoxic-ischemic injury to the brain
Failure of gas exchange across placenta - excessive or prolonged contractions, abruption, ruptured uterus
Interruption of umbilical blood flow - cord compression including dystocia, cord prolapse
Inadequate maternal placental perfusion, maternal hypotension or hypertension - often with IUGR
Compromised fetus - anaemia, IUGR
Failure of cardiorespiratory adaptation at birth - failure to breathe
Clinical manifestations start immediately or up to 48h after asphyxia
Mild - irritability, excessive response to stimuli, staring of the eyes, hyperventilation and impaired feeding
Moderate - marked abnormalities of tone and movement, cannot feed, may have seizures
Severe - no spontaneous movements or response to pain, fluctuate between hypotonia and hypertonia, prolonged seizures that don't respond to treatment, muti-organ failure
Respiratory support
Amplitude-integrated EEG - confirm encephalopathy and identify seizures
Anticonvulsants - clinical seizures
Fluid restriction - transient renal impairment
Treat hypotension - volume and ionotrope support
Monitoring and treatment of hypoglycaemia and electrolyte imbalance, esp hypocalcaemia
RCTs - mild hypothermia (33-34 C) reduces brain damage if started within 6 h of birth
Birth injuries
Soft tissue
Caput succedaneum - brusing and oedema of presenting part, above aponeurosis, resolves in a few days
Cephalohaematoma - haematoma below the periosteum, confined to the margins of the skull sutures; usually involved the parietal bone - resolves over several weeks
Chignon - oedema and brusing from ventouse delivery
Forceps marks to the face - transient
Nerve palsies
Breech deliveries or with shoulder dystocia
Erb palsy - upper nerve root, C5 and C6
Most recover by 2 years
Face palsy - compression of facial nerve against ischial spine - methicellulose drops to the eye
Clavicle - shoulder dystocia
Humerus/femur - shaft, from breech presentation or shoulder dystocia
The preterm infant
Respiratory distress syndrome
Deficiency of surfactant
Widespread alveolar colapse - inadequate gas exchange
Glucocorticoids are given if preterm delivery is anticipated
Surfactant therapy - from calf or pig lung, directly via trachea tube - reduce 40% mortality
Clinical signs
tachypnoea >60 breahts/min
laboured breathing with chest wall recession (sternal and subcostal indrawing) and nasal flaring
expiratory grunting
cyanosis if severe
X-ray - ground glass, air bronchogram
Happens in RDS
In up to 10% of infants ventilated for RDS - air leaks into the pleural cavity and causes a pneumothorax
Transillumination with a bright fibreoptic light source applied to the chest wall
Infants are ventilated with lower pressures - prevents pneumothoraces
Necrotising enterocolitis
Preterm infants - first few weeks of life
Bacterial invasion of ischaemic bowel wall
Fed with cow's milk formula - more likely to develop than just fed with breast milk
Stops tolerating feeds; there may be vomiting (sometimes bile-stained)
Abdominal distension and sometimes fresh blood in the stools
May become shocked - requiring artificial ventilation
Distended bowel loops
Thickening of bowel wall with intramural gas
Gas in the portal tract
Air under the diaphragm (bowel perforation)
Perforation - detected by X-ray or transillumination
Treat with surgery
Stop oral feeding - broad spectrum abx (cover both aerobes and anaerobes
Parenteral nutrition - ALWAYS needed
Maybe need artificial ventilation and circulatory support
20% Mortality!!!
Retinopathy (of prematurity)
Affects the developing blood vessels at the junction of the vascular and non-vascularised retina
Vascular proliferation - retinal detachment, fibrosis and blindness
35% of all VLBW infants
1% of VLBW - severe bilateral visual impairment - mostly in infants of <28 weeks
Bronchopulmonary dysplasia
Definition - infants who still require O2 therapy at post menstrual age of 36 weeks
Damage to the lungs comes from volume trauma - artificial ventilation, oxygen toxicity and infection
CXR - widespread areas of opacification(+/- cystic changes)
Short courses of steroids - some value
Most are weaned onto CPAP followed by addition ambient oxygen
Complications - infection (pertussis, rsv) and pulmonary hypertension - may lead to death
50% of newborns
High Hb concentration at birth - more breakdown
RBC life span - 70 days (Not 120)
Hepatic bilirubin metabolism - less efficient
<24h of Age
2 days to 2 weeks of Age
>2 weeks of Age
Encephalopathy - deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei
Effects - transient disturbance to severe damage and death
Acutely - lethargy and poor feeding
If severe - irritability, increased muscle tone (lies with arched back), seizures and coma
Sequelae - cerebral palsy, learning difficulties and sensorineural deafness
Introduction of anti-D Ig significantly reduced number of cases - used to happen in rhesus haemolytic disease
[Bilirubin] = 80 umol/L
Usually results from HAEMOLYSIS
Unconjugated bilirubin - can rise rapidly and reach high levels
Rhesus haemolytic disorder
Identified antenatally, monitored and treated
If born affected (RARE) - anaemia, hydrops and hepatosplenomegaly + severe jaundice
Other antigens - Kell and Duffy
ABO incompatibility
More common than RHD
Group O mothers - IgG anti-A-haemolysin
Hb level - normal or slightly low
No hepatosplenomegaly
Peak jaundice - first 12-72 hours
G6PD deficiency
Mediterranean, Middle-East and Far East or in African-Americans
Mainly males
Avoid - fava beans, aspirin, certain antibiotics
Sometimes family history
Spherocytes on blood slides
Physiological jaundice
No underlying cause
Adaptation to the transition from fetal life
Other causes must have been considered
Breast milk jaundice
More common and more prolonged in breast-fed infants
From delay in establishing breast-feeding
Other causes
Jaundice from haemolysis can still present in the first week
Crigler-Najjar syndrome (deficient or absent glucoronyl transferase)
Starts in head and face
All babies to be clinically checked for jaundice at 72h of life
Poor milk intake and dehydration exacerbate jaundice
Blue-green light (450 nm) converts unconjugated bilirubin into water-soluble pigment - excreted mainly in urine
Infant's eye are covered - otherwise uncomfortable
Temperature instability, rash and bronze discolouration
Exchange transfusion
Required if bilirubin is at dangerously high levels
Blood removed from baby is small aliquots (from arterial line or umbilical vein) and replaced with donor blood (via peripheral or umbilical vein)
Twice the infant's blood volume (2 x 80ml/kg) is exchanged
Persistent or prolonged neonatal jaundice
Could be BILIARY ATRESIA - important to diagnose early
Breast milk jaundice
Infection (esp UTI)
Congenital hypothyroidism
may caused prolonged jaundice before features of coarse facies, dry skin, hypotonia and constipation
affects 15% of healthy infants, disappears by 4-5 weeks
needs to be considered
Conjugated bilirubinaemia - dark urine and pale stools; may present with hepatomegaly and weight gain; cause may be neonatal hepatitis and biliary atresia
<48h after birth
Amniotic fluid gets infected with bacteria from birth canal
Fetal lungs in contact with infected amniotic fluid
Pneumonia - septicaemia and bacteraemia
Increased risk with prolonged or premature rupture of membranes
Chorioamnionitis - febrile mother during labour
Presents with: respiratory distress, apnoea and temperature instability
CXR and septic screen
CRP (takes 12-24h to rise)
Benzylpenicillin or amoxicilin
- cover for group B strep, listeria and other Gram +ves
- covers for Gram -ve
If neuro signs - CSF examined and cultured
>48h after birth
Source: infants environment
Source of nosocomially acquired infections
Indwelling central venous catheters
Invasive procedures
Tracheal tubes
Most common - staph epidermidis
Gram +ve - staph aureus
Gram -ve - e coli, pseudomonas, klebsiella
1st Line: Flucloxacillin and gentamicin - staphs and gram -ves
Vancomycin and/or meropenem
Neonatal meningitis - uncommon, but 20-50% mortality
Late signs- bulging fontanelle and hyperextension of neck and back
If likely - ampicillin or penicillin and cefotaxime
Group B Strep
10-30% of pregnant women have faecal or vaginal carriage
Causes early and late-onset sepsis
Early-onset - most have pneumonia; may also cause septicaemia and meningitis
If positive blood or CSF cultures - mortality is up to 10%
Late-onset - up to 3 months of age
Usually presents with meningitis or occasionally with focal infection (osteomyelitis or septic arthritis)
(preterm, pronlonged rupture of membranes, maternal fever during labour >38, maternal chorioamnionitis and previously infected infant)
Intrapartum anitbiotics given to mother with risk-factors
Listeria monocytogenes
Uncommon, but serious
Transmitted to mother in unpasteurised milk, soft cheeses and undercooked poultry
Passage to the feus is via the placenta
Features: meconium stained liquor, widespread rash, septicaemia, pneumonia and meningitis
Mortality - 30%
Sticky eyes - common - 3rd or 4th day of life
Clean with saline or water
Troublesome discharge and redness - staph or strep infection - neomycin ointment
Chlamydia trachomatis - purulent discharge + swelling of the eyelids at 1-2 weeks of age; organism identified with immunofluorescent staining
Oral erythromycin for 2 weeks
Mother and partner need to be checked and treated
Herpes simplex virus
Uncommon (1: 2000-30000)
Transmitted during passage during the birth canal
More common in preterm infants
Presentation - first 4 weeks, with herpetic lesions on the skin or eye, or with encephalitis or disseminated disease
Mortality and morbidity is high with disseminated disease even with aciclovir treatment
If mother has primary disease a C-section is indicated
Liver disease

Rudimentary digits
Limb hypoplasia
Full transcript