Paediatrics 1 Flashcards
Shunt direction for Ventricular Septal Defect
Left to Right
Effects of a moderate VSD
Enlarged atria and ventricles leads to pulmonary HTN and Congestive heart failure
Effects of Severe VSD
Severe pulmonary HTN and early onset heart failure
RF for VSD
Prematurity
Genetic Conditions - Downs, Edwards, Patau
Family Hx
Upper vs Lower RTI’s
Upper - rhintis, otitis media, pharyngitis, tonsilitis, Laryngitis
Lower - Bronchitis, croup, epiglottitis, Tracheitis, bronchiolitis, pneumonia
Clinical presentation of VSD
Often asymptomatic
Pansystolic murmur at lower left sternal border
Poor feeding
Tachypnoea
Dyspnoea
Failure to thrive
Diagnosing VSD
ECHO, ECG, XR
XR finding for VSD
Cardiomegaly
Tx for VSD
Diuretics for pulmonary congestion
ACE-i
Surgical repair
Complications of VSD
Eisenmengers, Endocarditis, Heart Failure
Shunt in ASD
Left to right
RF for ASD
Maternal smoking, FHx of CHD, Maternal diabetes, Maternal Rubella
Clinical Presentation of ASD
Tachypnoea, Poor weight gain, Recurrent Chest infections, Soft systolic ejection murmur in 2nd intercostal space, Wide flexed split S2 sound
Ix for ASD
ECG and Echo
Tx for ASD
Small - conservative, wait and weight it may close
Surgical closure if larger than 1cm
Complications of ASD
Stroke from DVT, AF, Pul Htn, Eisenmengers
Croup summarise
Viral - para flu
Spring/autumn
Self limiting
Worse at night
Barking sound
Stridor
Recession
Steroids help
Most common cyanotic congenital heart disease
Overriding aorta
Large VSD
Pulmonary stenosis
RVH
Epidemiology of ToF
More common in males
Rubella
Increased maternal age
Pathophysiology of ToF
Decreased right ventricular outflow. Dilated and displaced aorta.
Mild - asymptomatic but as heart grows they become cyanotic at 1-3 years
Moderate - Cyanosis and resp distress in first few months
Extreme - seen on antenatal scan, cyanosis quickly
Clinical Presentation of ToF
Irritability, Cyanosis, Clubbing, Poor feeding, Poor weight gain, Ejection systolic murmur in pul region and tet spells
What is a tet spell
Baby suddenly turns bluish and faints
Ix for ToF
CXR - boot shaped heart
MRI,Cardiac catheter
Echo
Tx for ToF
Prostaglandin infusion PGE1 to maintain ductus arteriosus
Beta blockers
Morphine to reduce resp drive
Surgical repair under bypass 3mo-4y but needs ICU
Why do you maintain the ductus arteriosus in ToF
To provide additional pulmonary blood flow to improve oxygen sats
Complications of ToF
Pulmonary regurg, Lifelong follow up
RF for ToF
Downs, Digeorge
What is Transposition of the Great Arteries (TGA)
Aorta rises from the right ventricle and pulmonary artery from the left ventricle
Epidemiology of TGA
More common in males
Maternal age over 40
Rubella
Maternal Diabetes
Alcohol consumption
Pathophysiology of TGA
Deox blood is delivered systemically
Mixing needs to be present to sustain life so a patent foramen ovale, VSD or patent ductus arteriosus must be present
Clinical presentation of TGA
Cyanosis in first 24 hours, Right ventricular heave, Loud S2 heart sound, Systolic murmur if VSD present,
Dx of TGA
Low SATS, ECHO, CXR shows egg on a string due to narrowed mediastinum and cardiomegaly, metabolic acidosis
Tx for TGA
PGE1 to ensure PDA
Surgical repair
What is a PDA
Persistent connection between the aorta and pulmonary artery
Shunt in PDA
Left to right
RF for PDA
Female and premature
Clinical presentation of PDA
Resp distress, Apnoea, Tachypnoea, Tachycardia, Continuous machinery murmur at left sternal edge
Dx of PDA
Echo, ECG/CXR
Tx for PDA
Cardiac catheterisation to close around 1 years old or sooner in more severe cases
Premature - Indomethacin or ibuprofen will inhibit prostaglandin and stimulate closure
What is croup
Acute laryngotracheobronchitis
Epidemiology of croup
Children ages 6mo-3yo
Common in autumn and spring
More common in boys
Pathophysiology of croup
Mucosal inflammation anywhere between nose and trachea
Caused by parainfluenza mainly but also Adenovirus, Rhinovirus, Enterovirus
Clinical features of corup
Mild: Barking cough with no stridor, no recession, child happy to eat or drink
Moderate: Frequent barking cough with audible stridor at rest, suprasternal recession, no agitated
Severe: Frequent barking cough, Prominent stridor, Sternal recession, agitated and distressed potentially tachy
Exam and Hx for Croup
1-4 days of non specific rhinorrhea, fever and barking cough
Worse at night
Stridor
Decreased bilateral air entry
Tachypnoea
Costal recession
Resp failure red flags
Drowsiness, Lethargy, Cyanosis, Tachycardia, Laboured breathing
Dx of Croup
FBC, CRP, U+E, CXR to exclude a foreign body
Tx of Croup
Symptoms from 48 hours-week
Paracetamol or Ibuprofen for sore throat
Admission if moderate/severe and if dehydrated
Single dose of dexamethasone 0.15mg/kg or prednisolone
Nebulised adrenaline for relief of severe symptoms
Oxygen if needed
Monitor for needed ENT intervention if suspected airway blockage
Complications of Croup
Otitis Media, Dehydration due to reduced fluids, Superinfection such as pneumonia
Define Bronchiolitis
Viral infection of the bronchioles
Epidemiology of Bronchiolitis
under 2’s
Common
Winter and spring peak
Caused by RSV
RF for Bronchiolitis
Breastfeeding for less than 2 mo
Smoke
Older siblings who could spread
Chronic lung disease of prematurity
Clinical features of Bronchiolitis
Symptoms onset 2-5 days
Low grade fever
Rhinorrhoea
Cough
Reduced feeding
Signs of resp distress: nasal flaring, tracheal tug, head bobbing, grunting, recession
Inspiratory crackles
Ix for Bronchiolitis
Nasopharyngeal aspirate for RSV culture
FBC, Urine, Blood gas
Home Tx for Bronchiolitis and prevention
Supportive at home
Palvizumab vaccine considered if child under 9 mo with chronic lung or child under 2 with severe immunodeficiency require long term vent
When to admit urgently in bronchiolitis
Apnoea
- Resp Rate > 70
- Central cyanosis
- SpO2 < 92%
When to do a non urgent admission in bronchiolitis
- Resp Rate > 60
- Clinical dehydration
Inpatient management for bronchiolitis
O2
Fluids
CPAP if in resp failure
Suctioning of secretions
Ribavirin for severe
What treatment has no evidence for use in bronchiolitis
Bronchodilation, Abx and steroids
What is Pneumonia
Infection of the LRT and lung parenchyma leading to consolidation
Epidemiology of Pneumonia
Highest incidence in infants
Viral cause more common in younger infants
Bacterial more common in older infants
Viral disease more common in winter
Aetiology of Pneumonia
Neonates: Group B strep, E.coli, Klebsiella, S.Aureus
Infants: Strep pnuem, Chlamydia
School age: Strep pneum, S.Aureus, Group a strep, Mycoplasma pneum
Clinical presentation of Pneumonia
Usually precede a URTI, Fever, SOB, Lethargy, Signs of resp distress, wheeze and hyperinflation when viral
Auscultation: dullness to percuss, crackles, Decreased breathing sounds, Bronchial breathing
Ix for Pneumonia
Clinical mainly
CXR - fluids in lungs
Tx for Pneumonia
Manage at home with analgesia
Admitted: O2 and Iv fluids
Abx:
Neonates: Broad spectrum
Infants: amox/co-amox
Over 5: Amox/Erythromycin
Complications of Pneumonia
Risk of parapneumonic collapse and empyema
Is whooping cough a URTI or LRTI
URTI
Whooping cough causative organsism
Bordatella Pertussis - Gram -ve bacillus
Epidemiology of Whooping Cough
Less common now due to vax
Impacts infants worse
Clinical presentation of Whooping cough
Catarrhal phase: 1-2w with coryzal Sx
Paroxysmal phase: week 3-6, inspiratory whoop
Cough worse at night
Spasmodic coughing episodes
Low grade fever
Sore throat
Convalescent phase - downgrade to cough and can last 3 mo
Dx for Whooping cough
Naso-pharyngeal swab with pertussis
FBC
Antibody test
Tx for Whooping cough
Macrolide
Prophylactic Abx for contacts
Isolate for 21 days after symptom onset or for 5 days after Abx
Complications of Whooping cough
Seizures, Pneumonia, Bronchiectasis, Encephalopathy, Otitis Media
What is Asthma
Reversible paroxysmal contriction of the airways with inflammatory exudate and followed by airway remodelling
Most common chronic condition in children
Aetiology of Asthma
Genetic, Premature, Low birth weight, Smoking, Early viral bronciolitis, Cold air, allergen exposure
Clinical presentation of asthma
Episodic wheeze, dry cough, SOB, Reduced peak flow
Ix for Asthma
- FEV1 significantly reduced
- FVC normal
- FEV1:FVC may be <70% if poorly controlled
- Reversible spirometry is highly suggestive of asthma
- ENO levels of nitric oxide correlate to inflammation
- Baseline chest x ray
Management of Asthma
Step 1: SABA PRN - Salbutamol
Step 2: ICS Preventer therapy - Beclomethasone
Step 3: LTRA Montelukast
Step 4: Strop LTRA if hasn’t helped and add LABA - Salmeterol
Step 5: Switch ICS/LABA for ICS MART: Formoterol and ICS
Step 6: Add a separate LABA
Step 7: High dose ICS (>400mcg), referral
Management of Asthma in under 5
Step 1: SABA PRN - Salbutamol
Step 2: SABA + 8 week trial of ICS if symptoms reoccur within 4 weeks, restart ICS
Step 3: Refer to specialist
What is viral indued wheeze
Episodic wheeze - symptom of viral URTI and symptom free between events
Multiple trigger wheeze - URTI and other factors trigger wheeze
Management of Viral induced wheeze
Symptomatic - Saba with spacer max of 4 hourly up to ten puffs
LTRA and ICS via spacer
Multiple trigger: trial ICS or LTRA for 4-8 weeks
What is Respiratory Distress syndrome
Affects premature neonates, before the lungs start producing adequate surfactant, common in below 32 w babies
Pathophysiology of Resp distress syndrome
Inadequate surfactant leads to high surface tension in alveoli leading to atelectasis as it more difficult for the alveoli to expand so inadequate gas exchange and hypoxia, hypercapnia and resp distress
Management of Resp distress syndrome
Dexamethasone to mothers with suspected preterm labour to increase surfactant production, Intubation and ventilation may be needed to fully assist breathing if distress is severe, Endotracheal surfactant via tube, CPAP, O2
Complications of resp distress syndrome
Short term - Pneumothorax, Infection, Apnoea, Intraventricular haemorrhage, Pul Haemorrhage, Necrotising Enterocolitis
Long term complications of resp distress syndrome
Chronic lung disease of prematurity, Retinopathy of prematurity, Nuerological, hearing, visual impairment
What is Bronchopulmonary dysplasia
Infants who still require oxygen at postnatal age of 36 weeks are described as having BPD
Bronchopulmonary Dysplasia aetiology
lung samage from pressure and vilume trauma of artificial ventilation, oxygen toxicity and infection
CXR - widespread opacification and sometimes cystic changes, fibrosis and even lung collpase
Tx for Bronchopulmonary dysplasia
Weaned onto CPAP followed by additional oxygen where needed and sometimes corticosteroids to facilitate weaning however there is a risk of neurodevelopmental issues with these
What is epiglottitis
inflammation and swelling of the epiglottis caused by infection. Life threatening emergency
Epiglottitis causative organism
Haemophilus influenzae B
Typical presentation of epiglottitis
Drooling, Tripod position, unvaxed, fever, sore throat, difficulty swallowing, muffled voice, scared and quiet child, septic and unwell
Ix for epiglottitis
If acutely unwell and obvious then dont investigate just treat them. Dont scare the child.
Can do a Xr of neck - thumb sign due to swollen epiglottis, can exclude a foreign body
Management of epiglottitis
Alert the most senior paediatrician available and anaesthetics.
Ensure airway is secure, prep for intubation and prep ICU
Tx once airway is secure: IV AbX (Ceftriaxone) and steroids (dexamethasone)
Prognosis for Epiglottitis
Most recover without intubation
Epiglottic abscess - pus around the epiglottis - similar tx to epiglottitis
Briefly summarise Laryngomalacia
Where part of the larynx above the vocals cords is structured in a way that partially blocks the airway
Chronic stridor
Omega shaped epiglottis
In infants peaking at 6 mo. intermittent stridor that is worse during feeding, upset, lying on back and during infection
Usually self resolving. Rarely surgery or a tracheostomy is needed
Define Cystic Fibrosis
Autosomal reccessive condition affecting mucus glands
Genetic mutation in CF
Mutation of the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7 - lots of variants with the most common being delta-F508 which codes for a chloride channel
CF incidence
1/2500
Key consequences on physiology of CF
Thick pancreatic and biliary secretions that blocks ducts resulting in lack of digestive enzymes
Low volume thick airway secretions - reduce airway clearance resulting in bacterial colonisation and increased infection
Congenital bilateral absence of vas deferens - male infertility
Presentation of CF
Screened for in bloodspot test
Meconium ileus is the first sign - not passing meconium in 24 hours with abdo distension and vomiting
Recurrent LRTI, Failure to thrive and pancreatitis
Symptoms of CF
Chronic cough, Thick sputum production, Recurrent RTI, Loose greasy stools, Salty child, Poor weight and height gain
Signs of CF
Low weight or height on chart, Nasal polyps, Clubbing, Crackles and wheeze, Abdo distension
Causes of clubbing in children
Hereditary clubbing, Cyanotic heart disease, IE, CF, Tuberculosis, IBD, Liver Cirrhosis
Dx of CF
Newborn blood spot, sweat test, Genetic testing
What is the sweat test
Gold standard for CF
Patch of skin chosen, Pilocarpine is applied, Electrodes next to patch, current causes sweating, lab is sent sweat to look for a chloride concentration of over 60 mmol/L
Microbial colonisers in CF
S. Aurues, Hib, Klebsiella, E.coli, Burkhoderia cepacia, Psedomonas aeruginosa
Pseudomonas Aeruginosa in CF
Hard to clear, resistant, reccomend isolating those infected. Keep away from other children with CF.
Tx - Tobramycin or ciprofloxacin
Management of CF
Chest Physio - several times a day to clear mucus and reduce infection and colonisation risk
Exercise - clears mucus and improves resp reserve
High calorie diet - due to malabsorption, increased resp effort and coughing
CREON - digests fats
Prophylactic fluloxicillin
Treat infections
Bronchodilators like salbutamol
Nebulised DNase
Nebulised hypertonic saline
Vax - pneumococcal, influenza and varicella
Monitoring for CF
Specialist clinics typically every six months, regular sputum monitoring, screening for diabetes, osteoporosis, vit d def, liver failure
Prognosis for CF
Median life expectancy of 47
- 90% develop pancreatic insufficiency
- 50% develop diabetes
- 30% develop liver disease
- Most males are infertile
What is Primary Ciliary Dyskinesia
Aka Kartagners syndrome. Autosomal recessive affecting the cilia. More common when there is consanguinity
PCD pathophysiology
dysfunction of motile cilia most notably in resp tract. build up of mucus in lungs which increases risk of infection
Sx for PCD
Similar to CF, lots of infection, poor growth and bronchiectasis, also affects fallopian tubes and flagella of sperm so reduced or absent fertility
What is PCD strongly linked with
Situs Inversus
What is Kartagners Triad
Three features of PCD:
- Paranasal Sinusitis
- Bronchiectasis
- Situs Inversus
What is Situs Inversus
All internal organs are mirrored in the body
25% of those with situs inversus have PCD
Dx of PCD
Recurrent infection. Family history looking for consanguinity. Imaging to look for situs inversus. Semen analysis, key test is to take a sample of ciliated epithelium
Management of PCD
Similar to CF and bronchiectasis
What is Pyloric Stenosis
Progressive hypertrophy of the pyloric sphincter causing gastric outlet obstruction
Epidemiology of Pyloric Stenosis
More common in boys, 1/500, Family Hx, First borns
Clinical presentation of Pyloric Stenosis
Presents at 4-6 weeks
Non bilious, forceful, projectile vomiting after feed
Will continue to feed despite vomiting
Weight loss
Dehydration
Constipation
Visible Peristalsis
Palpable olive sized pyloric mass felt
Ix for Pyloric Stenosis
Test feed with NG tube and empty stomach and feel for visible peristalsis and mass
USS - Hypertrophy of the muscle
Blood gas - Hypochloremic, Hypokalaemic Metabolic Alkalosis
Management of Pyloric Stenosis
Correct mentabolic imbalances - NaCl
Fluid bolus for hypovolemia
NG tube feed
Ramsteds Pyloromyotomy - feeding can commence after 6 hours
What is Hirschsprungs disease
Nerve cells of the myenteric plexus are absent in the distal bowel and rectum, specifically the parasympathetic ganglionic cells resulting in a lack of peristalsis
Epidemiology of Hirschprungs
90% present in neonates. Average age of presentation is 2 days. Males. Downs
Pathophysiology of Hirschprungs
Short segment is most common where it is confined to rectosigmoid section. Ganglion cells of submucosal plexus not present, failure of peristalisis and bowel movements causing obstruction, can lead to bacterial build up and enterocolitis and sepsis
Clinical Features of Hirschsprungs
Failure to pass meconium, Abdo distended, Bilious vomiting, palpable faecal mass, Empty rectal vault
Ix for Hirschsprungs
Rectal suction biopsy to test for ganglionic cells in anyone who has:
- delayed meconium, constipation early, family hx, distension, Faltering growth
Contrast enema
Management of Hirshsprungs
Iv Ibx, decompress, NG tube and surgery
What is malrotation and volvulus
Twisting loop of bowel leading to intestinal obstruction
When does malrotation and volvulus present
First month of life
Clinical presentation of malrotation and volvulus
Abdo pain, bilious vomiting, caecum in midline, reflux
Ix for volvulus
Barium enema, Abdo XR with contrast to look for obstruction (double bubble sign)
Tx for volvulus
Surgery
What is intussusception
One piece of the bowel telescopes inside another leading to ischaemia and bowel obstruction
Where is intussusception most common
distal ileum and ileocecal junction
Epidemiology of intussusception
3 mo to 3 years
Most common under 1 yo
most common cause of obstruction in neonates
RF for Intussusception
CF, Meckels, HSP, Rotavirus vaccine > 23 weeks
Clinical presentation of intussusception
Colic abdo pain, Pallor, sausage shape mass palpable RUQ, Redcurrant jelly stools, abdo distension, shock, peritonitis (Guarding, rigidity, pyrexia)
Ix for intussusception
USS: target shapes mass
Abdo XR: distended small bowel, absence of gas in bowel
Tx for intussusception
Medical emergency, IV fluids, Air enema using USS to stretch the walls of the bowel and reduce the intussusception and if this is unsuccessful then operate. If perforation then broad spectrum Abx e.g. Gentamicin
What is necrotising enterocolitis
Acute inflammatory disease affecting preterm neonates leading to bowel necrosis and multi system organ failure
Epidemiology of NEC
Low birth weight, Most common surgical emergency, presents in first 2 weeks, prematurity, Abx therapy > 10 days, genetic
Clinical presentation of NEC
New feed intolerance, vomiting with bile, Fresh blood in stool, Abdo distension, Reduced bowel sounds, Palpable abdo mass, Visible intestinal loops, sepsis
Ix for NEC
Bloods: Thrombocytopenia, neutropenia
Cultures
Blood gas: acidotic
USS: air in portal system, ascites, perforation
XR: riglers sign: both sides of bowel are visible due to gas in peritoneal cavity, dilated bowel loops, distended bowel, thickened bowel wall, air outlining falciform ligament
Tx for NEC
Nil by mouth, Bowel decompression by NG, IV Cefotaxime, surgery
What is Meckels Diverticulum
Congenital diverticulum of the SI containing ileal, gastric and pancreatic mucosa
Meckels incidence
2%
How far from the ileocaecal valve is Meckels
2cm
Risks with Meckels
Peptic ulceration
Clinical presentation of Meckels
Abdo pain, Rectal bleeding in children 1-2 yo, Obstruction due to intussusception and volvulus
Management of Meckels
Removal if symptomatic
What is biliary atresia
Obstruction of the biliary tree due to sclerosis of the bile duct, reducing bile duct flow
Epidemiology of Biliary atresia
Females, Neonatal cholestasis 2-8 weeks, associated with CMV, congenital malformations
Pathophysiology of Biliary atresia (types)
Type 1: Common bile duct obliterated
Type 2: Atresia of the cystic duct in the porta hepatis
Type 3: Most common atresia of the right and left ducts at level of porta hepatis
Clinical presentation of Biliary atresia
Jaundice post 2 weeks, Dark urine, Pale stools, Appetite disturbance, hepatosplenomegaly, abnormal growth, duodenal atresia
Ix for Biliary atresia
Serum bilirubin: Conjugated is high
LFT’s raised
Alpha 1 antitrypsin to rule out deficiency
Sweat test to rule out CF
USS to look for structural abnormalities
Management of Biliary atresia
Surgical dissection of abnormalities: Kasai procedure
Abx
Complications of Biliary atresia
Cirrhosis and HCC
Progressive liver disease
What is neonatal jaundice
Hyperbilirubinaemia in the neonate
Physiological vs pathological vs prologned jaundice
Physiological:
Breakdown of in utero Hb, immature liver cant break down bilirubin, starts 2-3 days of life
Pathological:
Onset less than 24 hours, G6PD def, Spherocytosis
Prolonged:
Jaunidce over 14 days, Biliary atresia, Hypothyroid, Breast milk jaundice resolves 1.5-4 months, UTI/infection
Aetiology of neonatal jaundice
Prematurity, small for dates, previous sibling with it
Clinical presentation of neonatal jaundice
Colour, Drowsiness, Signs of infection
Ix for neonatal jaundice
TCB (transcutaneous bilirubinometry) for over 35 weeks gestation
Serum bilirubin if not TCB
Total and Conjugated bilirubin
Coombs test
Infection screen
Management of Neonatal jaundice
Phototherapy, repeat tests, can do a transfusion
Complications of neonatal jaundice
Kernicterus - bilirubin induced encephalopathy and irreversible neurological damage
Secondary causes of constipation
Hirschprungs disease, CF, Hypothyroid, Spinal cord lesion, Sexual abuse, Intestinal obstruction, Cows milk intolerance
Clinical presentation of constipation
Less than 3 stools per week, Hard and difficult to pass, Rabbit dropping stool, straining, abdo pain, overflow soiling, palpable hard stools in abdo
Management of Constipation
Correct reversible factors e.g. diet, hydration
Laxatives: Movicol
Disimpaction regimen
Red flags for constipation and their associated conditions
Failure to pass meconium - Hirschsprungs
Failure to thrive - hypothyroid, coeliac
Gross abdo distension - Hirschsprungs or other
Sacral dimple above natal cleft - Spina bifida
Abnormal anus - abnormal anorectal anatomy
Perianal bruising - sexual abuse
Perianal fistualae - perianal crohns
What is otitis media
Infection of middle ear
Aetiology of otitis media
Viral
Pneumococcus/Haemolytic Streptococcus/HiB
Clinical presentation of otitis media
Ear pain, Fever, Bulging tympanic membrane, Discharge
What is secondary otitis media
Glue ear
May have hearing loss
Retracted eardrum
If it goes on for over 3 months then refer for grommets and adenoidectomy
Management of Otitis media
5 days Amox/Erythromycin
What is squint
AKA strabismus, misalignment of the eyes, images on retina dont match do double vision
Pathophysiology of squint
Bad connection of eyes to brain to brain reduces signal to one of the eyes so it becomes lazy and the problem worsens over time - amblyopia
What is concomitant squint
Differences in control of extra ocular muscles
What is esotropia
Inward position squint - affected eye deviated towards the nose
What is exotropia
Outward position squint - deviated to ear
What is hypertropia
Upward moving affected eye
What is Hypotropia
Downward moving affected eye
Aetiology of squint
Idiopathic, Hydrocephalus, Cerebral palsy, space occupying lesion, Trauma
Ix for Squint
Eye movement and inspection, Fundoscopy, Visual acuity, Hrischbergs test and cover test
Management of squint
start before age 8
Occlusive patch to force bad eye to develop
Atropine drops in good eye to cause blurring forcing good eye to develop
What is periorbital cellulitis
eyelid and skin infection in front of the orbital septum confined to the soft tissue layer
RF for orbital cellulitis
Boys
Previous sinus infection
Lack of Hib infection
Recent eyelid injury
Clinical presentation of Periorbital cellulitis
Swelling, redness, hot skin around eyelid and eye
Ix for periorbital cellulitis
Clinical
CT sinus with contrast to differentiate between orbital and periorbital
Management of Periorbital Cellulitis
Abx empirical e.g. Cefotaxime/Clindamycin
What is Epilepsy
Umbrella term for tendency to have seizures which are transient episodes of abnormal electrical activity in the brain
What is a Generalised tonic-clonic seizure
Loss of consciousness with tonic (rigidity) and clonic (rhythmic jerking) phase with possible tongue biting, incontinence, groaning and irregular breathing. Postictal period of confusion, drowsiness and irritability
Tx for generalised tonic clonic
Sodium valproate, lamotrigine or carbamazepine
What are focal seizures
Begin in temporal lobes and affect speech, memory and emotions. Present with hallucinations, flashbacks and deja vu.
Tx of focal seizure
Lamotrigine or levetiracetam
What is an absent seizure
Most common in children. Become blank and stare into space then return to normal. Usually 10-20 seconds
Tx for absent seizures
Ethosuximide
What is a myoclonic seizure
Sudden brief muscle contractions where they remain awake. Often part of juvenile myoclonic epilepsy
Tx for myoclonic seizures
Sodium valproate or levetiracetam
What are tonic/atonic seizures
Sudden tension/stiffness affecting the body
Tx for atonic seizures
Sodium Valproate or lamotrigine
Ix for epilepsy
full history
EEG after second simple tonic clonic
MRI brain for abnormalities
Blood electrolytes, glucose, cultures and LP
Management of acute seizures
Recovery position
Soft under head
Remove obstacles
Make a note of timings
Call an ambulance if longer than 5 mins
Side effects of Sodium valproate
Teratogenic, Liver damage, Hair loss and tremors
SE of Carbamazepine
Agrunlocytosis, Aplastic anaemia
SE of Ethosuximide
Night tremors, rashes and N+V
SE of Lamotrigine
DRESS syndrome, Leukopenia
What is Status Epilepticus
Emergency where seizures last over 5 mins or 2 or more seizures without regaining consciousness
Management of status epilepticus in community and hospital
Hospital - secure airway, high conc O2, Assess cardiac and resp function, IV lorazepam
Community - Buccal midazolam or rectal diazepam
What are febrile convulsion
Occur in children with a high fever 6 mo - 5 yo
Length of simple febrile seizure and type
less than 15 minute generalised tonic clonic
Length and type of complex febrile convulsion
Focal and last more than 15 mins or multiple times
Ix for febrile convulsion
Rule out other causes such as epilepsy, syncope, trauma, lesion and neuro infection
Management of febrile convulsion
manage infection. control fever with analgesia. Parental education
What is eczema
Chronic atopic condition caused by defects in the normal skin barrier, leading to gaps which let irritants, microbes and allergens to enter creating an immune response and inflammation
Triggers of eczema
Temp change, Dietary products, washing powders, cleaning products, stress
Clinical presentation of eczema
Infancy, dry red and itchy skin, sore patches over flexors, face and neck. Episodic flares
Management of eczema
Maintenance: Emollients e.g. E45 or diprobase. Use as often as possible especially after washing and before bed
Flare ups: Thicker emollient e.g. Cetraben or can use topical steroids e.g. Hydrocort and beclomethasone
Other: Topical tacrolimus, oral steroids, methotrexate
What is stevens-johnson syndrome
Disproportional immune response causing epidermal necrosis resulting in shedding of top layer of skin - less than 10% of body surface affected
Aetiology of stevens-johnson
Meds - Anti-epileptics, Abx, Allopurinol, NSAIDs
Infections - HSV, Mycoplasma pneumonia, CMV, HIV
Clinical presentation of stevens johnson
Non specific: fever, cough, sore throat, sore mouth, sore eyes, itchy skin
Purple/red rash which spreads and blisters
can affect urinary tract, lungs and internal organs
Management of stevens johnson
Steroids, Immunoglobulins, immunosuppressant
Complications of Stevens Johnson
Secondary infection: cellulitis, sepsis
Permanent skin damage
What is urticaria
Also known as hives, small itchy lumps which appear on the skin
What is urticaria associated with
angioedema
Pathophysiology of Urticaria
Release of histamine and other pro-inflammatory chemicals by mast cells in skin. Could be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic uritcaria
Aetiology of Urticaria
Allergies, Contact with chemicals/latex/nettles, Meds, Virus, Insect bites
What is chronic urticaria
Autoimmune condition where autoantibodies target mast cells and trigger them to release histamines and other chemicals
Tx of Urticaria
Antihistamines
For chronic - Fexofenadine
Steroids
Omalizumab - targets IgE
What is Nappy rash
Contact dermatitis in nappy area caused by friction between skin and urine/faeces in nappy. common in 9-12 mo. Breakdown can lead to candida or bacterial infection
RF for nappy rash
Delayed nappy change
Soaps
Diarrhoea
Oral Abx use -> candida
Preterm
Clinical presentation of nappy rash
Sore, red or inflamed skin
No rash on creases of the groin
Itchy rash - distress
Severe and long standing rash -> erosion and ulceration
Candida vs nappy rash
In nappy rash the flexures are spared, its patchy and red
Candida has beefy red papules and white scaling
Management of nappy rash
Switch to absorbant nappies
Change nappy often and clean skin
Maximise time out of the nappy
Infection - antifungal or abx cream
What are petechiae
Small, non blanching, red spots caused by burst capillaries
What is purpura
Larger, non blanching, red-purple macules or papules caused by leaking of blood from vessels under the skin
Urgency of child with non blanching rash?
Very urgent, immediate investigation due to risk of meningococcal sepsis
Name the differentials for non blanching rash
Meningoccocal septicaemia, HSP, ITP, HUS, Leukaemia, Mechanical, Traumatic and Viral
Explain the DDx for non blanching rash
Meningococcal septicaemia - fever, unwell manage with Abx
HSP - Purpuric rash on legs and buttocks, may also have joiny and abdo pain
ITP - rash over several days in an otherwise unwell child
Leukaemia - Gradual petechiae with other signs such anaemia, lymphadenopathy and hepatosplenomegaly
HUS - recent diarrhoea alongside oliguria and anaemia
Mechanical - coughing, vomiting, breath holding can produce petechiae
Traumatic - tight pressure on skin e.g. NAI
Viral illness can lead to rash
Ix for non blanching rash
FBC, U+E, CRP, ESR, Blood cultures, Meningococcal PCR, LP, BP, urine dip
Main cause of anaphylaxis
Food allergy with an IgE mediated reponse
Other causes of Anaphylaxis
Drugs, stings, latex, exercise, idiopathic
Management of Anaphylaxis
Adrenaline and long term management is avoiding allergens and prescribing epipen
What is kawasaki disease
Mucocutaneous, lymph node syndrome - a systemic medium-sized vessel vasculitis
Epidemiology of kawasaki
Young children under 5 with no clear cause or trigger, more common in boys of Japanese or Korean origin
Clinical presentation of kawasaki
Persistent high fever for more than 5 days, unwell and unhappy, widespread erythematous maculopapular rash and desquamation of the palms and soles, strawberry tongue, cracked lips, Cervical lymphadenopathy, bilateral conjunctivits
Ix for Kawasaki
FBC - Anameia, Leukocytosis, thrombocytosis
LFT - hypoalbuminaemia
Raised ESR
Urinalysis shows raised WBC
ECHO - rule out aneurysm
Disease course of kawasaki
Acute phase - child will be unwell with fever, rash, lymphadenopathy
Subacute phase - acute symptoms will settle but the arthralgia and risk of aneurysm continues
Convalescent stage - remaining symptoms return to normal and blood tests return to normal 2-4 weeks
Management of Kawasakis
High dose aspirin, IV Ig, inform public health
What is meningitis
Inflammation of the meninges
Meningitis causative agent
Gram negative diplococcus bacteria that occurs in pairs
What is meningococcal meningitis
When bacteria infects the meninges and CSF
What is most common cause of meningitis in neonates
Group B strep
Clinical presentation of meningitis
Fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures
Neonatal signs of meningitis
hypotonia, poor feeding, lethargy, hypothermia, bulging fontanelle
Two tests for meningitis
Kernig’s: lay patient on back and flex one hip and knee then straighten knee while keeping hip flexed which will produce pain or resistance
Brudzinski’s: lay patient on back and lift their head and neck off bed and flex chin to the chest, causes involuntary flexion of hips and knees
Criteria for an immediate LP
All children under 1 month with a fever
1-3 mo with a fever and unwell
Under 1 yo with fever and other signs of serious illness
Ix for meningitis
LP to be sent for meningococcal PCR
Community management for meningitis
Stat injection of Benzylpencillin then transfer to hospital
Management for meningitis in under 3 mo
IV Cefotaxime plus IV amoxicillin
Management for meningitis above 3 mo
IV Ceftriaxone
Post exposure prophylaxis for meningitis
Ciprofloxacin
Common causes of viral meningitis
HSV, VZV, enterovirus
Management of viral meningitis
Supportive, sometimes use aciclovir
Differences between Bacterial and viral meningitis CSF samples
Bacterial: Cloudy, High protein, Low glucose, High neutrophils, cultures bacteria
Viral: Clear, Mildly raised or normal protein, normal glucose, high lymphocytes, Negative culture
Is measles a bacteria or virus
Virus
Clinical presentation of measles
Fever, Koplik spots (blue/white spots on inside of cheeks), conjunctivitis, coryza, cough, rash that spreads downwards from behind ears to whole body - maculopapular
Management of measles
Supportive, avoid school for at least 5 days, Public health
Complications of measles
otitis media, pneumonia, febrile convulsions, encephalitis/subacute sclerosing panencephalitis
Clinical presentation of chicken pox
Fever, Vesicular rash beginning on head and trunk which spreads to peripheries, itching can lead to secondary infection
Management of chickenpox
Symptomatic, Immunocompromised given aciclovir, Avoid school until lesions have crusted over
Complications of Chicken pox
Bacterial superinfection, pneumonitis, DIC
What is rubella
mild disease in childhood that occurs in winter and spring
Incubation of 15-20 days
resp droplet spread
Clinical presentation of Rubella
Low grade fever, Maculopapular rash on face that spread to body
Rubella Tx
None needed, diagnosis made serologically if there is any risk of exposure for non immune pregnant women
Complications of rubella
Arthritis, Encephalitis, Myocarditis
Summarise diphtheria
Infection which causes local disease with membrane formation affecting the nose, pharynx, larynx or systemic with myocarditis and neuro manifestations
Generally been eradicated in UK
What is scalded skin syndrome
Caused by exfoliative staphylococcal toxin which causes separation of epidermal skin through the granular cell layers
Clinical presentation of scalded skin syndrome
Fever, Malaise, Purulent crusting localised infection around eyes,nose,mouth with widespread erythema and tenderness
What is the Nikolsky sign
Areas of epidermis seperate on gentle pressure leaving denuded areas of skin which then dry and heal without scarring
Management of scalded skin syndrome
IV Fluclox, Analgesia and fluids
Clinical presentation of Tuberculosis
Asymptomatic children have minimal signs of infection
If it spreads through lymphatic system - fever, anorexia, weight loss, cough and CXR changes such as hilar lymphadenopathy
Enlargement of peribronchial lymph nodes which can cause consolidation, obstruction and effusions
What is post-primary TB
infection can be local or spread across systems such as bones, joints, kidneys and CNS
Ix for TB
Gastric washing for 3 days to culture acid-fact bacilli through NG
Mantoux - however can be positive due to vax
IGRA - T cell response
Management of TB
RIPE therapy initially and then reduce to Rifampicin and Isoniazid after 2 mo - last 6 mo
After puberty - give pyridoxine to reduce peripheral neuropathy SE of Isoniazid
Contact trace
HIV Epidemiology
Affects 2 million children a year
Main transmission is during pregnancy, at delivery or breastfeeding
Ix for HIV
Over 18 mo - presence of antibodies
Under 18 mo - HIV DNA PCR
Clinical presentation of HIV
Most remain asymptomatic for years
Lymphadenopathy, recurrent bacterial infection, chronic diarrhoea, lymphocytic interstitial pneumonitis
What does a severe AIDS diagnosis often present with
Pneomocystis jirovecii pneumonia, severe faltering growth and encephalopathy
Tx for HIV
ART based on HIV load and CD4 count
Avoid breast feeding and active management of labour and delivery
What is encephalitis
Inflammation of the brain - can be infective or not
Most common cause of encephalitis
Viral, however bacterial and fungal are possible
Most common virus causing encephalitis
HSV 1 from cold sores in children
HSV 2 for neonates from genital herpes following birth
Clinical presentation of Encephalitis
Altered consciousness, Altered cognition, Unusual behaviour, Acute onset focal neurological symptoms, acute onset focal seizures, Fever
Ix for encephalitis
LP to send CSF for PCR
CT if LP is contraindicated
MRI after LP for visualisation
HIV testing is recommended
Management of Encephalitis
Herpes and VZV - Aciclovir
CMV - Ganciclovir
Repeat LP to ensure success before ending antivirals
Complications of encephalitis
Lasting fatigue, change in personality/mood/memory/cognition, headaches and chronic pain, Sensory disturbance, Seizures
Slapped cheek causative agent
Parvovirus B19
Slapped cheek pathophysiology
Virus infects erythroblastosis red cell precusors in bone marrow
Clinical presentation of slapped cheek
Erythema infectiosum - fever, headache, myalgia, rash on face which progresses to maculopapular rash on trunk and limbs
Complications of slapped cheek
Aplastic crisis: in children with haemolytic anaemia where there is increased red cell turnover and immunodeficiency
Foetal disease which can lead to death due to severe anaemia
Management of Slapped cheek
Supportive
What is impetigo
Superficial bacterial skin infection caused by S.aureus
Characteristic sign in impetigo
Golden crust
What are the two types of impetigo, explain them
Non bullous - around nose and mouth and exudate from lesions causes golden crust, no systemic symptoms and wont be unwell
Bullous - 1-2 cm fluid filled vesicles which then burst to cause golden crust, more common in neonates and under 2’s, will have systemic Sx such as fever and malaise
Tx for impetigo
Non-bullous - topical fusidic acid or antiseptic cream or fluclox if its widespread
Bullous - Fluclox
Complications of impetigo
Sepsis, Scarring, Post strep glomerulonephritis, scarlet fever, Staphylococcal scaled skin syndrome
Toxic shock syndrome causative agent
S.Aureus and Group A strep
Clinical presentation of toxic shock syndrome
Fever over 39
Hypotension
Diffuse erythematous, macular rash
Organ dysfunction: Mucositis, D/V, Renal impairment, Liver impairment, Clotting abnormalities and thrombocytopenia
Tx for toxic shock syndrome
Intensive care to manage the shock and areas of infection should be debrided
Abx such as Ceftriaxone and Clindamycin
After 1-2 weeks there is desquamation of the palms, soles, fingers and toes
Risk of recurrent infections
Scarlet fever causative bacteria
Strep pyogenes
RF for scarlet fever
Neonate, Immunocompromised, Concurrent chickenpox or flue
Clinical presentation of scarlet fever
Sore throat, fever, headache, fatigue, nausea and vom
Pinpoint, sandpaper like blanching rash initially on trunk which then spreads
Strawberry tongue
Cervical lymphadenopathy
Management of scarlet fever
Oral Abx such as benzylpenicillin for 10 days
tell public health
