Paediatrics Flashcards
what are the three core symptoms of ADHD?
inattention impulsivity hyperactivity
symptoms of inattention
easily distracted often appears not to be listening has difficulty sustaining attention during activities avoids or dislikes tasks requiring sustained attention forgetfulness disorganised loses important items
symptoms of hyperactivity
squirms and fidgets cannot remain seated runs or climbs excessively in inappropriate situations talks excessively cannot perform leisure activities quietly
symptoms of impulsivity
blurts out answers before question is finished has difficulty waiting turn interrupts or intrudes on others
how common is ADHD in school age children
4-7%
what is the male to female ratio of adhd in children and adults
childhood - M:F = 4:1 adulthood - M:F = 1:1
affect of adhd on mortality
untreated adhd has twice the childhood mortality than no adhd
ADHD crossover with developmental disorders
13% mental retardation 47% developmental coordination disorder 40% reading/writing disorder
ADHD crossover with psychiatric disorders
7% aspergers 33% tic disorders 60% oppositional defiant disorder
comment on thee pathophysiology of ADHD
Cortical maturation happens in the same order – from the back of the head to the front – but in ADHD it happens about 3-5 years later
how is a child assessed for ADHD
symptoms may not be present in highly structured environments where there are interesting activities like the assessment itself. therefore home videos or testimonials from those involved in the child’s care/education can be important.
proposed etiologies of ADHD
neuroanatomic/neurochemical CNS insults genetic origins (as hereditary as height) environmental factors
management of adhd
education adhd parenting programme school support and liason medical (methylphenidate, atomexetine or lisdexamfetamine)
what is the prevalence of ASD
1%
what is the m:f for asd
4:1
what are the three realms of asd
communication social interaction poor behaviour and imagination rigidity
what’s the asd thing where they repeat speech called
echolalia
asd management
education and information asd parenting workshops school liason and support manage comorbidity
types of anaemia common in paediatrics
iron deficiency haemolytic - membrane/enzyme/immune haemoglobinopathies aplasia
thrombocytopenias in paeds
immune - ITP neonatal alloimmune marrow failure
clotting factor disorders in paeds
haemoglobinopathies hypercoagulable states
haematopoiesis in children
at birth basically all bones are actively haematopoietic and in childhood it becomes central bone (vertebrae, sternum, ribs and pelvis)
causes of severe anaemia at birth
haemolytic disease of the newborn (erythroblastosis fatalis) bleeding (umbilical cord or internal haemorrhage)
signs and symptoms of erythroblastosis fatalis
severe anaemia compensatory hyperplasia of blood forming organs (spleen and liver)
treatment of erythroblastosis fatalis
prevention of sensitization with Rh immune globulin IU transfusion of affected fetus
what is the physiologic anaemia of newborns
normal drop in Hb from birth which reaches a nadir at 2 months
what causes physiologic anaemia of the newborn
decreaseed rbc production plasma dilution due to increasing blood volume neonatal rbcs have a shorter lifespan
describe the switch from HbF to HbA
from birth HbF decreases about 3% per week at 6 months it represents only 2% of total Hb
what is anaemia of prematurity
low birth weight infants have a poor erythropoietin response and this means the protein in breast milk may not be sufficient for hematopoiesis
signs of anaemia of prematurity
apnoea failure to thrive pallor decreased activity tachycardia
what are the 4 functional areas of the developmental assessment
1) gross motor 2) vision and fine motor 3) hearing speech and language 4) social, emotional and behavioural
what median age do they raise their heads 40 degrees in prone
6-8 weeks
what is the limit age for head control
4 months
what is the limit age for sitting upright without support
9 months
what median age for crawling
8-9 months
what is the limit age for pulling to stand
12 months
what median age walking independently
12 months
what is the limit age for walking independently
18 months
what median age fixing and following
6 weeks
what is the limit age for fixing and following
3 months
what median age for reaching for toys
4 months
what is the limit age for reaching for toys
6 months
what median age for palmar grasp
4-6 months
what median age for transferring from hand to hand
7 months
what is the limit age for transferring from hand to hand
9 months
what is the limit age for mature pincer grip
12 months
what median age for mature pincer grip
10 months
what is the median age for drawing line without demonstration
2 years
what median age for drawing circle without demonstration
3 years
what median age for drawing a cross without demonstration
3.5 years
what median age for drawing a square without demonstration
4
what median age for drawing a triangle without demonstration
5
what adjustment do you make for the drawing ages if you give them a demonstration
reduce by 6 months if they are copying you
how many bricks can they stack at 18 months
3
how many bricks can they stack at 2 yrs
6
how many bricks can they stack at 2.5
8
what is the limit age for a polysyllabic babble
7 months
what is the median age for being able to say 2-3 words other than mamma and dada
12 months old
what is the median age for 6-10 words other than mama and dada
18 months
what is the limit age for holding a spoon and getting food safely to mouth
18 months
what is the limit age for joining 2 words to make simple phrases
2 years
what is the limit age for making 3 word sentences
2.5 years
what is the limit age for being able to say 6 words with meaning (i.e. not mama or dada)
18 months
what is the limit age for smiling responsively
8 weeks
what median age for symbolic play
18-24 months
what is the limit age for symbolic play
2-2.5 years
what is the median age to be dry by day
2 years
what is the limit age to have fear of strangers
10 months
what is the median age for interactive play to begin evolving
2.5-3 years
what is the limit age for interactive play
3-3.5 years
how should you adjust the developmental assessment if a child is born pre-term
calculate their age from the expected date of their delivery this correction is no longer required after about 2 years of age
what is the normal range of Hb for a neonate
<140g/L
what is the normal range of Hb for a child aged 1 month to 12 months
<100g/L
what is the normal range of Hb for a child aged between 1 year and 12 years of age
Hb less than 110g/L
three broadest causes of anaemia
1) impaired red cell production 2) increased red cell destruction 3) blood loss
two different types of impaired red cell production
1) red cell aplasia 2) ineffective erythropoiesis
three causes of red cell aplasia
1) congenital (diamond blackfan anaemia) 2) transient erythroblastopenia of childhood (TEC) 3) parvovirus B19 infection
5 causes of ineffective erythropoiesis
1) iron deficiency 2) folic acid deficiency 3) chronic inflammation 4) chronic renal failure 5) lead poisoning
4 types of haemolytic disorder and an example of each
1) membranopathies e.g. hereditary spherocytosis 2) enzymopathies e.g. G6PD deficiency 3) hamoglobinopathies e.g. alpha and beta thalassaemias as well as sickle cell disease 4) immune e.g. haemolytic disease of the newborn
draw the flow diagram of simple diagnostic approach to anaemia in children
what are the diagnostic clues that the cause of anaemia is ineffective erythropoiesis
- normal or high reticulocyte count
- abnormal MCV
- low in iron deficiency
- high in folic acid deficiency
anaemia is often asymptomatic before Hb drops below
70g/L
management of iron deficiency anaemia
oral iron supplementation with nifarexx or sytron
this should be continued until Hb is normal and then a further 3 months
how quickly should Hb inrease on oral iron supplementation and what might it mean if it is not increasing at that rate
what is diamond blackfan anaemia
it is congenital red cell aplasia
caused by specific mutation
can present at birth but typically at 2-3 months age
treatment is with oral steroids
if steroid unresponsive then they can have monthly red cell transfusions
stem cell transplant is also an option down the line
what is transient erythroblastopenia of childhood
what can parvovirus B19 infection cause
it can cause red cell aplasia in children with inherited haemolytic anaemias not in healthy children
what are the diagnostic clues in red cell aplasia
normal bilirubin
negative coombs test
absent reticulocytes
how many times can bone marrow increase production of red cells in order to compensate haemolysis
8 times
what are the main causes of haemolytic anaemias in children
- immune haemolytic anaemias are uncommon so the main causes are the intrinsic abnormalities of the red cells
- membranopathies - e.g. heredetary spherocytosis
- haemoglobinopathies - e.g alpha or beta thalassaemias or sickle cell disease
- enzymopathies - e.g. Glucose-6-phosphate dehydrogenase deficiency
how common is hereditary spherocytosis
1/5000 live births
what is the inheritance pattern of hereditary spherocytosis
AD inheritance
what is the brief pathophys of hereditary spherocytosis
what is the presentation of hereditary spherocytosis
affected individuals could be asymptomatic
presentation is very variable
jaundice - could be severe in first few days of life, could be intermittent throughout childhood
anaemia - may be mild but could worsen transiently during infections
mild to moderate splenomegaly
aplastic crisis - very rare caused by parvovirus B19 infection
gallstones due to increased bilirubin infection
diagnosis of hereditary spherocytosis
blood film
treatment for hereditary spherocytosis
mostly mild so only treatment is oral folic acid supplementation
splenectomy if there is poor growth or severe anaemia
how many people worldwide does G6PD deficiency affect worldwide
100 million people worldwide
10-20% prevalence in people from central africa, the med, the middle east and the far east
what is the inheritance pattern of G6PD deficiency
x linked recessive so predominantly seen in males
what is the pathophys of G6PD deficiency
G6PD is the rate limiting enzyme in the pathway that prevents oxidative damage to red cells
so the cells are vulnerable to oxidative damage caused by certain drugs, infection and fava beans
G6PD deficiency presentation
neonatal jaundice
fever
malaise
abdominal pain
passage of dark urine
management of G6PD deficiency
patients need advice on spotting signs of acute haemolysis
patients should be given a list of drugs, chemicals and foods to avoid
transfusion is rarely required, even in acute haemolysis
which haemoglobinopathies are delayed until after 6 months of age and why
sickle cell and beta thalassaemias are delayed to 6 months of life because this is when HbF is decreased to non-functional levels
sickle cell and beta thalassaemia affect the beta globin gene
HbF does not require beta globin but it does require alpha globin so this is why alpha thalassaemias present at birth
how common is sickle cell disease
1/2000 live births
what is the sickle cell mutation
mutation in codon 6 of the beta globin gene that changes a glutamine to a valine
what is the inheritance pattern of sickle cell
autosomal recessive
what is the pathophys of sickle cell
HbS polymerises to rigid tubular spiral bodies with reduced lifespan
they can be trapped in microcirculation causing vaso-occlusion and ischaemia
this is exacerbated by low oxygen concentration, dehydration or cold
variation in disease severity is caused by either co-inheritance with other haemoglobinopathies or by genetic variation in the levels of HbF
describe the anaemia of sickle cell
all have moderate anaemia with clinically detectable jaundice from chronic haemolysis
describe the susceptibility to infection in sickle cell disease
- marked susceptibility to encapsulated organisms
- pneumococci
- haemophilus influenzae
- increased incidence of osteomyelitis caused by salmonella and other organisms
- the susceptibility to infection is caused by chronic microinfarction in the spleen causing hyposplenism
- the risk of overwhelming sepsis is highest in early childhood
describe the different types of painful crisis
- common mode of presentation in late infancy is hand foot syndrome
- dactylitis with swelling and pain of the fingers and or feet from vaso occlusion
- bones of limbs and spine are most common sites
- most serious type of painful crisis is acute chest syndrome which can lead to severe hypoxia and the need for mechanical ventilation and emergeny transfusion
precipitants for painful crisis in sickle cell
exposure to cold
dehydration
excessive exercise
stress
hypoxia
infection
causes of acute anaemia in sickle cell
- haemolytic crises - sometimes associated with infection
- aplastic crises - Hb may fall precipitously
- parvovirus B19 infection causes complete although transient cessation of red blood cell production
- sequestration crises - sudden splenic or hepatic enlargement, abdominal pain and circulatory collapse from accumulation of sickled cells in spleen
long term problems associated with sickle cell
- short stature and delayed puberty
- stroke and cognitive problems
- 1/10 have stroke
- 2/10 develop more subtle neurological damage
- adenotonsillar hypotrophy
- may cause sleep apnoea which could lead to nocturnal hypoxaemia, preciptiating a vaso-occlusive crisis
- cardiac enlargement from chronic anaemia
- heart failure from chronic anaemia
prophylaxis in sickle cell
- immunisations including
- pneumococcal
- haemophilus
- influenzae type B
- meningococcal infection
- once daily oral folic acid
- daily oral penicillin
- avoid exposure to precipitants
treatment of acute sickle cell crisis
oral and iv analgesia
infection should be treated with Abx
oxygen should be given if sats drop
exchange transfusion for acute chest syndrome, stroke and priapism
treatment for chronic problems
children with repeat admissions may benefit from hydroxycarbamide which works to increase HbF
bone marrow transplant for the most severely affected
hydroxycarbamide side effect
white blood cell suppression
sickle cell mortality during childhood
3% - usually due to bacterial infection
describe the difference between the two types of beta thalassaemia
- Beta thalassaemia major
- HbA cannot be produced at all because the mutations are so severe
- Beta thalassaemia minor
- small amounts of HbA and/or larger amounts of HbF can be produced due to the nature of the mutations
- this leads to milder disease
clinical features of beta thalassaemia major
- severe anaemia which is transfusion dependent from 3-6 months of age
- jaundice
- faltering growth
- extramedullary haemopoiesis is prevented with regular transfusions
- without them you get hepatosplenomegaly and maxillary overgrowth with skull bossing
managment of beta thalassaemia
- monthly red cell transfusions for life
- maintain Hb concentration above 100g/L in order to reduce growth failure
what are the risks of repeated blood transfusion
- chronic iron overload which if untreated causes:
- cardiac failure
- liver cirrhosis
- diabetes
- infertility
- growth failure
how many alpha globin genes are there
4
what is alpha thalassaemia major and how does it present?
- this is where there is deletion of all 4 alpha globin genes so HbA cannot be produced
- presents with
- fetal hydrops
- fatal in utero or within hours of delivery
- only survivable with monthly intrauterine transfusions until delivery followed by lifelong monthly transfusions after birth
what if 3 alpha globin genes are mutated
it’s called HbH disease and children have mild/moderate anaemia but occasional patients are transfusion dependent
what if one or two alpha globin genes is mutated
usually asymptomatic with mild or absent anaemia
what is the iron requirement of a child
1mg/kg/day
diagnostic clues for iron deficiency anaemia
what is aplastic anaemia
it is aka bone marrow failure
it is a reduction or absence of the three main lineages in the bone marrow leading to pancytopenia
what are the acquired causes of aplastic anaemia
hepatitis viruses
drugs such as those used in chemo
toxxins such as benzene glue
what is the clinical presentation of aplastic anaemia
anaemia - reduced red cells
infection - reduced white cells
bruising - thrombocytopenia
name two inherited aplastic anaemias and which one is more common
fanconi anaemia - most common one
shwachman diamond syndrome
what is the presentation of fanconi anaemia
- children have congenital abnormalities which may be spotted at birth
- short stature
- abnormal radii and thumbs
- renal malformations
- micropthalmia
- signs of bone marrow failure don’t normally become apparent until the age of 5 or 6
*
what is the difinitive treatment for fanconi anaemia
bone marrow transplant
which clotting factors does prothrombin time measure the activity of
activity of factors II, V, VII and X
which clotting factors does activated partial thromboplastin time measure the activity of
II, V, VIII, IX, X, XI and XII
how common is haemophilia A, what is the inheritance pattern and which clotting factor is deficient
haemophilia A is FVIII deficiency, it is 1/5000 male births and it is X linked recessive
which clotting factor is affected by haemophilia B, what is the inheritance pattern and how common is it
1/30,000 male births, it is factor IX deficiency and it is X linked recessive
draw the table on haemophilia A that includes columns for factor VIII level, severity and bleeding tendancy
what are the two most common situations surrounding presentation of haemophilia
40% is in neonatal period with intracranial haemorrhage, bleeding post-circumcision or prolonged oozing from heel prick
most of majority present around 1 yr of age with walking and crawling progressing
most common bleeding sites of haemophilia
into joints or muscles
what is the management for haemophilia
- recombinant factor VIII for haemophilia A
- recombinant factor IX for haemophilia B
- give these clotting factors whenever there is bleeding
- mild haemophilia A can be given desmopressin which stimulates endogenous release of FVIII and vWF
- desmopressin doesn’t work for haemophilia B
what are the two major roles of vWF
facilitates platelet adhesion to damaged endothelium
acts are the carrier protein for FVIII, protecting it from clearance
what is the most common subtype of vWD, when does it most commonly present and what are the clinical features
subtype 1 is most common and it is mild so may not be diagnosed until puberty (e.g. with menorrhagia) or adulthood
management of vWD
type 1 can be treated with desmopressin
more severe types have to be treated with plasma derived FVIII as recombinant contains no vWF and desmopressin is ineffective
name 4 acquired disorders of coagulation
haemorrhagic disease of the newborn due to vitamin K deficiency
liver disease
immune thrombocytopenia
disseminated intravascular coagulation
what platelet count constitutes thrombocytopenia
<150x109/L
what is the most common cause of thrombocytopenia in childhood
Immune thrombocytopenia (ITP)
aka
immune thrombocytopenic purpura
what causes ITP
destruction of circulating platelets by IgG antibodies
clinical features of ITP in children
most common between ages of 2 and 10
1-2 weeks after viral infection
short history of days to weeks
can cause mucoas bleeding such as epistaxis
profuse bleeding is rare despite platelets sometimes getting v low
what is important about the diagnosis of ITP
if they have any abnormal clinical features other than the thrombocytopenia they need to be investigated for ALL or aplastic anaemia with a bone marrow examintion
SLE could also be a differential
but if there are no other abnormal clinical features and it fits ITP clinical picture properly then it’s what it is
how often is ITP in children acute and how often is it chronic
in 80% of cases it is acute, benign and self-limiting
in 20% of cases it is chronic, lasting more than 6 months
what is the treatment for acute ITP
- Most can be treated at home unless there is evidence of severe bleeding
- Treatment options are
- Oral prednisolone
- IV anti-D
- IV Ig
- All of the above have bad side effects and need monitoring
what is the treatment for chronic ITP
supportive
rituximab (anti-B lymphocyte) can be used for those that have recurrent bleeding episodes
causes of DIC
Severe sepsis or other shock due to circulatory collapse
extensive tissue damage due to tissue damage
what are the features of DIC
- bruising
- purpura
- haemorrhage
- thrombocytopenia
- prolonged PT
- prolonged APPT
- low fibrinogen
- raised fibrinogen depletion products
- raised D-dimer
treatment for DIC
treat underlying cause and support with FFP
thrombosis in children is ______ and pretty much always caused by a _______ _______
thrombosis in children is rare and pretty much always caused by a hypercoagulable state
- types of congenital thrombophilia
- protein C or S (natural anti-coagulants) deficiency
- antithrombin deficiency
- factor V leiden mutation - it is malformed and resistant to degradation
- prothrombin gene mutation which is associated with very high levels of prothrombin in the blood
6 acquired hypercoagulable states
- catheter-related thrombosis
- DIC
- hypernatraemia
- malignancy
- SLE
- persistent antiphospholipid syndrome
what must you do in every child presenting with a thrombotic event
- not miss an inherited cause so do the following investigations
- assays for protein C and S
- PCR for factor V leiden mutation
- PCT for prothrombin gene mutation
write as much as you can from the child with petechiae diagram
what is classed as a fever in a child
anything over 37 C
red flag symptoms suggesting serious illness in children
- fever over 38 if aged less than 3 months
- fever over 39 if 3 months to 6 months
- pale, mottled or cyanosed colour
- neck stiffness
- reduced consciousness
- bulging fontanelle
- status epilepticus
- focal neurological signs
- seizures
- significant respiratory distres
- bile stained vomiting
- severe dehydration or shock
what are the empirical abx if they’re less than 1 month old
perenteral cefotaxime with ampicillin added to cover listeria
what are the empirical abx if they’re over one month of age
high dose ceftriaxone
what should be included in the septic screen
- blood cultures
- FBC including differential white cell count
- acute phase reactants
- urinalysis and urine MC&S
- consider if indicated
- CXR
- LP
- rapid antigen screen on blood/CSF
- meningococcal and pneumococcal PCR on blood/CSF samples
- PCR for viruses in CSF
is it more common for bacteria or viruses to cause meningitis
viruses are more common
does bacterial or viral meningitis typically have more severe problems
bacterial
what is the mortality of bacterial meningitis
5-10%
what proportion of bacterial meningitis is in children under 16
80%
what percentage of survivors of meningitis are left with neurological impairment
>10%
organisms most likely to cause bacterial meningitis in neonates to 3 months old
group b streptococcus
escerichia coli
listeria monocytogenes
most common bacteria causing meningitis in 1 month old to 6 years old
neisseria meningitides
streptococcus pneumoniae
haemophilus influenzae
most common organisms causing bacterial meningitis in children over 6 years old
neisseria meningitides
streptococcus pneumoniae
which bacteria causes lowest probability of long-term sequelae
neisseria meningitides which causes meningococcal septicaemia causes few neurological sequelae despite being able to kill in a number of hours
differentials for heads stiffness
tonsillitis and cervical lymphadenopathy
findings on examination of bacterial meningitis
fever
purpuric rash
neck stiffness
bulging fontanelle in infants
opisthotonus
positive brudzinski
positive kernig
signs of shock
focal neurological signs
altered consciousness levels
papilloedema
what is a positive brudzinski sign
flexion of the neck with the child supine causes flexion of the knees and hips
seen in meningitis
what is a positive kernig sign
with the child lying supine and with the hips and knees flexed there is back pain on extension of the knees
indicates meningitis
what are the contraindications for lumbar puncture
- cardiorespiratory instability
- focal neurological signs
- signs of raised ICP
- high BP
- coma
- low heart rate
- papilloedema
- coagulopathy
- thrombocytopenia
- local infection at site of LP
- if it causes undue delay in starting abx
draw the table for LP interpretation with the rows named normal, bacterial meningitis, viral meningitis, tuberculosis meningitis and encephalitis and the columns named appearance, white blood cells, protein, glucose
managment of bacterial meningitis
IM Benzylpenicillin while awaiting transfer to secondary care
IV ceftriaxone once in hospital
supportive care
cerebral complications of meningitis
hearing impairment
local cerebral infarction can result in epilepsy
hydrocephalus from impaired resorption of CSF - ventricular shunt may be required
cerebral abscess
what protection do you give the household contacts of someone who has had bacterial meningitis
meningococcal meningitis - rifampicin or ciprofloxacin to all household contacts
group C meningococcal meningitis should be vaccinated with meningococcal group C vaccine
how do you diagnose viral meningitis
by PCR of CSF, stool, urine, np aspirate and throat swabs
what are two differences between meningitis and encephalitis in presentation
encephalitis can be insidious
encephalitis often includes behaviour change
which organisms is impetigo caused by
s.aureus or group A strep
what are the most common organisms causing encephalitis
- Enteroviruses
- Influenza viruses
- Herpesviruses
- HSV
- VZV
- HHV-6
management of encephalitis
- All children with encephalitis should be treated with high dose IV acyclovir since it is safe and HSV encephalitis is very dangerous and destructive
- PCR of CSF to determine if it’s HSV
- If it’s HSV encephalitis then CT/MRI may show focal damage often to the temporal lobe
what causes toxic shock syndrome
staphylococcus aureus and group A streptococci can produce toxins that act as super antigens
characteristics of TSS
fever over 39C
hypotension
diffuse erythematous maculopapular rash
what do you see 1-2 weeks after onset of symptoms in toxic shock syndrome
desquamation of the palms, soles, fingers and toes
which systems can TSS affect
- mucousitis of the conjunctival oral mucosa and genital mucosa
- GI dysfunction - d&v
- renal impairment
- liver impairment
- clotting abnormalities and thrombocytopenia
- CNS - altered consciousness
management of TSS
- surgical debridement of infection site
- ceftriaxone with clindamycin
- clindamycin works to inhibit production of the toxin by the bacteria
- IV Ig can be given to neutralise the antigen
which organisms may cause necrotising fasciitis
S.aureus or group A strep
what is the danger with necrotising fasciitis
the area involved spreads rapidly and abx are not enough to treat
ITU is usually required due to systemic illness
IV abx are given but surgical debridement is also necessary
IVIg may also be given
who does impetigo most commonly occur in
infants and young children
it is more common in children with pre-existing skin conditions such as atopic eczema
what do the lesions look like in impetigo
usually on face, neck and hands
begin maculr, become papular and even bullous
characteristic honey coloured crusty lesions
what is the treatment for impetigo
flucloxacillin
what organisms cause periorbital cellulitis and what is the treatment
s.aureus and group A strep
treatment is with IV ceftriaxone to rapidly prevent posterior spread
what is nikolsky sign and what does it indicate
areas of epidermis seperate on gentle pressure
it indicates staphylococcal scalded skin syndrome
what is scalded skin syndrome
staphylococcal toxin causes exfoliative separation of the epidermal skin
mainly affects infants and young children
fever and malaise followed by widespread erythema and tenderness of the skin
what is the treatment for scalded skin syndrome
IV anti-staph abx like flucloxacillin
analgesia and monitoring of fluid balance is also needed
name all 8 human herpesviruses
HSV-1
HSV-2
EBV
CMV
VZV
HHV-6
HHV-7
HHV-8
What is eczema herpeticum
it is an emergency
it is widespreasd vesicular legions caused by HSV1 or HSV2
it happens on eczematous skin
can be complicated by secondary bacterial infection which may result in septicaemia
what are the complications from chicken pox
- these are rare but serious
- secondary bacterial infection
- fever will settly but recur a few days later
- encephalitis
- purpura fulminans
- in the immunocompromised host infection may result in severe progressive disseminated disease which has a mortality of up to 20%
- generalised encephalitis
- aseptic meningitis
- secondary bacterial infection
treatment for chickenpox
what is median incubation period for chickenpox
14 days
describe the typical vesicular rash in chickenpox
50-500 lesions
start on head and trunk and then progress to the peripheries
up to one week of papules, vesicles, pustules
itchy
if new lesions appear beyond 10 days it suggests defective cellular immunity
which cells does epstein barr virus have a particular tropism for?
B lymphocytes and the epithelial cells of the oropharynx
clinical features of epstein barr virus
fever
malaise
tonsillitis/pharyngitis
diffuse lymphadenopathy
prominant cervical lymph node swelling
splenomegaly
hepatomegaly
diagnosis of EBV is supported by
atypically large T lymphocytes seen on blood film
positive monospot test
serology
how long does infectious mononucleosis normally last?
and what is the treatment
1-3 months
treatment is symptomatic until they resolve
where the airway is compromised corticosteroids may be considered
what is the danger with cmv
subclinical infection in normal hosts
most people infected by adult age
can cause morbidity to the immunocompromised and to the developing foetus
what do HHV6 and HHV7 do?
- closely related and have similar presentations
- HHV6 is more prevalent
- classically cause
- exanthema subitem aka roseola infantum
- high fever and malaise for a few days
- generalised maculopapular rash which appears as the fever wanes
- exanthema subitem aka roseola infantum
- can be fever without rash or can be subclinical
- clinically similar picture to rubella or measles
what is common slip up with HHV6 and HHV7
Occasionally what happens is the infant is seen by a doctor in the early stages of the illness and is prescribed antibiotics and when a rash appears it is erroneously attributed to allergic reaction to the drug
What are the 4 syndromes that human parvovirus B19 can cause
- asymptomatic - 65% adults have antibodies
- erythema infectiosum aka slapped cheek syndrome
- viraemic phase of fever, malaise, headache and myalgia
- followed by characteristic rash on cheek
what is hand foot and mouth disease
painful vesicular lesions on hands, feet and mouth and sometimes buttocks
systemic features generally mild
subsides within a few days
caused by coxsackie virus
which type of viruses are the most common cause of viral meningitis in high income countries
enteroviruses
complications of measles
- respiratory
- pneumonia
- secondary bacterial infection
- otitis media
- tracheitis
- neurological
- febrile seizures
- EEG abnormalities
- encephalitis
- subacute sclerosing panencephalitis (sspe)
- other
- diarrhoea
- hepatitis
- appendiciitis
- corneal ulceration
- myocarditis
how frequently does SSPE occur and what is it
it is a complication of measles where 7 years after infection, 1/100,000 cases lose neurological function and progress to dementia and death over several years
how frequently does encephalitis occur as a consequence of measles
1/5000 cases
which time of year does mumps occur
spring and winter
how is mumps spread
droplets
what is the usual disease course of mumps
- incubation period of 15-24 days
- 30% of cases are subclinical
- onset is with fever, malaise and parotisis
- fever disappears within 3-4 days
- infectious for 7 days following parotid swelling
complications of mumps
- hearing loss - usually unilateral and transient
- meningitis/encephalitis
- orchitis - usually unilateral and while sperm count may drop, infertility is rare
what is rubella like and are there any complications
- usually mild
- low grade fever if at all
- maculopapular rash is first sign of infection
- starts on face but spreads centrifugally
- rash fades over 3-5 days
- complications are reare
- arthritis
- encephalitis
- thrombocytopenia
- myocarditis
- the real danger is with congenital rubella syndrome so it should be confirmed by serology if there is risk of exposure to a non-immune pregnant woman
9 non-infectious causes of prolonged fever
- systemic onset juvenile idiopathic arthritis
- systemic lupus erythematosus
- vasculitis including kawasaki
- IBD
- sarcoidosis
- malignancy
- macrophage activation syndromes
- lymphophagocytic lymphohistiocytosis
- drug fever
- FII
what age does kawasaki mainly affect
6 months to 4 years of age with a peak at the end of the first year of life
diagnosis of kawasaki
- clinical diagnosis
- based on fever of 5 days and 4 of the following
- non-purulent conjunctivitis
- red mucous membranes
- cervical lymphadenopathy
- rash
- red and oedematous palms and soles
- peeling of fingers and toes
- in infants they may have an incomplete clinical picture so have a high index of suspicion
what are children with kawasaki like
they are strikingly miserable and this isn’t improved with oral anti-pyretic agents
what are the bloods like in kawasaki
they have high inflammatory markers and a platelet count that rises in the second week of illness
what is the management of kawasaki
they need IV Ig and aspirin
they need an echo at 6 weeks
what’s the feared complication and the mortality of kawasaki
- coronary arteries affected in 1/3 of affected children –> aneurysms
- mortality is 1-2%
how would you diagnose active TB in children
diagnosis in children is even harder than in adults
clinical features are non-specific
sputum samples are unobtainable in children under 8
since they swallow their sputum, gastric washings on three consecutive mornings can be used to identify M.tuberculosis
what are the microbiological techniques used to identify TB
- Staining techniques are for acid fast bacilli using Ziehl Neelsen stains
what is the treatment for TB
- triple or quadruple therapy with
- rifampicin
- isoniazid
- pyrazinamide
- ethambutol
- this is decreased to rifampicin and isoniazid after 2 months
- total treatment is usually for 6 months
vomiting child red flag symptoms and what they indicate
- bile stained vomit - intestinal obstruction
- haematemesis - peptic ulceration, gastritis, oesophageal varices
- projectile vomiting - pyloric stenosis
- abdominal pain on movement - surgical abdomen e.g. appendicitis
- blood in the stool - intussesception, gastroenteritis
- severe dehydration - DKA, severe gastroenteritis, systemic infection
- headache or seizures - raised ICP
- failure to thrive - GORD, coeliac
what is a chronic cough in children
>3 weeks
‘barking cough’ is characteristic of _____
croup
