emergency paeds Flashcards
paeds resp rates infant (upto 1 year) toddler (1-3) preschooler (3-6) school-age (6-12) adolescent (12-18)
Infant (birth–1 year) 30–60/m Toddler (1–3 years) 24–40/m Preschooler (3–6 years) 22–34/m School-age (6–12 years) 18–25/m Adolescent (12–18 yrs) 12–16/m
paeds HR Infant (birth–1 year) Toddler (1–3 years) Preschooler (3–6 years) School-age (6–12 years) Adolescent (12–18 years)
Infant (birth–1 year) 100-160/m Toddler (1–3 years) 90 -150 /m Preschooler (3–6 years) 80 -140/m School-age (6–12 years) 70 -120/m Adolescent (12–18 years) 60 -100/m
immunisation history
Birth – BCG for at risk infants
2 months – DTaP, IPV, HIB, Hep B
PCV
Men B
Rotavirus
3 months – DTaP, IPV, HIB, Hep B
Rotavirus
4 months – DTP, IPV, HIB, Hep B
Men B
PCV booster
12 months – HIB/ Men C
PCV booster
Men B booster
MMR
3/4 years – DPT Polio
MMR
14 (School yr 9) Td/IPV
Men ACWY
when does a kid smile sit unaided walk talk handedness
Smile – 6 weeks Sit unaided – 6 months Walk – 12 months Talk – 12 months Handedness
clinical Sx
mechanism
Mx
of paracetamol
Early:
• abdominal pain, vomiting
Later (12 h to 24 h):
• liver failure
Mechanism initial gastric irritation Toxic metabolite (NAPQI) produced by saturation of liver metabolism
Mx
Risk assessed by measuring plasma paracetamol concentration
Treat with intravenous acetylcysteine if concentration is high or liver function abnormal
clinical Sx
mechanism
Mx
of button batteries
Abdominal pain
Gut perforation and stricture formation
mechanism
Leakage: corrosion of gut wall due to electrical circuit production
Mx
X-ray of chest and abdomen to confirm ingestion and identify position
Endoscopic removal is recommended if in the oesophagus, the object fails to pass, or symptoms are present (e.g. abdominal pain or melaena)
clinical Sx
mechanism
Mx
of CO
Early:
• headache, nausea
Later:
• confusion, drowsiness leading to coma
mechanism
Binds to haemoglobin causing tissue hypoxia
Mx
High-flow oxygen to hasten dissociation of carbon monoxide
The role of hyperbaric oxygen therapy is unclear
clinical Sx
mechanism
Mx
of salicyclates
Early:
• vomiting, tinnitus
Later:
• respiratory alkalosis followed by metabolic acidosis
Mechanism
Direct stimulation of respiratory centre
Uncouples oxidative phosphorylation leading to metabolic acidosis and hypoglycaemia
Mx
Plasma salicylate concentration 2–4 h after ingestion helps to estimate toxicity
Alkalinization of urine increases excretion of salicylates.
Haemodialysis also effectively removes salicylate
clinical Sx
mechanism
Mx
of TCAs
Early:
• tachycardia, drowsiness, dry mouth
Later:
• arrhythmias, seizures
mechanism
Anti-cholinergic effects, interference with cardiac conduction pathways\
Mx
Treatment of arrhythmias with sodium bicarbonate
Support ventilation
clinical Sx
mehcanism
Mx of
ethylene glycol
Early:
• intoxication
Later:
• tachycardia, metabolic acidosis leading to renal failure
mechanism
Production of toxic metabolites that interfere with intracellular energy production
Mx
Fomepizole inhibits the production of toxic metabolites; alcohol may also be used but has more adverse effects
Haemodialysis to remove toxic metabolites in severe cases
clinical Sx
mechanism
Mx
alcohol
Hypoglycaemia
Coma
Respiratory failure
Direct inhibitory effect on glycolysis in the liver and neurotransmission in the brain
Monitor blood glucose and correct if necessary. Support ventilation if required
Blood alcohol levels may help to predict severity
clinical sx
mechanism
mx
of iron
Initial: vomiting, diarrhoea, haematemesis, melaena, acute gastric ulceration
Latent period of improvement
6–12 h later: drowsiness, coma, shock, liver failure with hypoglycaemia, and convulsions
Long term: gut strictures
mechanism
Local corrosive effect on gut mucosa
Disruption of oxidative phosphorylation in mitochondria leads to free radical production, lipid peroxidation, and metabolic acidosis
Mx
Serious toxicity if >75 mg/kg elemental iron ingested
Serum iron level 4 h after ingestion is the best laboratory measure of severity
Intravenous desferoxamine chelates iron and should be administered in cases of moderate-to-severe toxicity
clinical Sx
mechanism
Mx of
hydrocarbons ie. paraffin, kerosene
Pneumonitis
Coma
mechanism
Low viscosity and high volatility makes aspiration easy, resulting in direct lung toxicity
Direct inhibitory effect on neurotransmission in the brain
Mx
No specific antidote – supportive treatment only
clinical sx
mechanism
Mx of
organophosphorus pesticides
Cholinergic effects:
• salivation, lacrimation, urination, diarrhoea and vomiting, muscle weakness, cramps and paralysis, bradycardia. and hypotension
Central nervous system effects:
• seizures and coma
Inhibition of acetylcholinesterase resulting in accumulation of acetylcholine throughout the nervous system
Supportive care
Atropine (often in large doses) as an anticholinergic agent
Pralidoxime to reactivate acetylcholinesterase
factors increased risk of recurrence for self harm
lack of regret, evidence of planning, e.g. leaving a note, and a lack of protective social factors
surgical cuases of abdominal pain
acute appendicitis
other causes if abdo pain that are not abdo originated
• lower lobe pneumonia may cause pain referred to the abdomen
• primary peritonitis is seen in patients with ascites from nephrotic syndrome or liver disease
• diabetic ketoacidosis may cause severe abdominal pain
• urinary tract infection, including acute pyelonephritis,
- pancreatitis -> acute abdo pain, serum amylase
Sx of acute appendicitis
– Anorexia
– Vomiting
– Abdominal pain, initially central and colicky (appendicular midgut colic), but then localizing to the right iliac fossa (from localized peritoneal inflammation)
signs of acute appendicitis
– Fever
– Abdominal pain aggravated by movement, e.g. on walking, coughing, jumping, bumps on the road during a car journey
– Persistent tenderness with guarding in the right iliac fossa (McBurney’s point). However, with a retrocaecal appendix, localized guarding may be absent, and in a pelvic appendix there may be few abdominal signs.
Mx of appendicitis
appendicectomy - uncomplicated
generalised guarding consistent w perforation -> fluid resuscitation and intravenous antibiotics are given prior to laparotomy
define non-specific abdominal pain
- abdominal pain which resolves in 24–48 hours.
- accompanied by an upper respiratory tract infection with cervical lymphadenopathy
what is intussusception
invagination of proximal bowel into a distal segment. It most commonly involves ileum passing into the caecum through the ileocaecal valve
most common cause of intestinal obstruction
3 m-2yrs
most serious complication of intussusception
stretching and constriction of the mesentery resulting in venous obstruction, causing engorgement and bleeding from the bowel mucosa, fluid loss, and subsequently bowel perforation, peritonitis and gut necrosis
presentation of intussusception
- Paroxysmal, severe colicky pain with pallor – during episodes of pain, the child becomes pale, especially around the mouth, and draws up the legs. There is recovery between the painful episodes but subsequently the child may become increasingly lethargic.
- May refuse feeds, may vomit, which may become bile stained depending on the site of the intussusception.
- A sausage-shaped mass – often palpable in the abdomen
Passage of a characteristic redcurrant jelly stool comprising blood-stained mucus – this is a characteristic sign but tends to occur later in the illness and may be first seen after a rectal examination.
• Abdominal distension and shock.
how to confirm diagnosis of intusussception
US and also monitor treatment TARGET SIGN
Unless there are signs of peritonitis, reduction of the intussusception by rectal air insufflation is usually attempted by a radiologist
what is the compression ventialtion ratio
compression:ventilation ratio: lay rescuers should use a ratio of 30:2. If there are two or more rescuers with a duty to respond then a ratio of 15:2 should be used
DDx for a red swollen eye
- pre-septal cellulitis • Orbital or Post-septal cellulitis. • Allergicconjunctivitis. • Bacterial conjunctivitis. • Trauma. - sub-periostal/orbital abscess - cavernous sinus thrombosis
Features of pre-septal cellulitis
- redness and discharge from one eye
- affected eye ‘stuck shut’ in the morninh
- colour/consistency depends on cause
- caused by bacteria (staph aureus, H strep, H.influenzae) chlamydia, viruses
Definition of preseptal cellulitis
inflammatory disease of the orbit limited to the tissues anterior to the orbital septum.
definition of orbital cellulitis
inflammatory disease of the superficial and deep structures of the orbit.
aetiology of preseptal
cellulitis
- Commonly follows URTI and sinusitis (ethmoid commonest).
- Respiratory pathogens (Streptococcus, Haemophilus) commonest. • Other sources: spread from skin, lachrymal ducts, middle ear etc.
Mx of cellulitis
- Admit. • IV access. • FBC/CRP, cultures. • Nose swab. • IV Ceftriaxone. • ± IV Metronidazole • (if sinuses involved) • Prompt ENT and ophthalmology review - 4h obs - Consider CT scan
Sx of meningitis
- Fever
- Irritability
- Lethargy / Drowsiness
- High pitched cry
- Loss of consciousness
- Seizures
- Poor feeding
- Vomiting
- Photophobia
DDx of fever headache and neck stiffness
- Bacterial meningitis.
- Viral meningitis.
- Viral encephalitis.
- Tuberculous meningitis.
- Cerebral abscess.
- Hydrocephalus.
- Non-accidental injury
acute Mx of bacterial meningitis
Call for senior help
Airway: apply 15L/min facial O2
Breathing: support as necessary
Circulation: IV or IO cannula
Bloods: Gas (HCO3, BE, lactate), glucose. FBC, CRP, clotting, U&E
check circulation (CRT, HR, BP) - Rx PRN
IV 20ml/kg 0.9% NaCl fluid bolus
Disability: assess: level of consciousness (GCS)
Neurology - cranial nerves, focal. Raised ICP.
Exposure - temperature rashes
LP contraindications
- cardiorespiratory instability
- signs of raised ICP: coma, low HR, high BP, papilloedema -> needs CT
- coagulation abnormalities , thrombocytopenia
- after seizures - until stabilised
- focal neurological deficits
- sogns of infection at the LP site
- concerns about menigococcal septicaemia
what is normal CSF
clear
<5 lymphocytes
0.14-0.4g/L
>50% BG
bacterial menigititis CSF
Appearance white cells protein glucose organisms
turbid
100-10000 neutrophils
increased protein
decreased glucose
S. pneumoniae - 14 days
H. influenzae - 10 days
N. Meningitis - 7 days
neonates
strep group B
Ecoli
Listeria
viral meningitis Appearance white cells protein glucose organisms
clear
<1000 lymphoctyes
normal protein
usually normal
Enteroviruses Echo, coxsackie Parechovirus Herpesviridae Herpesvirus 1 & 2 Varicella zoster CMV, EBV Herpesvirus 6 & 7 adenovirus influenza RSV measles mumps
TB meningitis Appearance white cells protein glucose organisms
turbid clear/viscous
10-500 lymphocytes
increased protein
decreased glucose
Mycobacterium TB
viral encephalitis Appearance white cells protein glucose organisms
clear
usually <1000 lymphocytes
normal protein
normal
same as viral menigitis
acute Mx of meningitis
<28 days: 3o cephalosporin + Amoxicillin + Gentamicin
1-3 mo: 3o cephalosporin + Amoxicillin
IV amoxicillin + IV cefotaxime
> 3 mo:
3m: IV cefotaxime (or ceftriaxone)
3o cephalosporin ± Amoxicillin (? Listeria)
+ Acyclovir (all age groups – until microbiology seen)
- Steroids
NICE advise against giving corticosteroids in children younger than 3 months
dexamethsone should be considered if the lumbar puncture reveals any of the following:
frankly purulent CSF
CSF white blood cell count greater than 1000/microlitre
raised CSF white blood cell count with protein concentration greater than 1 g/litre
bacteria on Gram stain - Fluids
treat any shock, e.g. with colloid - Cerebral monitoring
mechanical ventilation if respiratory impairment - Public health notification and antibiotic prophylaxis of contacts
oral ciprofloxacin is now preferred over rifampicin
N. meningitidis H. influenzae Strep pneum Group B strep E.coli Listeria
N. meningitidis - 7 H. influenzae - 10 Strep pneum - 14 Group B strep - 14 E.coli - 21 cefotaxime/ceftriaxone
Listeria - 21
other Mx of meningitis
steroids: only in childre older than 3m. <12h since 1st AB dose + purulent CSF
IV fluids: normal maintenance.
2/3 if SIADH: low serum Na/osmolality
high urine Na/osmolality
CT scan: other intracranial pathologies
Hearing test: in all within 6 weeks of presentation
acute complications of meningitis
hearing impairment local vasculitis - CN palsies - focal neuro signs - septic shock
- DIC: due to sepsis and coagulopathy
raised IC pressure: due to cerebral oedema
increased BP
decreaesd pulse/GCS
SIADH: fluid retention and reduced serum Na
hydrocephalus: obstructed by oedema/infection
cerebral abscess/subdural empyema
long term complications of meningitis
hearing loss - commonest complication, damage to cochlear hair cells
local vasculitis: focal neuro lesions
local cerebral infarction: cause seizures, can lead to epilepsy
subdural effusion - more common in infants-> bulging fontanelle, enlarging head size and/or seizures; may be asymptomatic
learning difficulties; developmental deficits
Hx and examination of barking cough and noisy breathing
preceding Sx - runny nose, fever other Sx- toxicity (very high, To) choking episode/trigger drooling voice changes/hoarseness cyanotic episodes
VACCIANTION STATUS
abnormal respiratory sounds/stridor
respiratory status - RR, WOB
DDx for barking cough and noisy breathing
viral croup (laryngeotracheoronchitis)
Acute infections
- epiglottitis
- bacterial tracheitis
- diphtheria
- peritonsilar abscess
- reteropharyngeal abscess
other non infection
- foreign body
- anaphylaxis
- burns
- UA trauma
- angioedema
- VC dysfunction
what is croup
Sx
typical age
aetiology
triad - hoarse voice - barking cough - stridor \+/- fever
6m and 6yr
aetiology
parainfluenza virus (commonest)
influenza virus, RSV, adenovirus, measles
what is stridor
- High-pitched, high-energy usually inspiratory sound.
• Caused by turbulent airflow over the upper airway.
• Expiratory with severe UA or tracheal narrowing
what is stretor
- Low-pitched, high-energy snoring sound.
* Caused by nasal obstruction, tonsil ± adenoid hypertrophy and neuromuscular weakness
what is wheeze
- High-pitched whistling usually expiratory sound.
• Suggests narrowing of lower airways.
what is the westley score include
CROUP
level of consciousness -> normal 0, disorientated= 5
cyanosis - none=0, with agitation=4, at rest=5
stridor none=0, wiht agitation=1, at rest=2
air entry - normal=0, decreased=1, markedly decreased=2
retractions- none=0, mild=1, moderate=2, severe=3
welsey score <4
severity
description
Mx
mild
Occasional barky cough.
No stridor.
No/mild retractions
Mx
Oral dexamethasone (0.15mg/kg).
Score 0 – no treatment needed.
Score <2 – discharged home; otherwise observe for 1 hour.
westley severity score 4-6
moderate
Frequent barky cough.
Stridor at rest. Mild to moderate retractions No/little distress or agitation
prompt senior review oral dexamethasone (0.15mg/kg). (or nebulised budesonide (2mg) is struggling with oral meds) oxygen if pO2 <92% observe respiratory status
westley severity score
>6
Severe
Frequent barky cough.
Stridor at rest. Marked retractions Significant distress and agitation
Mx
prompt senior review
nebulised adrenaline (0.4mg/kg) of 1:1000 solution (1ml=1mg)
aetiology of epiglottitis
Acute inflammatory swelling of epiglottis and surrounding tissues. Life-threatening emergency because of high risk of airway obstruction. Most common between 1 and 6 yrs but occurs at any age.
Most commonly caused by Haemophilus influenzae.
clinical presentation of epiglottitis
onset over hours
appearance-> toxic, very unwell, anxious, restless, irritable
temp - >38.5 severe sore throat cant drink drooling absent cough soft whispering stridor muffled, reluctant to speak
Mx of epiglotittis
Regardless of apparent severity, deterioration can occur rapidly.
• Prompt senior review.
• Call ICU, anaesthesia and ENT. • Avoid distressing the child.
• Secure airway in theatre.
DDx for fever and rash
Measles.
• Rubella (German measles).
• Slapped cheek (Fifth disease)(Parvovirus).
• Roseola infantum (Sixth disease)(Herpes 6/7). • Enterovirus (echo, coxsackie).
• Scarlet fever (Group A Streptococcus)
• Kawasaki disease
• Systemic onset juvenile idiopathic arthritis
what are measles
highly contagious
caused by RNA paramyxovirus
incubation period: 10 days to fever
14 days to rash
rash
koplik spots
conjunctivitis and coryza
cough
complications of measles
Respiratory: OM, croup, tracheitis, pneumonia. Neurological: febrile seizures, encephalitis, SSPE Other: Diarrhoea, hepatitis, myocarditis.
what is roseola infantum
- Usually in younger children (6mo-2yr). • 3-4 days of fever and malaise.
- Widespread rash when fever subsides.
what is rubella
Mild disease; incubation 15-20 days.
• Prodrome mild (low grade fever) or none.
• Widespread rash spreading from face.
• Lymphadenopathy (sub-occipital and post-
Temp oC
auricular) prominent.
slapped cheek syndrome what is it
Parovirus B19
• Fever, malaise, headache, myalgia.
• Rash appears on face a week later.
• Progress to maculopapular (‘lace-like’) rash on trunk and limbs
what is scarlet fever
Diffuse erythematous eruption generally associated with pharyngitis (Strep A).
Cough
• Rash: Diffuse blanching erythema.
raised papules-sand-paper feel
starts in groin and axilla; spreads to trunk and extremities
ass w strawberry tongue
history septicaemia
Fever
Poor feeding
Miserable, irritable, lethargy
History of focal infection, e.g. meningitis, osteomyelitis, gastroenteritis, cellulitis
Predisposing conditions, e.g. sickle cell disease, immunodeficiency
signs on examination of septicaemia
Fever
Tachycardia, tachypnoea, low blood pressure
Purpuric rash (meningococcal septicaemia)
Shock
Multiorgan failure
aetiology of septicaemia
Carried in nasopharynx: rate low in infants/young children
Droplet spread; needs prolonged close contact.
RFs of meningococcal septicaemia
age season - winter smoking preceding influenza A infection living in 'closed/semiclosed' community
Mx of pre-hospital (primary care) and emergency care
IM benzypenicillin
high flow oxygen
blue light ambulance
notify ICU and anaethesia pre-arrival appropriate senior staff present rapid ABCDE assessment high flow O2 IV/IO access: blood tests, IV ceftriaxone, Iv fluid bolus
early inotrope support
early airway support
DDx of acute antalfgic gait
- transient synovitis
- septic arthritis
- osteomyelitis
- trauma NAI
- Malignancy (leukaemia, neuroblastoma)
- perthes disease
- juvenile idiopathic arthritis
define transient synovitis
irritable hip. It is caused by temporary (transient) irritation and inflammation in the synovial membrane of the joint (synovitis). It is the most common cause of hip pain in children aged 3 – 10 years. It is often associated with a recent viral upper respiratory tract infection.
presentation of transient synovitis
Ix
- Limp
- Refusal to weight bear
- Groin or hip pain internal rotation abduction
- Mild low grade temperature
Ix
US -> fluid in joint
Mx of transient synovitis
symptomatic
simple analgesia
3-9 -> if limp s present for less than 48 hours and they are otherwise well
NEED CLEAR SAFETY NET ADVICE - attend A&E if the Sx wosern or develop fever
follow up at 48 hours and 1 week
what is septic arthritis
common bacteria
presentation
infection inside a joint
common under 4 years
staph aureus neisseria gonorrhoea - Group A streptococcus (Streptococcus pyogenes) - Haemophilus influenza - Escherichia coli (E. coli)
- Hot, red, swollen and painful joint
- Refusing to weight bear
- Stiffness and reduced range of motion
- Systemic symptoms such as fever, lethargy and sepsis
joint drainage and irrigation
what is used to measure likelihood of SA (modified Kocher criteria)
Fever >38.5oC
• WCC >12 x 109/L
• CRP >20
• Inability to weight bear
None <0.2%; 1: 3% 2: 40%
3: 93.1%
4: 99.6%
acute Ix for bone/joint infection
FBC - useful to differentiate (TS/SA; leukaemia)
CRP highly sensitive
Blood culture - should always be obtained, low yield
x-ray - always perform at baseline
US - very sensitive to identify joint effusion in SA
synovial fluid - always be obtained before ABx
+ve gram stain helps ABx choice
drainage of pus aids
Mx of bone/joint infection
- Ix: FBC, CRP, BC, Hip US
- early surfical referral for pus drainage
- do NOT delay empiric IV ABx
ABx
<3 months: IV cefotaxime or ceftriaxone
> 3 months: IV ceftriaxone
switch to oral w improvement
ABx duration: SA 2-4 weeks; OM 2-6 weeks
DDx for traumatic limp
1-4
- DDH
- septic arthritis/osteomyelitis
- Transient synovitis
Toddlers fracture
Non-accidental injury
DDx for atraumatic limp child 5-9
transient synovitis
Perthes disease
Juvenile idiopathic arthritis
DDx of adolescent >10
slipped capital femoral epiphysis
juvenile idiopathic arthritis
DDx for suspected allergic reaction
allergic reaction anaphylaxis skin: acute urticaria GUT: food poisoning, gastroenteritis Respiratory: URTI, irritant rhinoconjunctivitis. choking, viral wheeze, acute asthma exacerbation CVS: vasovagal syncope, panic attack
define anaphylaxis
Severe, life-threatening allergic reaction that is acute in onset and can cause death
criteria for anaphylaxis
acute onset of illness involving skin mucosa or both ie urticaria, angioedema
and at least one of the following
- resp compromise ie dyspnoea, wheeze, stridor, hypoxaemia, reduced PEF
- reduced BP or end organ dysfunction ie. hypotonia (collapse), syncope, incontinence
two or more of the following after exposure to likely allergen for that patient (mins to hours)
- skin or mucous membrane involvement
- resp compromise
- cardio compromise
- persistent GI Sx - crampy abdominal pain, vomiting
reduced BP after exposure to known allergen for that pt (mins to several hrs)
- infant child: low age specific systoli or >30% drop
- adolescent <90 or >30% drop
what is urticaria
- Also called hives, wheals or welts.
- Common condition affecting up to 20% of population. Typically intensely pruritic erythematous plaque.
May be associated with angioedema (swelling). Commonly categorized by chronicity:
• Acute: <6 weeks; triggers allergy, URTI, idiopathic.
• Chronic: >6 weeks; spontaneous or physical triggers
Mx of urticaria
- History and examination to make diagnosis.
- In new-onset acute urticaria where assessment does NOT suggest underlying cause, NO investigations; may consider FBC and CRP if worried about vasculitis. - High-dose non-sedating antihistamines
- ± Oral glucocorticosteroids.
Mx of paracetamol overdose
ingestion <1h and >150 mg/kg
give oral charcoal and IV anti-emetic
risk of liver toxicity based on paracetamol dose
<150mg/kg - unlikely
> 250mg/kg likely
> 12g total - potentially fatal
delay sampling to 4h after ingestion
-Paracetamol level.
• U&E – baseline renal status/risk of AKD.
• LFT – monitor ALT levels for hepatotoxicity.
• Glucose – hypoglycaemia common in liver necrosis.
• Clotting screen – INR as PT best indicator of liver necrosis.
• Venous gas –acidosis in 10% of acute liver failure.
common causes of seizures in children
- febrile convulsions
- Known epilepsy ± acute illness
• Meningitis or encephalitis
•Hypoglycaemia/hypocalcaemia
• Metabolic/Poisoning - trauma - accidental/non accidental
- drugs
- raised ICP
Hx of seizure
complications
before fit - aura/temperature during fit - duration - shaking - tongue biting - limbs involved - incontinence
- Epilepsy?; medication, compliance, Rx change.
- Fever, trauma, poisoning ingestion.
Hypoxia, hyperthermia, DIC.
• Resp: Airway obstruction; aspiration.
Pulmonary oedema; drug depression.
• CVS: Arrhythmia, Hypertension.
Ix
FBC, U&E, LFT, Clotting, Gas, Culture.
• Metabolic screen, toxicology, drug levels ± CT
features of a febrile convulsion
How will you prevent further recurrences and reassure parent
6 months - 5 years - no previous neurology
- generalised in nature
- <15 mins duration
- no IC infection/metabolic disturbance
- simple or complex
- not epilepsy
- very common in children
- due to high temp
- give antipyretic to control temperature
- prevent injury
- has a very good prognosis as they tend to stop as the children grows
- no increased risk of developing epilepsy
features of infantile spasms
age of onset 3-12 months sudden violent flexor spasms of head, trunk and limbs followed by extension of arms. • Last 1-2 seconds; occur multiple/day. • Often with developmental regression. • EEG: hypsarrthymia; Rx ACTH, steroids.
features of an absence epilepsy
age of onset 4-12 years; girls>boys - sudden onset; last few seconds (<30s) - ass w automatisms - flickering of eyes, purposeless movement of eyes/mouth EEG: 3 per second hx spike and eave -spontaneous remission in adolescence
Mx of croup
oral dexamethasone no tolerated nebulised budesonide -> rapidly decreases laryngeal mucosal inflammation -> reducing the duration and severity of croup
red flags sign of children at any age
>60 breaths/minute grunting reduced skin turgor non-blanching rash neck stiffness seizures bulging fontanelle.
essential examination for hip pain in children and why
abdomen - appendicitis
axillae anf groin - lymphadenopathy, hepatosplenomegaly and pallor points heamatological malignancy
hip
scrotum - testicular torsion
features of perthes disease
5-10 uears
avascular necrosis of the femoral head
features limp painful at times limb shortened stiffness and reduces range of movement x-ray: early changes include widening of joint space, later changes include decreased femoral head size/flattening
Diagnosis
plain x-ray - femoral head Fragmentation (radiolucency) and re-ossification (radiodensity)
technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms persist
AP + Lateral pelvic xray
Complications
osteoarthritis
premature fusion of the growth plates
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
Ix for slipped upper femoral epiphysis
x ray of the hip AP and lateral
Klein’s line is drawn
along the superior border of the femoral neck and should intersect with the growth plate.
Failure to do so suggests early SUFE.
Mx
bed rest + minimum weight bearing
surgical fixation if worsening
Signs of meningitis
Fever • Irritable • Difficult to examine • Altered LOC • Neck stiffness* • Bulging fontanelle* anterior fontanelles closes at 18 months • Opisthotinos • +ve Brudzinski sign* • +ve Kernig sign*
RFs of DDH
firstborn child, female sex, family history of DDH, breech presentation at birth, and oligohydramnios.
what is juvenile idioptahic arthritis
<16 lasts for more than 6 weeks
features pyrexia salmon-pink rash lymphadenopathy arthritis uveitis anorexia and weight loss
Ix
ANA positive
RF - (-ve)
Symptoms of osteomyelitis
inital mx
- cause -> staph aureus, strep, haemophilus influenzae
- severe pain
high temp
tenderness
joint movements is not affected
In young child/infant
Widespread limb pain difficult to localize on examination Pseudoparalysis Bone or limb swelling Erythema Refusal to bear weight or sit down Limping Older children tend to localize pain
Mx
- analgesia
- commence IV ABx better after 24-48hrs -> oral ABx for 6w
FAILS
- surgical drainage/debridement of osteomyelitis
lead to pathological fracture
Mx of Bone Joint infection
complications
<3m IV cefotaxime/ceftriaxone
> 3m IV flucoxacillin
allergic - vancomycin
2–4 weeks for SA
• 4–6 weeks for OM. oral ABx
• 2–6 weeks for pyomyositis
- Chronic infection
- Relapse
- Reinfection with different bacterial agent
- Abscess or sequestrum
- Residual pain and rigidity
- Bone deformity
- DVT
Signs of raised ICP
papilloedema reduced consciousness neurological signs cushing reflex decerebrate posturing
Ix for meningitis
bloods - FBC, U&E, CRP
ABG
blood culture
LP if CT shows no ICP
chicken pox virus name
incubation
features
Mx
varicella zoster 10-21 days fever initially itchy, rash starting on head/trunk before spreading. Initially macular then papular then vesicular systemic upset is usually mild
Mx
- calmine lotion
skl -> until all the lesions are dry and have crusted over (usually about 5 days after the onset of the rash).
complications
- secondary bacterial infection of lesions - NAIDs, invasive group A streptococcal soft tissue infections may occur resulting in necrotizing fasciitis
pneumonia
encephalitis (cerebellar involvement may be seen)
disseminated haemorrhagic chickenpox
arthritis, nephritis and pancreatitis may very rarely be seen
Ix of Bone Joint infection
- FBC + CRP
- Blood cultures
- synovial fluid before AB initiation
- xray -> : Frequently normal at baseline. Repeat
imaging 10-21 days from symptom onset shows
appearance of osteolytic changes or periosteal
elevation - US for joint effusion
- MRI within 3-5 days of onset
bone scan
