Paediatrics Flashcards
ABCDE approach to a child
Airway:
Listen for stridor
Assess for foreign body or secretions (drooling, look in throat, XR)
Breathing:
watch for 30 seconds-1 minute for RR
Recession (subcostal, intercostal, sternal), nasal flaring, tracheal tug, accessory muscle use
Oxygen saturation (<94 significant illness, <90 alarming)
Auscultation (wheezing, crepitations in bronchiolitis, bronchial breathing)
Circulation:
Colour: pallor, mottled
Radial pulse rate (brachial for <6 months) (>160bpm for 1 YO, >150 for 1-2 years and >140 for 2-5 YOs)
Hydration signs: wet nappies, mucous membranes, skin turgor, capillary refill and peripheral temperature of hands and feet
Auscultate heart sounds
Blood pressure if very unwell
Disability (neuro): Alertness and activity Responsive to surroundings Behaviour (irritable, clingy), distinguish from true irritability (sign of raised ICP) by if the child can be distracted or consoled at all. If they cannot it is likely more true irritability. AVPU score/Glasgow Coma Scale Pupils if very unwell Limb tone and movement Joint swelling RASHES Capillary glucose if decreased alertness
Everything else:
Ears, Nose, Throat exam: ensure positioning of child is appropriate and parents secure them safely
Temperature: measure with tympanic membrane thermometer or tempa dot strip or axilla (recommended for babies)
Feel stomach for tenderness, organomegaly, masses etc.
Green features of traffic light system and management
Responds normally to social cues
Content and smiling
Stays awake or wakes quickly
Strong, normal crying
No red or amber symptoms
Circulation and hydration
Normal skin and eyes
Moist mucous membranes
No amber or red symptoms
management:
Supportive care advice
Safety netting for worsening symptoms and when to phone back/attend A+E
orange features of traffic light system
> 39 degrees in children aged 3-6 months
Pallor reported by parents
Not responding normally to social cues
No smile
Wakes only with prolonged stimulation
Decreased activity
Nasal flaring
Tachypnoea >50 in ages 6-12 months or >40 in >12 months
Oxygen saturation <95% on air
Crackles in chest auscultation
Tachycardia >160bpm ages <12 months
>150bpm in ages 12-14 months
>140 bpm in ages 2-5 years
Cap refill >3 seconds
Dry mucous membranes
Poor feeding in infants
Reduced urine output
Age 3-6 months
Temperature >39
Fever for >5 days
Rigors
Swelling of limb or joint
Non-weight bearing limb/not using an extremity
management:
Safety netting advice for parents to be managed at home (clinical judgement)
Advice on warning symptoms and when to following up for urgent medical review
Arrange primary care review/follow-up
Liaise with other healthcare professionals, including out of hours, to ensure direct access for the child if further assessment is needed
Consider hospital admission if:
Age <3 months with suspected unexplained UTI
Feverish illness with no obvious cause, unwell for longer than expected
Significant parent anxiety or difficulty coping
Red features of traffic light system and management
> 38 degrees in infants aged 0-3 months
Hypothermia
Pale
Mottled
Ashen or cyanotic
No response to social cues
Appears ill to healthcare professional
Does not wake or stay awake if roused
Weak, high pitching or continuous crying
Grunting
Tachypnoea >60
Moderate or severe chest indrawing
Reduced skin turgor
Age <3 months with temperature of >38
Non-blanching skin rash
Bulging fontanelle
Neck stiffness
Status epilepticus
Focal neurological signs
Focal seizures
management:
Urgent transfer to hospital
fever
Background:
Elevation of body temperature above daily normal variation (>37-38 degrees C usually)
Very common presentation in children in primary and secondary care
Fever in young children >6 months are often not serious
Fever in children aged 3-6 months have a higher chance of being serious and must be taken seriously
Fever in a child <3 months is unusual and concerning - requires hospital admission for Ix
Aetiology:
Viral infections (most common)
Bacterial infection - meningitis
Non-infectious cause - Kawasaki disease (fever >5 days)
fever presentation and investigation
Presentation:
Temp >37 degrees
Symptoms of causative agent (infection or systemic signs)
Investigation/diagnosis:
Traffic light system
Assess age: 1+ (green), 6-12 months (orange), <6 months (red)
Assess risk: prematurity, cardiac disease, syndromal
History - assess parental perception and child’s presentation/history, associated symptoms of D+V, rash, maternal fever/premature delivery, significant medical conditions, immunosuppression, recent antipyretic drug or antibiotic use
Immunisation history !!
Recent foreign travel, recent contact with serious infectious diseases, parental beliefs or previous experiences or severe febrile illness.
fever management
Management:
Antipyretics to help reduce fever and improve symptoms (DOES NOT HELP CAUSE) such as calpol, paracetamol or ibuprofen
Avoid overwrapping or undressed clothing, avoid tepid sponging, encourage fluid intake
Fever in young children >6 months are often not serious
Fever in children aged 3-6 months have a higher chance of being serious and must be taken seriously
Fever in a child <3 months is unusual and concerning - requires hospital admission for Ix
Red column - urgent hospital admission
acute cough
Background:
Very common in young children especially in URTIs
Usually <3 weeks for infection (acute)
Very uncommon to have a chronic cough in young children (passive smoking)
Aetiology:
Most commonly viral infection
Infants under 12 months - often bronchiolitis
acute cough presentation, investigation and management
Presentation:
Cough
Can be characteristic such as whooping cough (pertissus) or barking cough (croup)
Can be with or without a wheeze or chest sounds
Investigation/diagnosis:
ABCDE for respiratory distress
ENT exam (aside from if epiglottitis is suspected)
Vital signs - oxygen, temperature, cap. Refill,
Assess for other symptoms - chest, hydration, cap. Refill, skin turgor, low urine output, poor feeding or wet nappies
Home life symptoms - pets, passive smoking, fumes
Management:
Asthma symptoms - SABA inhaler via spacer, hospital admission if severe respiratory distress
Hospital admission for temp >38 in ages <6 months, inadequate fluid intake (<50% normal), decreased activity, <3 months with cough and fever (croup)
Diarrhoea and vomiting
Background:
Very common in children, often caused by gastroenteritis, often children have more than one episode per year
Pathology:
Depends on underlying cause
Gastroenteritis - upper gastrointestinal tract infection (stomach and intestines)
Aetiology:
GI infections (gastroenteritis) most commonly from viral infections (rotavirus or norovirus) or bacterial (E. coli, campylobacter, shigella)
Systemic infections
Surgical conditions (intussusception, pyloric stenosis)
Diarrhoea and vomiting presentation, investigation and management
Presentation:
Gastroenteritis - diarrhoea usually lasting 5-7 days, most resolve within 2 weeks, vomiting for 1-2 days, most stop within 3 days
Investigation/diagnosis:
Dehydration assessment
vitals
Management:
Gastroenteritis - self limiting, supportive care, replacement fluid intake to prevent dehydration
Oral rehydration solution for those at risk of dehydration
IV fluids only for persistent vomiting of oral rehydration solution or suspected shock
Encourage small regular foods, avoid solids unless dehydration is normal
intussusception
Background:
Primary - 95% of infants and children, usually ages 3-12 months
Secondary - in adults, much less common.
Mortality is very low within the first 24 hours but very high in irreducible or gangrenous cases
Complications - ischaemia of the bowel, risk of gangrene or necrosis, bowel obstruction if involved loops become blocked.
Pathology:
Telescoping prolapse of a portion of intestine into the lumen of the adjacent portion of intestine
Aetiology:
Primary - has no obvious cause, disharmony between ileum and cecum in GE
Secondary - underlying cause present such as polyps, inverted Meckel diverticulum etc.
Risk factors: Ages 3-12 months (primary) Males 2:1 (primary) Meckel's diverticulum Polyps
intussusception presentation and investigations and management
Presentation:
Paroxysms of abdominal colic (screaming and pallor, leg raising, with intermittent settling between bouts of pain)
Bilious vomiting from obstruction
Red-currant jelly stool (late sign)
Dance’s sign - empty RIF + sausage shaped mass in mid abdomen or RUQ
Signs of shock - lethargy, poor feeding, hypotonia
Investigation/diagnosis:
USS diagnostic showing target or doughnut sign in cross section
Management:
Obstruction - NMB, nasogastric tube feeding, IV fluid resus before attempting reduction
Air enema - diagnostic and therapeutic
Operation - gentle reduction or resection if irreducible or gangrenous
constipation
Background:
Very common paediatric problem
Encopresis - faecal incontinence, not considered pathological until 4 years of age. It is usually the sign of chronic constipation where the rectum becomes stretched and loses sensation. Large hard stools main remain in the rectum and only loose stools are able to bypass the blockage and leak out
Pathology:
less bowel peristalsis leading to less bowel movements
Hard stools leading to difficulty passing
Aetiology:
Most are idiopathic or functional constipation - no significant underlying cause other than lifestyle factors
Secondary - Hirschsprung disease, CF, hypothyroidism
Encopresis - faecal impaction, spina bifida, hirschsprung disease, CP, learning disability, psychological stress, abuse
constipation risk factors and presentation
Risk factors: Habitually withholding stools Low fibre diet Poor fluid intake and dehydration Sedentary lifestyle Psychological problems (safeguarding)
Presentations: Very variable between individuals < 3 x weekly Hard stools, difficult to pass Rabbit dropping stools Abdominal pain Straining and painful passage Rectal bleeding associated with hard stools Holding abnormal posture (retentive posturing) Faecal impaction - overflow soiling with incontinence of loose and smelly stools Palpable mass in abdomen Loss of sensation of need to open bowels
constipation investigations and management
Lifestyle factors history
History for RED FLAGS:
Not passing meconium within 48 hours of birth (CF or hirschsprung’s disease),
Neurological signs or symptoms (cerebral palsy/spinal cord lesion),
Vomiting (intestinal obstruction or Hirschprung’s)
Ribbon stool (anal stenosis)
Abnormal anus, abnormal lower back or buttocks
Failure to thrive (coeliac disease, hypothyroidism, safeguarding)
Acute severe abdominal pain and bloating (obstruction or intussusception)
Management:
Recommend high fibre diet and good hydration
Start laxatives (movicol first line), continue long term and slowly wean off as good bowel habits develop
Faecal impaction - disimpaction regimen with high dose laxatives then taper off
Encourage and praise good toilet habits to improve habits
Bowel diary
Encephalitis
Background:
Inflammation of the brain, causing abnormal cerebral function (unlike meningitis)
Encephalitis - preceded by an infectious prodrome (temperature, rash, LAP, cold sores, conjunctivitis, meningeal signs)
Encephalopathy - no infectious prodrome e.g. hypoglycemia, hepatic encephalopathy, DKA, hypoxic brain injury, uremia, drugs, SLE, wernicke’s etc.
Pathology:
Inflammation of the brain often causing cerebral abnormality leading to altered mental status, motor and sensory deficits
Aetiology:
Usually viral (HSV 1-2, arboviruses, CMV, VZV, HIV, Measles, mumps, rabies, japanese B encephalitis, west nile virus, tick-borne encephalitis etc.)
Non-viral - bacterial meningitis, TB, malaria, listeria, lyme disease, legionela, leptospirosis, aspergillosis, cryptococcus, schistosomiasis, typhus.
Risk factors:
Meningitis
Immunocompromised
encephalitis presentation and investigation
Presentation: Altered personality Decreased GCS score Confusion drowsiness, coma Fever Headaches Neck stiffness and pain Seizures Focal neurological signs History or travel or animal bites Infectious prodrome (temperature, rash, LAP, cold sores, conjunctivitis, meningeal signs)
Investigation/diagnosis:
GCS score
ABCDE assessment
Bloods - cultures, viral PCR, U+Es,
Contrast enhanced CT (before LP), or MRI if allergic to contrast
LP - typically moderate protein and lymphocyte increase, decreased glucose
EEG
encephalitis management
Management:
Hospitalisation
IV Acyclovir within 30 minutes of arrival for 14 days (empirical treatment for HSV)
Specific therapies for CMV (ganciclovir), toxoplasmosis based on blood cultures or PCR
Supportive therapy in HDU/ICU
Phenytoin for seizures, treat increased ICP
Repeat LP to ensure successful treatment prior to stopping antivirals
Complications - high ICP, seizures, mortality is 70%
meningitis
Background:
Infection of the meninges, usually bacterial
Associated with high mortality
Complications - VTE, severe cerebral oedema or abscess, hearing loss, seizures and epilepsy, cognitive impairment, memory loss, cerebral palsy with FNDs (limb weakness, spasticity)
Viral - usually benign, self-limiting within 4-10 days with no serious sequelae
Chronic meningitis - long history of vague symptoms (headache, lassitude, anorexia, vomiting, signs of meningism later in disease
Pathology:
Microorganisms infect the meninges from the ears, nasopharynx, cranial injury, congenital defects leading to inflammation
Infection may spread to the blood leading to septicemia
Aetiology: MPH
Most commonly meningococcus (neisseria meningitidis), Pneumococcus (strep. pneumonia) or Haemophilus influenzae worldwide
Viral - enterovirus, polio, mumps, HSV, epstein-barr virus
Fungal infection
meningitis risk factors and presentation
Risk factors:
Cranial injury
Infection
Immunocompromised
Presentation:
Headache
Neck stiffness (nuchal rigidity) - Brudzinski’s neck sign
Fever
Photophobia
Vomiting
Kernig’s sign (inability to fully extend the knee when the hip is flexed 90 degrees)
Papilledema
Meningococcal septicaemia - non-blanching, purpuric skin rash (starts as small pin pricks spreads quickly and turns into red/purple blotches), signs of shock (tachycardia, tachypnoea, hypovolemia)
Complications - progressive drowsiness, lateralizing signs, cranial nerve lesions
meningitis investigations
Rash - glass test for blanching
ABCDE assessment
GCS score
Bloods - cultures (CONFIRMS BACTERIAL SEPSIS), viral PCR, syphilis serology, U+Es, LFTs
CXR
Contrast CT for FND, papilloedema,, LOC or seizures (before LP to exclude high ICP)
LP - diagnostic CSF microscopy (DO NOT PERFORM IF BACTERIAL SEPSIS SUSPECTED)
meningitis LP results
Normal - clear, <5 white cells, all lymphocytes, 0.2-0.4 protein, normal pressure 10-20
viral - clear, 5-1000 white cells, lymphocytes, 0.4-1 protein, normal or slightly high opening pressure
bacterial - cloudy and turbid, 100-50,000 white cells, neutrophils, >1 proteins, <40% plasma glucose, high opening pressure
TB - cloudy and viscous, <500 white cells, lymphocytes, 1-5 protein, <30% plasma glucose, high opening pressure
meningitis management and prophylaxis
All cases must be notified to local public health authority allowing contact tracing
Non-blanching rash:
Immediate hospitalisation
Benzylpenicillin 1200mg slow IV or IM OR cefotaxime 1g IV before transfer to hospital
Start IV antibiotics once admitted, tailor to blood culture results
Mx:
Ideally perform LP to confirm before starting ABX but this should not delay ABX
<3 months - Cefotaxime 2g/6 hourly initially + amoxicillin (covers listeria contracted during pregnancy)
Above 3 months old - ceftriaxone
Change ABX based on cultures, vancomycin for penicillin resistance
Steroids for bacterial meningitis to reduce loss of hearing and neurological damage (DEXAMETHASONE give 4x daily for 4 days to children >3 months)
IV fluids and inotropes for septicaemia signs
Prophylaxis:
Oral rifampicin or ciprofloxacin to eradicate nasopharyngeal carriage of organism
Given to those with prolonged contact with infected patient in household setting during 7 days prior to illness onset
Vaccine for meningococcal group C and haemophilus influenzae is part of routine UK childhood immunisation
stridor
Background:
Noise heard on inspiration, from partial obstruction at the larynx or large airways
More common in children as their airways are narrower and more flexible than adults, meaning obstruction occurs more dramatically and faster.
Pathology:
Partial obstruction of the larynx or large airways causing whistling high pitch notes on inspiration due to the decreased diameter of the airway passage.
Aetiology:
Infective - croup (laryngotracheobronchitis), bacterial tracheitis, epiglottitis, laryngitis
Non-infective - congenital (laryngomalacia, web/stenosis, vascular rings), anaphylaxis, haemangiomas or papillomas, thermal or chemical trauma, foreign body or vocal cord paralysis.
stridor presentation and other signs of respiratory distress
High pitched, wheezing, musical sound on inspiration
Other signs of respiratory distress:
Swallowing difficulty/drooling
pale/cyanosed
Accessory muscle breathing
Nasal flaring
Subcostal retraction/recession (indrawing of the abdomen just below rib cage, belly breathing)
Downward plunging of trachea with respiration (tracheal tug)
stridor infective and non-infective differentials and investigations
infective:
croup
epiglottitis
bacterial tracheitis
retropharyngeal abscess
non-infective:
inhaled foreign body
subglottic haemngioma
C1 esterase inhibitor deficiency (hereditary angioedema)
hypoglycaemia
investigations ABCDE examination Vital signs - temp, RR, HR, breathing Respiratory examination Bloods - U+Es, Ca, FBC
croup/laryngotracheobronchitis (LGB)
Background:
Leading cause of stridor with a barking cough
Most severe in children under 3 years old (typically 6 months - 2 years)
Pathology:
Viral upper respiratory tract infection causing inflammatory oedema involving the larynx, causing a hoarse voice and barking cough and partial airways obstruction leading to stridor.
Aetiology:
95% viral - parainfluenza, influenza, adenovirus, respiratory syncytial virus (RSV), measles etc.
Bacterial - klebsiella, diphtheria (rare, can lead to epiglottitis)
Fungal - rare
Risk factors:
Ages 6 months - 2 years
croup presentation, investigation and management
Presentation:
Stridor and barking cough with no drooling - almost always croup
Increased work of breathing
Barking cough occurring in clusters of coughing episodes
Hoarse voice
Stridor
Low grade fever
Steeple sign - tapering trachea seen on XR
Investigation/diagnosis: ABCDE examination Respiratory examination Vital signs CXR
Management:
Mild
Generally self-limiting, within 48 hours should improve (parainfluenza viral infection especially),
Supportive treatments (fluids and rest), sit them up during coughing and comfort, avoid school while ill and vulnerable people.
Good hygiene to avoid spreading.
Any child under 6 months with signs of difficulty breathing or dehydration must be admitted to hospital
Moderate - severe - admit to hospital
Dexamethasone (prednisolone in GPs) 150 mcg/kg can be given orally and repeated again in 12 hours PRN
Supportive oxygen
Nebulised budesonide 2 mg
Nebulised adrenaline (failure to improve with steroids or adrenaline - consider bacterial tracheitis)
Intubation and ventilation
bacterial tracheitis
Background:
Pseudomembranous necrotising tracheitis
Most serious in young children due to relatively small sized trachea, easily blocked by swelling.
A severe bacterial infection of the trachea capable of producing airways obstruction
Usually considered part of the lower respiratory tract however can produce upper airway obstruction if severe.
Pathology:
Thick mucopurulent exudate and tracheal mucosal sloughing (pseudomembrane) that is not able to be cleared with coughing and risks occluding airway
Defects in the cartilage leads to inability to support the trachea, collapse of the trachea due to hacking or barking cough
Aetiology:
Most commonly staph aureus
Often follows recent viral URTI
bacterial tracheitis presentation and investigation
Presentation: Often history of a recent URTI with an acute deterioration Toxic appearance Barking cough with thick sputum Inspiratory stridor Scratchy feeling in throat Tracheal tenderness Chest pain Fever Earache, headache, dizziness Increased effort to breathe (accessory muscle use, stridor, grunting, nasal flaring)
Investigation/diagnosis:
ABCDE assessment
Respiratory examination - rule out croup and epiglottitis
Bronchoscopy for direct vision of exudates or pseudomembrane on trachea
CXR - subglottic narrowing
Vital monitoring
ECG monitoring during treatment
bacterial tracheitis management
Severe:
IV antibiotics (broad spectrum)
ITU/ICU admission for intubation and supportive ventilation
ECG monitoring, oxygen saturation, capnography, BP monitoring
epiglottitis
Background:
Rare but has high mortality rate due to risk of respiratory arrest
Medical emergency
Pathology:
Bacterial URTI leading to inflammation and swelling of the epiglottis
This can potentially cause airway obstruction
Aetiology:
Haemophilus influenzae type B most commonly
Strep pyogenes
Risk factors:
M:F 3:1
Peak age of infection is 2-7 years
epiglottitis presentation and investigation
Presentation: Often acute history of infection Sore throat Drooling (head forward, tongue out) Prefer to sit, leaning forward (tripod position) Fever Dyspnoea Stridor Hot potato muffled voice Dysphagia Tender anterior neck Enlarged anterior neck nodes Voice hoarseness Thumb sign seen on lateral XR of neck
Investigation/diagnosis:
ABCDE assessment
Vitals examination
Lateral neck XR - thumb sign + exclude foreign body
Nasopharyngeal intubation by anaesthetist to diagnose
Bloods - culture
Epiglottis culture
DO NOT EXAMINE THE THROAT - CAUSES RESP> ARREST
epiglottitis management and prognosis
Management:
Prevention - vaccine programme against haemophilus
DO NOT DISTRESS PATIENT - can cause airway closure
ITC admission, alert senior paediatrician and anaesthetist to secure airway
Oxygen by mask until anaesthetist arrives
Nebulised adrenaline
IV dexamethasone
Nasopharyngeal intubation by anaesthetist to diagnose
IV pen G + ceftriaxone 2g/12 hourly
Antipyretic (ibuprofen)
Cricothyrotomy in emergency
Prognosis:
Most recover without intubation
Those that are intubated often recover fully within a few days
Common complication is epiglottic abscess, collection of pus around the epiglottis which also threatens the airways. Treatment is similar to epiglottitis.
eczema
Background:
Chronic relapsing inflammatory condition of the skin
Complications - lichenification, secondary infection, refractory eczema
Pathology:
Excessive skin growth leading to immature keratocytes on outer skin layers and improper laying of keratocytes leads to improper skin barrier formation
Leads to excess loss of water and skin buried defects allowing pathogens etc. to enter
This leads to skin inflammation and easy irritation
The itch, scratch cycle is when inflammation causes itching, the patient scratches the area and this leads to further histamines release in the tissues causing increased itch and so on.
Aetiology:
Unknown
Triggers - heat, allergens, infection, sweating, severe stress
Risk factors:
Personal history of atopic conditions - asthma, hay fever, eczema
Familial history of atopy
eczema presentation, ix, mx
Presentation: Itchy Erythematous Dry, scaly patches May weep Nail pitting and ridging Commonly on extensor aspects (INFANTS) or flexor aspects (CHILDREN and ADULTS)
Investigation/diagnosis:
Clinical - itch + history of atopy, general dry skin, visible eczema rash, onset in first 2 years of life
Management:
Avoid triggers, keep nails short and avoid scratching (educate on itch scratch cycle)
Apply emollient liberally (thin creams - e45, aveeno, thick creams - 50:50 ointment, hydromol, cetraben ointment)
Topical hydrocortisone 7 days for flares
Antihistamines
Antibiotics (flucloxacillin) for secondary infection
Later life - tacrolimus (ages 2+) or pimecrolimus (ages 2-16)
Phototherapy and immunosuppressants for severe cases
steroid ladder
Mild = hydrocortisone
Mod = eumovate
Potent = betnovate
Very potent = dermovate
nappy rash
Background:
Very common in young children wearing nappies
Common complication is secondary yeast infection with candida species
Severe long standing nappy rash can lead to erosions and ulcerations
Pathology:
Contact dermatitis +/- secondary candida infection
Inflammation of the skin in response to urine and faeces contact
Aetiology:
Prolonged wearing of soiled nappies
Risk factors: Most common between ages 9-12 months Not regularly changing infant Not washing or drying well/using talcum powder Tight fitted nappies
nappy rash presentation, ix and mx
Presentation: Sore, itchy Erythematous Spread around the nappy region only (perianal, genital region) Tends to spare the skin creases Worsened after wearing nappies Improves with less nappy use Candida - rash extending into skin folds, well demarcated scaly border, circular pattern to rash, satellite lesions near main rash.
Investigation/diagnosis:
Clinical
Swab for resistance or uncertainty
Management:
Leave nappies off for as long as possible
Change regularly, use barrier emollient creams liberally
Talcum powder after washing to help properly dry the area
Loose fitting nappies to avoid irritation
Mild hydrocortisone cream for 7-14 days for inflammation
Daktacort cream (miconazole + hydrocortisone) or antifungal cream for suspected candida infection 2-3x daily for 7-10 days after the rash clears
eczema herpeticum
Background:
Viral herpes simplex or VZV skin infection in those with atopic dermatitis
Pathology:
Atopic dermatitis leads to poor skin barriers in some areas making contact with viral lesions easier for spreading and causes more widespread severe skin flare up
Aetiology:
Most commonly HSV-1 or VZV
Risk factors:
Atopic dermatitis
eczema herpeticum presentation, ix and mx
Presentation: Widespread, painful, vesicular rash - affects any area Pus filled vesicles, sometimes itchy After bursting, leave punched out ulcers with red base Fever Lethargy Irritability Reduced oral intake LAP
Investigation/diagnosis:
Clinical diagnosis
Viral swabs to confirm
Management:
Aciclovir (oral for mild-mod or IV if severe)
Complications - bacterial superinfection needing antibiotics
Hand foot and mouth disease and presentation
Background:
Complications - dehydration, bacterial superinfection, encephalitis
Pathology:
Incubation usually 3-5 days
Viral infection transmitted via lesion contact or respiratory droplets
Aetiology:
Coxsackie A virus
Presentation:
URTI - fatigue, sore throat, dry cough, fever
After 1-2 days small mouth ulcers appear followed by blistering red spots across the hands, feet and mouth mostly
Painful ulcers, particularly on the tongue
May be itchy
hand foot and mouth disease ix and mx
Investigation/diagnosis:
Clinical diagnosis
Dehydration status
Management:
Supportive - good fluid intake, simple analgesia and antihistamines if itchy or painful
Spontaneously resolves within 7-10 days
Educate on high transmission - avoid sharing towels, bedding, wash hands regularly especially when handling dirty nappies
chicken pox
Background:
Complication: chickenpox induced pneumonia, bacterial superinfection, dehydration, conjunctival lesions, encephalitis/ataxia
Do NOT use NSAIDs as this worsens the rash and symptoms
Pathology:
Highly contagious, spread via direct contact with lesions or infected respiratory droplets
Patients become symptomatic 10 days - 3 weeks after exposure
Stops being contagious after lesions have crusted over
After viral infection presents, virus can lay dormant in sensory dorsal root ganglion cells and cranial nerves which can reactivate later in life as shingles or ramsay hunt syndrome
Aetiology:
VZV infection
chicken pox presentation
Presentation:
Vesicular, raised rash, widespread
Erythematous
Blistering lesions
Usually starts on the trunk or face and spreads outwards over 2-5 days
Eventually lesions scab over and stop being contagious
Fever
Itch
General fatigue and malaise
In pregnancy <28 weeks can cause congenital varicella syndrome
In pregnancy around time of delivery can cause life threatening VZV infection
chicken pox ix and mx and prevention
Investigation/diagnosis:
Clinical
Management:
In neonates - IV acyclovir
Usually no treatment in otherwise healthy children
Aciclovir in immunocompromised patients 14 years + presenting within 24 hours.
Calamine lotion and chlorpheniramine (antihistamine) for itching
Avoid school and pregnant women and immunocompromised patients until lesions dry and crust over (5 days usually)
Prevention:
Ig VZV given to unexposed pregnant women
Pityriasis rosea
Background:
Very common in teenagers and young adults
Generalised self limiting rash with unknown cause
NOT contagious - no need to keep off school
Pathology:
Not fully understood
Aetiology:
May be caused by HHV-6 or HHV-7 but no definitive cause is known
Risk factors:
More common in women
More common in ages 10-35
Pityriasis rosea presentation, Ix and Mx
Presentation:
Prodromal - headache, fatigue, loss of appetite, general malaise
Rash begins with large Herald patch - faint pink/red scaly patch usually >2cm on the torso
2 days after the rest of the rash spreads - faint red/pink, slightly scaly and oval shaped lesions usually <2cm
Can form characteristic ‘christmas tree’ pattern on ribs or torso
Dark skin - lesions can be grey coloured or darker in colour than skin
Itchy
Investigation/diagnosis:
Clinical diagnosis
Management:
Resolves spontaneously within 3 months
Can leave skin discolouration for an additional few months
Educate on course and that it is NOT contagious
Symptomatic relief (emollients, topical steroids, antihistamines) for itching
Erythema infectiosum
Background:
AKA slapped cheek/5th disease
Very common childhood infection occurring between the ages of 3-15 years
Pathology:
Spread via droplet transmission, blood/bone marrow transplant or vertical transmission (mum-baby)
Typically takes 4-20 days incubation
Lifelong immunity after being exposed to the virus
Aetiology:
Parvovirus B19
Risk factors:
Most common in children
Erythema infectiosum presentation and differentials
Presentation:
Asymptomatic in 25% of infections
Non-specific coryza symptoms
Headaches
Rhinitis
Sore throat
Low grade fever
Typically 7 days after being symptoms free develop facial rash - slapped cheek red face rash
Can spread to the rest of the body 2-3 days after appearing on the face
Arthropathy (more common in adults than children)
Differentials:
Rubella: very similar rash over the whole body
Measles: check for Koplik spots
Scarlet fever: look for strawberry tongue
Roseola: similar rash
Drug eruption: new medications?
erythema infectiosum Ix and Mx
Investigation/diagnosis:
Clinical diagnosis
If uncertain/pregnant - PCR test for parvovirus B19
Bloods - specific to IgM and IgG checking for immunity and current infection
Management:
Self limiting viral infection
Regular OTC analgesia, symptomatic management
Avoid any immunocompromised or pregnant people
Do NOT need to avoid school, but do need to make anyone pregnant at the school aware
Pregnancy:
30% chance of passing infection onto baby
Baby fatality 10% if infected, higher in the first trimester
Can cause congenital abnormality
If been in contact with someone infected, must be investigated (ask if any previous history of parvovirus in childhood, bloods and PCR)
If they have active infection: refer to foetal medicine unit to check for foetal infection
Impetigo
Background:
Contagious infection, should keep children off school during
Classified into bullous (always caused by staph. aureus) and non-bullous
Complications - cellulitis, sepsis, scarring, post. Strep glomerulonephritis, staph. Scalded skin syndrome, scarlet fever.
Pathology:
Superficial bacterial skin infection
Occurring when bacteria enter via break in skin barrier
Bullous impetigo - staph. Aureus bacteria produce epidermolytic toxins that break down proteins holding the skin together.
Causes fluid filled vesicles to form under the skin
Aetiology:
Most commonly staph. Aureus bacteria
Less commonly strep. pyogenes
Risk factors:
Eczema or dermatitis
Bullous - more common in neonates and children <2 years
Impetigo presentation
Non-bullous - typically around the nose/mouth. Exudate dries into ‘GOLDEN CRUST’. Often do NOT cause systemic symptoms
Bullous - 1-2 cm vesicular lesions that grow in size then burst. Exudate dries forming ‘GOLDEN CRUST’. Heal without scarring. Lesions can be painful and itchy. More common for systemic symptoms to occur (fever, malaise) and this is called staphylococcal scalded skin syndrome.
impetigo Ix and Mx
Investigation/diagnosis:
Clinical diagnosis
Swab of lesions to confirm
Management:
Fusidic acid (topical) for localised non-bullous impetigo
Antibiotics (flucloxacillin) for widespread or more severe impetigo
Advice on good hand hygiene, not touching lesions, avoiding sharing face towels and cutlery, must be kept off school while unwell until lesions heal or have been treated with antibiotics for at least 48 hours.
Paronychia
Background:
Common infection of the skin next to the nail
Chronic paronychia - infection/inflammation for >6 weeks
Pathology:
Infection of the skin besides the nail fold
Aetiology:
Bacterial (staph. aureus) or fungal infection (candida)
Risk factors:
Hands in water for long periods of time (cleaners, bartenders, beauticians etc.)
Injury to the skin around the nail (nail biting, eczema or splinters)
Artificial nails
Gloves for prolonged period of time
Paronychia presentation, Ix and Mx
Presentation: Collection of pus Swelling Erythema Painful and tender Nail may become infected or damaged
Investigation/diagnosis:
Clinical diagnosis
Swab for uncertain species and treatment
Management:
Fusidic acid and warm water soaks, simple analgesia 1st line
Flucloxacillin or erythromycin for bacterial infection
Pus drainage
Chronic paronychia - keep hands warm and dry, avoid triggers, wear comfortable shoes (toenails), treat underlying skin conditions, hydrocortisone for inflammation, clotrimazole cream or terbinafine oral antifungals. Operation to open infected area and allow drainage and healing
Non-blanching rash
Background:
Associated with bacterial meningitis, all non-blanching rash is treated as meningococcal sepsis until proven otherwise
Pathology:
Large purple rash from haemorrhage/bleeding under the skin from blood vessel leaking into skin tissue
Petechiae - Small <3mm, non-blanching red/purple spots from burst capillaries
Purpura - larger 3-10mm non-blanching, red/purple, macules or papules from leaking blood vessels under the skin
Aetiology:
Bacterial meningitis (meningococcal septicemia)
henoch-Schonlein purpura (HSP)
Idiopathic thrombocytopenic purpura (ITP)
Acute leukaemias
Haemolytic uraemic syndrome (HUS)
Mechanical cause - strong coughing, vomiting, breath holding
Traumatic - tight pressure on the skin e.g. non-accidental injury
Viral illness - influenza and enterovirus typically
non-blanching rash presentations
Non-blanching rash
Purpura
HPS - rash on legs and buttocks, may have associated abdominal or joint pains
ITP - develops over several days in otherwise well child
Acute leukaemias - gradual development of petechiae, anaemia, LAP and hepatosplenomegaly
HUS - rash with oliguria and anaemia often recent diarrhoea
Mechanical - petechiae around the ‘superior vena cava distribution’ above the neck and most prominent around the eyes
Traumatic - specific areas only
Non-blanching rash Ix and Mx
Investigation/diagnosis:
Exclude meningitis, HUS, leukaemias, HSP etc.
Bloods - FBC, U+Es, CRP, ESR, coagulation, ESR, blood cultures,
Meningococcal PCR
LP
BP - HTN associated with HSP and HUS and hypotension with septic shock
Urine dipstick - proteinuria and haematuria suggest HUS
Safeguarding
Management:
Urgent referral and investigation in secondary care unless there is a clear unconcerning cause
Manage underlying cause
Ringworm/tinea infection
Background:
Tinea capitis - affecting the scalp
Tinea pedis - affecting the foot (athletes foot)
Tinea cruris - of the groin or leg
Tinea corporis - of the torso/body
Onychomycosis - fungal nail infection
Tinea incognito - more extensive fungal skin infection resulting from use of steroids on the area. Often occurs when misdiagnosed as dermatitis, accelerates growth of fungus by weakening the immune system via steroid use
Pathology:
Spread via contact with infected individual, animal or soils
More likely to occur in areas with sweaty, moist, damp environments such as changing rooms
Aetiology:
Ringworm - tinea fungal infection of the skin
Most common fungus causing ringworm is trichophyton
tines infection risk factors and presentation
Risk factors:
Tinea capitis - more common in children
Presentation:
Itchy, erythematous and scaly rash
Well demarcated
Often one or several rings/circular shaped areas that spread outwards
Edge is more prominent than the centre
Tinea capitis - associated with hair loss, itching, dryness and erythema of the scalp
Athletes foot (tinea pedis) - white/red flakey, cracked, itchy patches between the toes. May split and bleed.
Onychomycosis - thickened, discoloured and deformed nails
Tinea incognito - fewer scales, less well-demarcated border
tines infection Ix and Mx
Investigation/diagnosis:
Clinical diagnosis
Scraping for microscopy and culture to confirm
Management:
Antifungal creams - clotrimazole and miconazole
Antifungal shampoos - ketoconazole (tinea capitis)
Oral antifungal medications - fluconazole, griseofulvin and itraconazole
Nail infection - amorolfine nail lacquer for 6-12 months or oral terbinafine if this fails (needs LFTs before and whilst taking)
Daktacort for mild itching
Lifestyle advice:
Loose, breathable clothing
Keep affected area clean and dry
Avoid sharing towels, clothes and bedding
Use separate towel for feet (tinea pedis)
Avoid scratching and spreading to other areas
Wear clean dry socks every day
Verruca and warts
Background:
Benign epidermal neoplasms
Over 100 subtypes of HPV and different subtypes associated with different clinical lesions
Types: (examples not exhaustive list)
Common warts: dome shape nodules, common on hands, may have fine digit like projections caused by HPV 2, 27 and 57
Plane warts: smooth, flat topped papules common on the face, may have brownish colour and caused by HPV 3 and 10
Plantar warts: found on soles of feet, can be painful and scaly, may have dark punctate spots caused by HPV 1, 2, 4, 27 and 57
Anogenital warts: occur on genitals and spread through sexual contact. May be small or coalesce into larger lesions called condylomata acuminata caused by HPV 6 and 11
Filiform warts: eye or face typically have fingerlike projections
Epidermodysplasia verruciformis: rare genetic condition of chronic cutaneous infection starting out as flat warts then developing into skin cancer
Pathology:
Spread via direct contact with lesion or sharing towels, damp environment like pools etc.
Aetiology: Human papillomavirus (HPV)
HPV infection presentation
Presentation:
Infections of mucous membranes like URT can cause respiratory papillomatosis causing voice changes and high pitched breath sounds if the larynx is infected
Anal and genital infections tend to be skin coloured, range in size and have califlower like surface. Typically painless, can be itchy, burning local pain or bleeding
HPV investigation and prevention
Investigation/diagnosis:
Clinical diagnosis
Mucous membrane infections may need endoscopy (if URT suspected) or regular pap or acetic acid tests of cervix after 21 years old even if symptoms are subclinical
Cervical smears detect HPV virus after 25 years old every 3 years until age 50 when becomes every 5 years
Definite diagnosis needs biopsy microscopy confirmation
Prevention:
HPV vaccine nationally against HPV 16 and 18
Now switched to protect against HPV 16, 18, 6 and 11 so is also protective against genital warts
Wart and verrucae management
Black tape method: cut a piece of duct tape as close to the size of the wart as possible. Leave tape on wart in place for 6 days (if falls off, replace) after 6 days remove the tape and soak the area in water. Repeat the process until the wart is gone or for up to 2 months.
Most resolve without treatment: watch and wait if not painful
Topical salicylic acid first line: pared down wart prior to application then daily treatment for at least 12 weeks
Cryotherapy: 2 wkly liquid nitrogen given by clinician. May be painful and cause bleeding. Avoid in young children
Anogenital: may resolve spontaneously, remain same or increase in size. Need to be referred to a sexual health clinic for diagnosis, STI screening and management. There is a very long latent period of HPV so reassure pt it does not mean infidelity
Podophyllotoxin cream/solution self application for soft, non-keratinised external warts for 3 days BD
Imiquimod 5% for keratinised lesions and non-keratinised external lesions apply 3 x weekly until resolution or for up to 4 months
Surgical removal
All treatments cause burning, itch and pain
Condoms not reliably protective
95% genital warts not associated with high risk neoplasm transformation however types 16 and 18 are high risk of anogenital cancers
Otitis externa
Background:
Acute (<3 weeks)
Chronic (>3months)
Very common and more than 1% of people will be diagnosed with the conditions each year
Affects all ages but incidence peaks between ages 7-12
Complications can include abscess, inflammation of tympanic membrane, malignant otitis
Pathology:
Inflammation of the external ear canal +/- infection
Aetiology:
Bacterial infection
Disturbing/damaging cell lining of the ear canal e.g. excessive cotton bud use or hot tubs causing inflammation
Risk factors:
Diabetes or radiotherapy to the head/neck increase the risk of malignant otitis
Otitis externa presentation and investigation
Presentation:
Ear pain, itching, discharge and hearing loss
Swollen, red or eczematous ear canal and/or external ear
Usually systemically well and not bothered by infection
Ear may leak fluids, look wet and crusty and may smell
Investigation/diagnosis:
History/clinical diagnosis
Ear examination
Ear swab for persistent or recurrent symptoms
Otitis externa management
Paracetamol or ibuprofen (codeine for severe pain up to 60mg) analgesia
Topical preparation (Otomize spray) containing dexamethasone and neomycin. Also can use steroid eye drops for simple otitis externa cases. Use for 7 days but up to 14 if symptoms persist, 2-3 drops 3-4x daily. Tilt ear up and back (or back and down if child <3 years), press tragus and keep head tilted to the side for a few moments to help keep fluid in the ear
Do NOT prescribe steroids if there is a perforation ! NO OTOMIZE SPRAY
https://www.safemedication.com/how-to-use-medication/ear-drops
General advice to keep ears clean, dry, avoid using cotton buds, moisturising any eczema etc.
Follow up recommended for those with severe otitis externa, chronic OE, diabetes or are immunocompromised
Suspected malignant otitis - urgent admission
Chronic otitis externa:
If fungal infection is suspected - clotrimazole or other antifungal prep used. 7-14 days T/QDS.
Irritation suspected - prescribe corticosteroid prep
Unknown cause - topical corticosteroid without antibiotic, can prescribe acetic acid spray alongside
Inadequate response - continue steroid but reduce strength
Still no response - consider trial of antifungal drug e.g. clotrimazole
Otitis media
Background:
Very common in children
Complications - otitis media with effusion (glue ear), hearing loss, perforation, recurrent infection, mastoiditis, abscess
Pathology:
Infection of the middle ear (between tympanic membrane and inner ear, where the cochlea, vestibular apparatus and nerves are located)
Bacteria enter through the throat via the eustachian tube
Often preceded by viral URTI
Aetiology:
Commonly viral infection
Strep. Pneumoniae most commonly for bacterial infection
Otitis media presentation and investigation
Presentation:
Ear pain
Reduced hearing
Fever
Cough
Coryzal symptoms
Sore throat
General malaise
Fever, vomiting, irritability and lethargy or poor feeding especially in younger children
Bright red, inflamed tympanic membrane with bulging appearance due to fluid build up
Perforation - allows discharge to travel through
Investigation/diagnosis:
ENT examination
Otitis media management
Severely unwell or uncertain diagnosis or in those <3 months with temperature 38 or those aged 3-6 months with temp 39+ - urgent paediatric referral
Mostly self limiting within 3 days but can last up to a week
Simple analgesia and supportive care (fluids)
Antibiotics for those <2 YOs with bilateral otitis media, with otorrhea (discharge)
Delayed prescription for if not cleared up within 3 days or if condition worsens
Amoxicillin 1st line for 5 days, erythromycin and clarithromycin for allergy
Glue ear overview
Background:
Otitis media with effusion
Pathology:
Middle ear is inflamed (otitis media) with fluid and causes hearing loss in affected ear
Eustachian tube becomes blocked and causes middle ear secretions to build up within the middle ear space
Possibility of secondary bacterial infection due to fluid stasis
Aetiology:
Eustachian tube blockage
Risk factors:
Otitis media
Presentation:
Hearing reduction
Dull tympanic membrane with air bubbles or visible air fluid level but can look normal
Otitis media if infection present
Investigation:
ENT exam
Audiometry to establish hearing loss
Management:
Spontaneously resolves within 3 months
Hearing aids or grommets if other comorbidities or not healing
Tonsillitis
Background:
Very common with URTIs
Peak age between 5-10 and 15-20 YOs
Complications - chronic tonsillitis, quinsy, otitis media, scarlet fever, rheumatic fever, post. Strep GN, post strep. Reactive arthritis
Pathology:
Inflammation of the tonsils
Waldeyer’s tonsillar ring - ring of lymphoid tissue making up the adenoid, tubal, palatine and lingual tonsils. The palatine tonsils are typically affected in tonsillitis
Aetiology:
Viral infection most commonly
Bacterial infection (strep. A and strep pyogenes most often)
Tonsillitis presentation, Ix and Mx
Fever Sore throat Odynophagia Poor oral intake Headache Vomiting Abdominal pain Swollen, bilaterally enlarged tonsils +/- white exudate
Investigation/diagnosis:
Centor criteria
Fever pain score - fever in 24 hours, purulence, attended within 0-3 days onset, inflamed tonsils, no cough or coryza
Exclude red flags for quinsy, meningitis and encephalitis
Management:
Viral tonsillitis - supportive Mx only, good fluid intake, analgesia for pain and fever
Safety net for persistent fever above 38.3 degrees, worsening condition
Consider delayed prescription in those with fever pain score of 2-3
Antibiotics (penicillin V/phenoxymethylpenicillin 10 day course, clarithromycin in allergy) for score 4+
Peritonsillar abscess/quinsy overview
Background:
Often follows tonsillitis
Common in teens and young adults as well as children
Pathology:
Trapped pus forming an abscess within a region of the tonsils
Aetiology:
Bacterial infection causing pus and abscess formation - most commonly strep. pyogenes , staph aureus and H. influenzae
Presentation: Unilaterally enlarged tonsils Difficult to differentiate tonsils Deviated uvula Sore throat Hot potato voice Trismus - unable to open mouth LAP and tender lymph nodes Neck pain Odynophagia
Investigation/diagnosis:
Throat exam
Clinical diagnosis
Management:
Referral to secondary ENT care for incision and drainage under GA
Antibiotics (co-amoxiclav)
Dexamethasone to settle inflammation and help recovery in some cases
Molloscum contagiosum overview
Background:
Complication can include bacterial superinfection rarely
Pathology:
Spread through direct contact or sharing items like towels or bedsheets
Aetiology:
Poxvirus - molluscum contagiosum virus
Presentation:
Small, flesh coloured papules with characteristic central dimple
Typically appear in crops of multiple lesions in a local area
Investigation/diagnosis:
Clinical diagnosis
Management:
Avoid sharing towels/flannels
Avoid picking and scratching as can cause secondary infection or scarring
Self resolving within 18 months and skin returns to normal after this
Treat any secondary bacterial infection - fusidic acid or antibiotics
Specialist referral for extensive lesions or in problematic areas like eyelids, anogenital areas etc.
Sunburn
Background:
Common, acute inflammatory response of skin to exposure to UV radiation
Pathology:
UVR causes vasodilation and release of mast cell mediators leading to inflammatory response
Less intense or short duration exposure leads to increase skin pigmentation which provides further protection against UVR induced damage
Aetiology:
UV radiation exposure
Risk factors: Duration of UVR exposure Height of sun (midday = worst) Type of UVR - UVB more potent Increasing altitude Environmental reflection Lack of sun cream or protective clothing Lighter skin pigmentation Moist skin Face, neck and torso skin is less resistant Areas of vitiligo more prone to burn Photosensitivity - SLE, acne medication (EPIDUO) Sunbed use
Sunburn presentation, Ix and Mx
Presentation: Red and hot skin Blanches on pressure Painful and tender Usually 2-6 hours post exposure Peaks 12-24 hours after onset Vesicles and bullae may form Headache, chills, malaise, N+V if more severe
Investigation/diagnosis: Assess area and degree of burn Assess for dehydration Assess for degree of pain Heat Stroke or exhaustion signs - high body temp, fatigue, weakness, dizziness, LOC, headache, N+V, rapid pulse, myalgia, altered behaviour
Management:
SAFE SUN EXPOSURE - sun creams and covering clothing
Refer deep dermal and full thickness burns, all circumferential burns, superficial burns with >3% total body surface area in those aged 16+ or >2% in those under 16. Refer those involving hands, feet, perineum, genitalia or flexures, suspected dehydration, heat stroke, shock or sepsis.
Safeguard for non-accidental injury or neglect.
Majority resolves spontaneously - good fluid intake, aloe vera after sun to soothe symptoms, emollients, simple analgesics
Herpes simplex virus
Background:
Most individuals are infected with HSV-1 by 1-2 years of age (1 = above waist)
HSV-2 tends to be with onset of sexual activity (2 = below waist)
Usually is asymptomatic
Most contagious when virus filled lesions are present but can also be shed when asymptomatic
In individuals with atopic dermatitis can present with very severe herpes virus blistering in these areas due to weakness of skin barriers (eczema herpeticum) and also can have very similar severe viral blisters in those with burn injuries.
Complications include meningitis or encephalitis if viral infection reaches the brain (typically in the TEMPORAL LOBE)
Pathology:
Primary infection occurs through a break in the mucous membranes of the mouth, throat, eyes, genitals or skin abrasions. Can also be spread via vertical transmission
Virus internalised in cells then begins lytic cycle of proliferation
Cells burst and virus spreads to other cells
Can also infect sensory neurons and lays latent there in the trigeminal ganglia (oral herpes) or sacral ganglia (genital warts) and lies dormant until an immunocompromised state allows for the virus to travel back down the neurons and infect the cells
Triggers include stress, skin damage and viral illness.
Aetiology:
HSV-1 and HSV-2
Enveloped, double stranded DNA viruses
Risk factors:
Triggers include stress, skin damage and viral illness.
Herpes simplex oral infection presentation, Ix and Mx
Oral: Often asymptomatic Tingling or burning sensation Blisters appearing on the sides of the mouth, heal within a few weeks and often painful Lesions on palate, lip, gums, tongue LAP Pharyngitis
Investigation/diagnosis: Clinical diagnosis PCR viral DNA Viral cultures Viral antibodies
Management: Usually self limiting Topical or systemic antivirals within prodromal phase to help speed up recovery Topical analgesic OTC for oral lesions Acyclovir, famciclovir or valacyclovir
slipped upper femoral epiphysis background and pathology
Background:
Acute - 10-15% occurs suddenly and normally spontaneously
Chronic - 85% is a steady slippage occurring progressively
Typically seen in ages 10-13, adolescence
Stable - can walk
Unstable - unable to walk (10% case) and is high risk of osteonecrosis
Pathology:
A slippage between the neck and head (capital epiphysis) of the femur
Physis (growth plate) of the femur is weak and unstable during the growth phase before ossification and is supported by the perichondrial ring helping resist shearing forces holding the head and neck together.
Weakness in the proximal femoral physis/perichondrial ring or factors inducing stress to the hip joint at the growth plate during growth periods leads to displacement of the capital femoral epiphysis
The metaphysis (neck of the femur) is displaced anteriorly and superiorly leads to slipped state
If severe can cut off blood supply causing avascular osteonecrosis
slipped upper femoral epiphysis causes
Mechanical - local trauma, obesity
Hormonal - testosterone weakening the physis
Hypothyroidism
Radiotherapy and chemotherapy to the hip
slipped upper femoral epiphysis presentation
Uni or bilateral (usually unilateral)
Discomfort in the hip, groin, medial thigh or knee during walking
Limping
Pain accentuated in running and jumping
Limited hip motion especially internal rotation
When flexed the hip externally rotates
Mild-moderate shortening of the affected leg in chronic cases
slipped upper femoral epiphysis Ix and mx
Investigation/diagnosis:
Clinical
XR using Kline’s line or trethowan’s sign using frog leg lateral XR view
Management:
Immobilise limb, non-weight bearing
Analgesia and orthopaedic referral
Surgery to stabilise the joint via percutaneous pin fixation
osgood schlatter disease background and pathology
Background:
Common cause of knee pain in adolescents
More common in boys during periods of rapid growth
Pathology:
Repeated pulling on the tendons on the growth plate of the tibia causing repeated microtrauma, inflammation of the apophysis resulting in apophysitis during fast growth of the bones
osgood schlauer disease presentation
Knee pain over the tibial tuberosity during activity like running or jumping
Usually unilateral but can be bilateral
Localised pain worse with exercise improves with rest
Swollen and tender tibial tuberosity
No effusion
osgood schlauer disease Ix and mx
Investigation/diagnosis:
Knee examination and hip examination (referred pain)
Management:
Usually settles over weeks or months but can persist for 1-2 years
Simple analgesia
Intermittent ice pack application especially after activity
Patients may continue normal activity but may need to modify the duration, frequency or intensity (limiting running or jumping)
transient synovitis background, pathology and causes
Background:
AKA irritable hip
The most common cause of limp in children
Often follows a viral infection or after a fall/injury
Most common in ages 3-10
Self resolving
Pathology:
Inflammation of the synovial lining of the joint (usually the hip joint)
Cross immune inflammation resulting in inflammation of the joints following a viral infection
aetiology:
viral infection
trauma or injury
transient synovitis presentation
New onset limp Pain in hip, knee, groyne or thigh Refusal to weight bear Usually unilateral Systemically well but may follow recent viral infection
transient synovitis Ix and mx
Investigation/diagnosis:
Hip examination R/O septic arthritis, juvenile arthritis
Management:
Self-resolving condition
Rest - should begin to improve within 3 days and better within 2 weeks
NSAIDs analgesia
Avoid sports and strenuous activity until they are completely better
juvenile idiopathic arthritis and subtypes
Refers to condition affecting children and adolescents where autoimmune inflammation occurs in the joints
Diagnosed where there is arthritis without any other cause lasting >6 weeks in patient under the age of 16
Key features are joint pain, swelling and stiffness
Subtypes: Systemic Polyarticular Oligoarticular Enthesisits related Juvenile psoriatic
systemic JIA
AKA still’s disease
Systemic illness that can occur throughout childhood
Typical features are subtle salmon pink rash, high swinging fevers, enlarged lymph nodes, weight loss, joint inflammation and pain, splenomegaly, muscle pain, pleurisy and pericarditis
Antinuclear antibodies and RFs typically negative but inflammatory markers CRP, ESR, platelets and serum ferritin are raised
Key complication is macrophage activation syndrome with severe immune system activation and massive inflammatory response. Acutely unwell child with disseminated intravascular coagulation, anaemia, thrombocytopenia, bleeding and non-blanching rash.
Life threatening emergency - key investigation is finding low ESR
polyarticular JIA
In 5 joints or more
Tends to be symmetrical and can affect small joints of hands and feet as well as large joints
Minimal systemic symptoms (mild fever, anaemia, reduced growth)
RF -ve usually described as seronegative; seropositive patients tend to be older children/adolescents and disease more similar to rheumatoid arthritis in adults
oligarticular JIA
Involves 4 joints or less
Usually only affects single joint (monoarthritis)
Tends to be larger joints and more common in girls under age 6
Classic feature is anterior uveitis (must be referred to ophthalmologist)
Tend not to have systemic symptoms and inflammatory markers are normal/mild
ANAs often positive but RF usually negative
enthisitis related JIA
More common in male children over age 6
Thought of as a paediatric version of seronegative spondyloarthropathy conditions (ankylosing spondylitis, psoriatic arthritis, reactive arthritis and inflammatory bowel disease-related arthritis. Patients have inflammatory arthritis in the joints as well as enthesitis)
MRI can demonstrate enthesitis but cannot distinguish cause (stress or autoimmune)
Majority of patients are HLA B27 positive
Prone to anterior uveitis and should be referred to ophthalmologist even if asymptomatic
Tender to localised palpation of entheses: commonly in IP, wrist, greater trochanter, quad insertion at ASIS, quad/patella tendon, achilles, MCP areas
juvenile psoriasis arthritis
Seronegative arthritis associated with psoriasis
Pattern of joint involvement varies but associated with several skin signs: psoriasis, nail pitting, onycholysis (separation of nail from bed), dactylitis, enthesitis
JIA management
Paediatric rheumatology referral and MDT NSAIDs Steroids (oral, IM, intra articular) DMARDs (methotrexate) TNF inhibitors (etanercept, infliximab)
perthes disease background and pathology and risk factors
Background:
Perthes’ disease is a degenerative condition affecting the hip joints of children
Typically between the ages of 4-8 years.
Around 10% of cases are bilateral
Pathology:
It is due to avascular necrosis of the femoral head, specifically the femoral epiphysis.
Impaired blood supply to the femoral head causes bone infarction.
Risk factors:
Perthes’ disease is 5 times more common in boys.
Perthes disease presentation, Ix and Mx
Presentation:
hip pain: develops progressively over a few weeks
limp
stiffness and reduced range of hip movement
x-ray: early changes include widening of joint space, later changes include decreased femoral head size/flattening
Investigation/diagnosis:
plain x-ray
technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms persist
Management:
To keep the femoral head within the acetabulum: cast, braces
If less than 6 years: observation
Older: surgical management with moderate results
Operate on severe deformities
Prognosis
Most cases will resolve with conservative management. Early diagnosis improves outcomes.
Complications
osteoarthritis
premature fusion of the growth plates
EBV/MONO background and pathology
Background:
EBV AKA human herpesvirus 4 is widespread and one of the most common human viruses worldwide
Member of the herpes virus family
Most people are infected with EBV at some point in their lives
Most common cause of infectious mononucleosis (85-90% of cases)
Pathology:
Spread commonly through bodily fluids (saliva)
Infects B lymphocytes and epithelial cells
Can cause infectious mononucleosis in roughly 50% of primary infections
Also associated with tumours such as Burkitt’s lymphoma, Hodgkin’s disease, B-lymphoproliferative disease
Nasopharyngeal carcinomas and oral hairy leukoplakia can also be associated.
In congenital infection can cause X linked lymphoproliferative syndrome
Can also play a role in autoimmune diseases like SLE, RA and MS but pathology is unknown.
Primary infection is often mild or asymptomatic or causes mumps.
After primary infection the virus becomes latent however in immunocompromised individuals may reactivate
Aetiology:
HHV-4/EBV viral infection
Risk factors:
Immunocompromised - risk of reactivation of latent infection
EBV/MONO presentation
Fatigue Fever Inflamed throat Lymphadenopathy Hepatosplenomegaly Rash
EBV/MONO Ix and prevention
Clinical diagnosis (difficult due to vague presentation) PCR and viral antibodies (MONOSPOT test - looks for heterophile antibodies) Bloods - FBC (WCC and monospot test), LFTs (raised ALT)
prevention:
good hygiene, avoid kissing or sharing bodily fluids, personal items such as drinks
EBV/MONO management
Usually self limiting within 2-4 weeks, fatigue can last for longer
Do not need to isolate from school (with infectious mononucleosis)
Arrange hospitalisation for signs of dehydration, stridor or complication such as ruptured spleen
Avoid exercise for at least one month after recovery due to risk of splenic rupture
Fluid intake
Rest
Avoiding kissing, sharing personal items, drinks
Regular analgesia as needed
Treat immunocompromised states
Vesicoureteric reflux (VUR) overview
Background:
Abnormal backflow of urine from the bladder into the ureter and kidney.
Relatively common abnormality of the urinary tract in children and predisposes to urinary tract infection (UTI)
Found in around 30% of children who present with a UTI.
As around 35% of children develop renal scarring it is important to investigate for VUR in children following a UTI
Pathophysiology:
ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
therefore shortened intramural course of the ureter
vesicoureteric junction cannot, therefore, function adequately
Aetiology:
Developmental anomaly
Presentations
antenatal period: hydronephrosis on ultrasound
recurrent childhood urinary tract infections
reflux nephropathy
term used to describe chronic pyelonephritis secondary to VUR
commonest cause of chronic pyelonephritis
renal scar may produce increased quantities of renin causing hypertension
Investigation/diagnosis:
VUR is normally diagnosed following a micturating cystourethrogram
a DMSA scan may also be performed to look for renal scarring
The table below summarises the grading of VUR
Grade
I - Reflux into the ureter only, no dilatation
II - Reflux into the renal pelvis on micturition, no dilatation
III - Mild/moderate dilatation of the ureter, renal pelvis and calyces
IV - Dilation of the renal pelvis and calyces with moderate ureteral tortuosity
V - Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity
Complications:
Pyelonephritis
Recurrent UTI
febrile seizure background and features
Background:
Febrile convulsions are seizures provoked by fever in otherwise normal children. They typically occur between the ages of 6 months and 5 years and are seen in 3% of children.
Clinical features:
usually occur early in a viral infection as the temperature rises rapidly
seizures are usually brief, lasting less than 5 minutes
are most commonly tonic-clonic
types of febrile seizure and characteristics
Simple - <15 mins - generalised seizures (tonic clonic most commonly) - typically no recurrence within 24 hours - should have complete recovery within an hour
Complex - 15-30 minutes - focal seizures - may have repeat seizures within 24 hours
Febrile status epilepticus - > 30 minutes
febrile seizure management and prognosis
Management following a seizure
children who have had a first seizure OR any features of a complex seizure should be admitted to paediatrics
Prognosis
the overall risk of further febrile convulsion = 1 in 3. However, this varies widely depending on risk factors for further seizure. These include: age of onset < 18 months, fever < 39ºC, shorter duration of fever before seizure and a family history of febrile convulsions
If there are recurrences, try teaching parents how to use rectal diazepam or buccal midazolam. Parents should be advised to phone for an ambulance if the seizure lasts > 5 minutes
regular antipyretics have not been shown to reduce the chance of a febrile seizure occurring
febrile seizure link to epilepsy
risk factors for developing epilepsy include a family history of epilepsy, having complex febrile seizures and a background of neurodevelopmental disorder
children with no risk factors have 2.5% risk of developing epilepsy
if children have all 3 features the risk of developing epilepsy is much higher (e.g. 50%)
cystic fibrosis background and pathology
Background:
One of the most common life threatening autosomal recessive conditions
1 in 2000 live births
1 in 25 people carry a copy of the faulty gene (carriers)
All UK babies undergo screening programme
Pathology:
Mutations in the CF transmembrane conductance regulator (CFTR) gene on chromosome 7
Deranged transport of chloride and/or other ions, such as Na and bicarbonate
Leads to an alteration in viscosity and tenacity of mucous produced at the epithelial surfaces and to increased salt content in sweat gland secretions
The changes in the composition of airway surface liquid predispose the lung to chronic pulmonary infections and bronchiectasis.
The lungs of babies born with CF are structurally normal at birth, frequent respiratory infections soon develop and are the presenting feature.
The resultant inflammatory response damages the airway, leading to progressive bronchiectasis, airflow limitation and eventually respiratory failure.
20% develop ABPA (allergic bronchopulmonary aspergillosis).
Mycobacterial colonisation affects up to 20% of children, making a rapid deterioration
of condition.
In the newborn, thick tenacious intestinal secretions cause small bowel obstruction
(meconium ileus), an early manifestation of CF.
cystic fibrosis causes and risk factors
Aetiology:
Mutations in the CF transmembrane conductance regulator (CFTR) gene on chromosome 7
Risk factors:
Caucasian
Family history
cystic fibrosis presentation in neonates
Meconium ileus [obstruction due to impaction of thick meconium] FTT (Failure to thrive) Rectal prolapse Fatty stool Cyanosis Finger clubbing Bilateral lung crackles
cystic fibrosis presentation in children and young adults
Respiratory: cough, wheeze, recurrent infections, bronchiectasis, pneumothorax, haemoptysis, respiratory failure, cor pulmonale - nasal polyps, sinusitis Bilateral lung crackles Fatty stool Cyanosis Finger clubbing
GI:
Pancreatic insufficiency (DM, Steatorrhoea), Malabsorption
Intestinal obstruction (content impaction),
Gallstones, Cirrhosis, GORD, …
Other
Male Infertility
Osteoporosis, Arthritis, Hypertrophic pulmonary osteoarthropathy (HPOA)
Vasculitis
cystic fibrosis investigations
Usually based on sweat test and genetic assessment
Sweat test - sweat Na and Cl >60mmol/L (1st line)
Genetic blood DNA analysis screening and counselling
Faecal elastase - exocrine pancreatic dysfunction
Bloods - FBC, U+Es, LFT, clotting screen, vitamins A, D and E, glucose tolerance test annually from 12 years
Sputum culture
CXR - hyperinflation
Abdominal USS - fatty liver, cirrhosis, chronic pancreatitis
DEXA bone scan - osteoporosis
Spirometry - obstructive lung disease
cystic fibrosis management
Holistic management (psychosocial + physical wellbeing): MDT: physician, GP, physiotherapist, specialist nurse, and dietician
Chest:
Respiratory Physiotherapy (postural drainage, airway clearance techniques). Abx
(Antibiotics) for acute infective exacerbations and prophylactically.
Mucolytics, Bronchodilators
Chronic Pseudomonas infection is an important predictor of survival.
Annual CXR surveillance
GI
Pancreatic enzyme replacement, vitamin supplements (A, D, E, K) …
Other: Mx of CF-related DM Screening (DEXA scan) >> treatment of osteoporosis Advanced lung disease: Oxygen Diuretics (cor pulmonale) Non-invasive ventilation Lung or heart/lung transplantation
cystic fibrosis prognosis and complications
Complications:
Pseudomona
Lung damage associated with persistent infection with P. aeruginosa is a major cause of
morbidity and mortality in patients with CF.
Nebulized antipseudomonal antibiotic therapy, e.g. Tobramycin, improves lung
function, slows the rate of respiratory decline and decreases the risk of infective
exacerbations and hospitalisation in these patients.
Regular sputum culture for Pseudomonas allows early detection and treatment.
Prognosis:
Today: Median survival is now ~ 41yrs in the UK.
In future: A baby born today would expect to live longer.
Post-lung-transplant survival = 5 years.
