paeds Flashcards
(211 cards)
1
Q
define colic and what advice would you give parents?
A
paroxysmal crying with pulling up of the legs for over 3 hours on 3+ days of the week for at least 1 week.
Reassure parents and advise them to do what they can to reduce stress e.g. enlist family/friends help
Movement (carry cot on wheels), let the baby finish the breast first (hind milk easier to digest), warm baths, burping baby, belly rubs.
2
Q
What is cows milk protein intolerance?
A
Immune mediated allergic response to naturally occurring milk proteins whey and casein. Can be IgE-mediated, non-IgE mediated or mixed.
3
Q
Describe the pathophysiology underlying CMPI
A
IgE mediated = Type 1 hypersensitivity - CD4+ TH2 cells stimulate B cells to produce IgE antibodies -> mast cell degranulation + cytokine release in an anaphylactic response on re-exposure to allergens after sensitisation
Non-IgE mediated = T cell activation against CMP
4
Q
How does a CMPI usually present?
A
<3/12 in formula/mixed fed infants. Tends to be more severe and acute onset after feeding in IgE mediated.
vomiting, abdo pain ± colic, reflux, diarrhoea, pruritis, erythema, atopic eczema, lower resp tract sx (cough, SOB, wheeze), can get urticaria, angio-oedema of lips/tongue/face, anaphylaxis, severe = faltering growth
5
Q
Risk factors for CMPI
A
atopy or a family history of atopy
6
Q
Differential diagnosis for ?CMPI
A
allergic reaction to other food/non-food allergen
anatomical abnormality - meckels, pyloric hypertrophy, etc
chronic GI disease - reflux, coeliac, IBD, gastroenteritis
pancreatic insufficiency - hx CF?
UTI
7
Q
How is ?CMPI investigated?
A
Usually clinical dx but may refer for RAST testing for specific IgE antibodies if faltering growth + 1 sx, 1 acute systemic or severe delayed reaction, atopy, clinical/persistent parental suspicion.
8
Q
Mx of CMPI
A
Refer to pads if severe sx e.g. failure to thrive
Counsel parents - many will grow out of it (55% IgE by 5, non-IgE most by 3), elimination diet with re-evaluation in 6-12m(/until 9-12/12) to assess tolerance - refer parent to MAP guidelines milk ladder
Nutritional counselling and regular growth monitoring
Formula fed = trial extensively hydrolysed formula, if still symptomatic or very severe then 2nd line AA formula
Breast fed = mom eliminates cows milk from her diet
9
Q
A 6 month old baby boy is brought into the GP by his mother with a rash on his bottom, O/E well-demarcated erythematous maculopapular rash with slight scaling in areas, skin folds are spared.
What is the likely diagnosis and what management would you advise?
A
Irritant dermatitis nappy rash
Mx - use disposable nappies as these retain less moisture, change them frequently and ideally have nappy-free periods, careful drying and use of emollient/barrier creams such as sudocream.
10
Q
a 9 month old baby is brought into the GP by his father with a rash on his bottom. O/E there is an erythematous maculopapular rash affecting the bottom and inguinal folds, with papular satellite lesions, superficial pustules and scaling seen.
What is the likely diagnosis + appropriate management?
A
Candida dermatitis nappy rash (affects skin folds, satellite lesions)
Mx - use disposable nappies and change frequently, ideally have nappy-free periods, careful drying, use of emollients and topical imidazole, cease use of barrier creams until candida has settled.
11
Q
a 1 year old is brought to the GP by her mother with a rash on her bottom. O/E there is are salmon pink patches on with scaling on the bottom and inguinal folds, you also note diffuse, yellow, greasy scales on the scalp.
What is the likely dx + appropriate mx?
A
Seborrheic dermatitis nappy rash (+ cradle cap)
Mx - use disposable nappies and change frequently, ideally have nappy-free periods, careful drying, use of emollients barrier creams e.g. sudocream.
12
Q
Differential diagnosis for vomiting in an infant
A
Posseting - effortless regurgitation of milk during feeds
Physiological - as long as it is not significant or excessive (destroying carpets=?pathological)
Overfeeding - >150ml/kg/day
Gastro-oesophageal reflux or gastritis
Pyloric stenosis - projectile vomiting ~8wks
Any infection - UTI, infective gastroenteritis
Adverse food reaction e.g. CMPI
Rarer - pharyngeal pouch, obstruction (bilious vomiting), RICP, DKA
13
Q
A 6month old is brought to the GP with a 9 hour history of fever. Her mother reports her to be getting worse - increasingly ‘out of it’ and drowsy, taking less feed than usual (around half), she last had a wet nappy approximately 8 hours ago. O/E she is drowsy and does not interact with you, little reaction to parents, no skin rashes, HR 165, CRT3s, RR 53, temp 39, O2 sats 94% on air.
How would this child be stratified and what should the management plan be?
A
Amber - ‘out of it’ apathy, not responding to social clues, no smile, drowsy; RR>50, O2 <95, HR>160, CRT>3s, poor UO and half feeding.
Mx - need to ensure they are seen face to face, no known dx = refer to paeds for further assessment, otherwise may be able to safety-net - verbal and/or written info on warning symptoms, how to access further healthcare, follow up appt and liaise with other HCP (e.g. out of hours providers to ensure direct assessment if needed).
14
Q
A 1yr old is brought to the GP with a 9 hour history of fever. Her mother reports her to be getting worse - increasingly drowsy and tearful, taking less feed than usual (around half), she last had a wet nappy approximately 8 hours ago. O/E she is pale and appears ill, is crying weakly, and shows subcostal recession and moderate chest wall indrawing. HS 1+2+0, abdo SANT, chest crackles heard L base. HR 165, CRT3s, RR 61, temp 39, O2 sats 94% on air.
How would this child be stratified and what should the management plan be?
A
Red - pale, weak cry, appears ill to HCP, tachypnoea, moderate chest indrawing
mx - urgent referral to paeds specialist to be seen within 2h.
15
Q
How would you manage a severely unwell child with no obvious source of fever?
A
Sepsis 6 + urine ± LP
Urine dip for UTI (>3m; younger clean catch MC&S)
FBC, U&Es, blood culture, CRP, VBG
CXR
LP if clinically indicated
Fluids - bolus 20ml/kg if lactate >2
Abx - 0-1m = cefotaxime + amoxicillin + gentamicin, 1-3m = ceftriaxone + amoxicillin, >3m = ceftriaxone
16
Q
When and in whom would you expect to see an intraventricular haemorrhage?
A
Within first 72h of life, pre-mature neonate with very low birthweight (<1.5kg)
17
Q
How are IVHs usually diagnosed? Clinical sx and Ix
A
Often asymptomatic but may see seizures, cerebral irritability, bulging fontanelle, hydrocephalus due to clot obstructing CSF outflow.
Premature <32/40 = cranial US on day 4-7 to assess; >32 weeks if clinically indicated.
18
Q
How are IVHs managed and what complications may arise?
A
Mx - supportive care, hydrocephalus may require shunt insertion
Complications - learning disability, cerebral palsy, hydrocephalus. May recover completely.
19
Q
What is neonatal apnoea and what causes it? How is it prevented and managed?
A
Failure to make respiratory effort for over 20 seconds, or less than 20 seconds with accompanying bradycardia
Causes - prematurity, infection, hypothermia, aspiration, congenital heart disease. Prevent with maternal IM corticosteroids.
Mx - physical stimulation and IV caffeine
20
Q
What is retinopathy of prematurity?
A
Incomplete maturation of the retina in-utero usually seen in <32/40, vascularisation of the retina begins centrally spreading outwards and is driven by hypoxia. Baby born early means O2 drives abnormal BV development - friable and grow outside the plane of the retina = liable to bleed into the eye which can cause retinal scarring, detachment and blindness. This is exacerbated by O2 supplementation.
21
Q
How is retinopathy of prematurity picked up/diagnosed and managed?
A
babies born before 32 weeks gestation or with very low birthweight (<1.5kg) are screened for it.
- Born =<27/40 = screen at 30-31 weeks gestational age
- Born >27wks = screen 4-5 weeks of age
Screen at least every 2 weeks by ophtho until sufficient vascularisation of retina, rx diode laser therapy
22
Q
Define neonatal sepsis
A
Serious bacterial or viral blood infection in first 28d of life, it can be classed EONS (in first 72h of life) or LONS (onset between 3 and 28d of life)
23
Q
Which are the most likely causative organisms in early onset neonatal sepsis?
A
Group B streptococcus and E.Coli, coagulase negative staph, H.Influenzae, listeria
24
Q
Risk factors for early onset neonatal sepsis
A
Mother - known carrier of GBS (prev baby with GBS sepsis, prenatal test), UTI, intrapartum pyrexia 38+, ROM 18+hrs, evidence of maternal chorioamnionitis
25
What are the most likely causative organisms in LONS and list risk factors for this
gram + organisms - mainly coagulase negative staphylococci, also s.aureus; E.Coli, pseudomonas, klebsiella.
Central line and catheters, congenital malformations, severe illness, immunodeficiency, poor cord care.
26
Clinical presentation of neonatal sepsis
respiratory distress most common - grunting, nasal flaring, tachypnoea/apnoea
seizures
sx of shock - tachycardia, low UO, low BP, resp distress
jaundice
feed intolerance inc vomiting
abdo distension
labile temperature, abnormal HR, poor O2 sats
27
How would you manage a neonate with ?sepsis
A-E assessment and initiate sepsis 6 bundle
- Bloods - culture, blood gas, CRP, FBC
- LP, ?urine MC&S, ?CXR
- Fluid - bolus 10-20ml/kg, maint 120-150ml/kg day 5-28
- Abx
- EONS - IV benzylpenicillin + gentamicin
- LONS - IV flucloxacillin + gentamicin
- ?meningitis - IV cefotaxime + amoxicillin
28
Causes of neonatal seizures
```
Metabolic - hypoglycaemia (r/o immed), hypo/hyper-natraemia, hypocalcaemia, hypomagnesaemia
HIE
Infection - meningitis, encephalitis
Kernicterus
Inborn error of metabolism
Intracranial haemorrhage/infarction
Structural CNS lesion
Neonatal withdrawal from maternal drugs/substance
Idiopathic
```
29
How may neonatal seizures present?
Subtle signs - blinking, chewing, eye deviation, lip smacking, staring, cycling/boxing, apnoea
Repetitive jerking, stiffening and posturing limbs/trunk
EEG can confirm
30
How would you manage neonatal seizure?
A-E assessment
Rule out hypoglycaemia
Blood - FBC, U&Es, Ca, Mg, VBG; ?culture/metabolic screen/LP
Arrange EEG; if poss Cerebral Function Analysis Monitor
Rx seizures if prolonged (>3mins or 4+ in hour) IV phenobarbitol
31
What is hypoxic-ischaemic encephalopathy?
Clinical syndrome of brain injury in neonates due to prolonged or severe hypoxia during birth causing ischaemic brain damage. Severe = CP, death
32
Causes of HIE
Maternal shock, intrapartum haemorrhage, amniotic fluid embolism, prolapsed or nuchal cord
33
How might HIE present?
Antenatal - foetal distress on CTG (abnormal HR + contraction patterns), RFM, cramps, PV bleed
Postnatal - cord blood gas acidosis, low Apgar score at 5 and 10mins, seizures, difficulty feeding, breathing problems, hypotonia, organ damage/failure, abnormal level of conscious (up or down)
34
How is HIE managed?
in NICU, resuscitation, supportive care (ventilation, circulatory support, rx acidosis and seizures), therapeutic hypothermia if moderate/severe.
35
Define neglect
Persistent failure to meet Childs basic physical /psychological needs that is likely to result in serious impairment of Childs health and development
36
Define child abuse
Deliberate infliction of harm to a child or failure to prevent harm, may be physical/sexual/emotional/bullying/online abuse
37
How old should a child be when they first smile?
6 weeks
38
How old should a child be when they have no head lag on pulling to sit?
3 months
39
At what age would you expect a child to be able to sit?
6 months - pull self to sitting, sit with a straight back when held
7-8 months - sit without support
40
How old should a child be when they can pull themself to standing?
9 months
41
How old should a child be when they start crawling?
9 months
42
How old should a child be when they start cruising and then walking unsupported and at what age would you refer to a specialist if this has not yet happened?
cruising 12 months
| 13-15 months, refer at 18
43
By what age should a child be able to hop on one leg?
4 years old
44
Describe the social interaction you may see in normal childhood development
```
6 weeks - first smile
3 months - laughs, enjoys friendly handling
6 months - not shy
9 months - shy but can play basic games like peek a boo or pat a cake
12 months - waves bye bye
18 months - plays alone
2y - plays near but not with others
4y - plays with other children
```
45
Describe the speech development and milestones you would expect to see in a normal child
6 months - 2 syllables
9 months - 'mama' 'dada' understands no
12 months - knows and responds to own name
12-15 months - knows 2-6 words (refer at 18months)
2 yrs - combines two words
3y - 3-5 word sentences, what and who questions
4y - why, when and how questions
46
At what age would you expect a child to be able to build a tower of 3 blocks?
18 months
47
At what age would you expect a child to be able to copy a circle?
3y
48
Who receives a BCG vaccine and when do they receive it?
at risk of TB (e.g. family case in last 6 months) get it at birth
49
Childhood vaccine schedule
2 months - 6 in 1 + oral rotavirus + MenB
3 months - 6 in 1 + oral rotavirus + PCV
4 months - 6 in 1 + MenB
12-13months - HiB/MenC + MMR + MenB + PCV
2-8 - annual flu vaccine
3-4 - MMR + pre-school booster (dip/tet/whoop/polio)
12-13 - HPV vaccine
13-18 - MenACWY + dip/tet/polio booster
50
What is in the 6 in 1 vaccine and when is it given?
2/3/4 months; dip/tet/whoop/polio/HiB/HBV
51
In what scenario should vaccinations be delayed?
acute febrile illness/intercurrent infection
52
Features of trisomy 21?
Short stature
Hypotonia
Face = upslanting palpebral fissures, epicanthic folds, brush field spots, round/flat face, small low-set ears, protruding tongue
Flat occiput
Single palmar crease
Sandle-gap deformity
Duodenal atresia, Hirschsprung's disease, congenital heart defect
53
What complications might you see of T21?
learning difficulties, repeated respiratory infections ± hearing impairment from glue ear, congenital heart defect (endocardial cushion defect, VSD, TOF, PDA)
ALL, hypothyroidism, early onset Alzheimers, cataracts, subfertility
54
How would you expect croup to present and what is the causative organism?
Stridor - caused by laryngeal oedema, inflammation and secretions
Cough - barking cough commonly worse at night
Fever and coryzal sx
Parainfluenza viruses
55
How is croup graded and what does this mean for management?
Mild - occasional cough, no stridor or sternal recession
Moderate - frequent cough, stridor and sternal recession at rest
Severe - frequent cough, stridor and sternal recession at rest WITH agitation/lethargy
Mild - stat dose PO dexamethasone, safety net usually self-limiting and will resolve within 48h but can last up to 1 week, fluids and paracetamol/ibuprofen, seek medical advice if cough worsens and stridor/recession.
Moderate/severe - admit for observation to prevent resp failure, stat PO dexamethasone, highflown O2/neb adrenaline if required.
56
How would you expect epiglottitis to present?
Rapid onset, continuous stridor, significant pyrexia and generally unwell (T>39), drooling/pooling of saliva with muffled voice no cough. Used to be disease of childhood but HiB vaccination now (2m/3m/4m/12m) means more commonly presenting in adults.
57
How do you manage acute epiglottitis?
As soon as it is suspected call anaesthetist and ENT. Do not examine throat, keep child with mom and do not approach/intervene as any upset can cause airway obstruction due to increased oedema/inflammation.
58
Most common causative organisms of bronchiolitis?
RSV, more rarely mycoplasma/adenovirus/parainfluenza
59
How does bronchiolitis typically present?
coryza, dry cough, breathlessness, wheeze, fine crackles, poor feeding
60
What signs/symptoms would make you admit patient with suspected bronchiolitis?
Respiratory distress (grunting, severe recessions, RR>70), hypoxia, feeding 50% usual amount.
61
How is bronchiolitis managed?
Supportive - oxygen if required and NG tube if poor feeding.
62
What is the causative organism of whooping cough?
Bordetella pertussis
63
How does whooping cough present? How would you investigate it?
2-3 days of coryza, then paroxysmal coughing (usually worse at night or after feeds, may vomit after, lasts for 10-14 WEEKS) ± inspiratory whooping (forced inspiration against closed glottis), in infants may have episodes of apnoea
Nasal swab PCR, may see lymphocytosis on FBC
64
How is whooping cough managed?
Notifiable disease
Admit infants under 6 months old, anyone with severe breathing difficulties or a significant complication
Onset of cough <21d ago = PO clarithromycin
Exclusion from school until 48h of abx or 21 days from sx onset if not using abx
Offer prophylactic abx to household members who have been contacts in last 21d who are not fully vaccinated.
65
Describe the pathophysiology of cystic fibrosis
Characterised by an autosomal recessive mutation on chromosome 7 affecting the CFTR gene which codes cAMP-regulated Na/Cl channels. This causes exocrine secretions to become more viscous, which may manifest clinically as recurrent chest infections, pancreatic insufficiency, malabsorption, meconium ileus etc.
66
How may cystic fibrosis present?
Screened on neonatal blood spot screening (Guthrie testing) day 5-9.
May present as neonate with meconium ileus
Later - recurrent pneumonias, failure to thrive, steatorrhoea, slow growth
67
What test is used to diagnose CF? Is it always correct?
Sweat test - abnormally high sweat chloride. false positives - glycogen storage disease, malnutrition, diabetes insipidus, hypo(para)thyroidism, G6PD, adrenal insufficency. false negatives - skin oedema
68
How is CF managed?
Counselling for patient and family - direct to online resources and support groups; genetic counselling
MDT very important! inc transition paeds to adult services
Chest physio at least twice a day to dislodge mucus (teach parents how to do it), postural drainage.
High calorie high fat diet, pancreatic enzyme and vitamin supplementation
Minimise contact with other CF patients (cross infection with pseudomonas, burkholderia)
Heart and lung transplant
69
How would asthma present in a child?
Episodes of wheeze, breathlessness, chest tightness or cough with diurnal variability, but minimal symptoms between attacks. Recorded observation of wheeze by HCP. Hx of atopy. Ideally a recorded PEF/FEV1 which is significantly lower during symptomatic periods. Lack of sx suggestive of other dx.
70
Describe the pathophysiology of asthma
Dendritic cells present allergens to TH2+ T cells which are then activated and stimulate the humeral immune system to produce cytokines which promote inflammation and bronchoconstriction, with increased proliferation of mast cells, eosinophils and dendritic cells.
71
Risk factors for childhood asthma
Atopy, family hx of atopy, low birth weight, prematurity, parental smoking
72
Important factors to elucidate in ?asthma hx
```
Cough/wheeze/SOB/chest tightness
Sx frequency
Sx severity
Any identifiable triggers
Age of onset
How is this affecting the child in terms of school attendance, ability to take part in hobbies, sleep? Have they had to attend hospital for it?
Any treatments tried?
PMH - other allergies, prev viruses/eczema/hayfever
FHx atopy
```
73
What investigations might you perform for ?asthma?
Often a clinical dx but can perform as baseline tests
SPIROMETRY - baseline FEV1/FVC, and if unsure of dx can perform baseline spirometry and trial with bronchodilators to check for improvement
Baseline CXR, PEFR
Exhaled NO
Can do exercise testing or skin prick testing to identify specific allergens but not to identify asthma itself.
74
Describe the management of asthma in children
Stepwise treatment step up/down until at the minimum intervention which controls symptoms. At each step ensure compliance and correct spacer technique, ensure written asthma management plan
1) Short acting B2 agonist (salbutamol)
2) + Low dose ICS as regular preventer (beclometasone; can jump straight to this step if sx 3+ times a week or at night)
3) + Leukotriene receptor antagonist
4) Switch LTRA to LABA if not effective
5) SABA + Maintenance + Reliever Therapy (low ICS)
6) SABA + MART (moderate dose ICS)
7) SABA + MART (high dose ICS)/additional drug such as theophylline
75
Define a severe asthma attack
```
O2 <92
PEF 33-50% best or predicted
too breathless to talk/feed
HR >125 if 6+, >140 if 1-5
RR >30 if 6+, >40 if 1-5
use of accessory neck muscles
```
76
Define a life threatening asthma attack
```
O2 <92
PEF <33% best or predicted
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis
```
77
How would you manage an acute asthma attack
High flow O2
Salbutamol (mild/mod = spacer, severe = nebuliser) ± nebuliser ipratroprium bromide
PO prednisolone 3/7
2nd line = consult specialist for ?IV salbutamol, add MgSO4
78
Causes of diarrhoea in children
Acute = can be early sign of sepsis so beware! Usually gastroenteritis due to rotavirus infection, initial fever and vomiting, biggest risk is dehydration which requires oral rehydration therapy.
Chronic
- breastfed infant - normal for their stools to be liquid
- CMPI
- toddler diarrhoea - undigested food
- coeliac disease
- post gastroenteritis lactose intolerance
79
describe pathophysiology of coeliac disease?
T-cell mediated immune reaction to gluten causing small intestine epithelial cell destruction and villous atrophy.
80
How would you expect a child with coeliac disease to present?
Usually 9-24 months
Malabsorption - failure to thrive, weightloss, loose stools, steatorrhoea, abdo pain/distension, anorexia, muscle waste. Miserable child with behavioural changes.
Could present with extra-intestinal symptoms - dermatitis herpetiformis, osteoporosis, delayed puberty, short stature, IDA, arthritis.
81
How would you investigate ?coeliac disease
serology - total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)
ttg only weakly positive then IgA endomysial abtibodies (EMA)
Positive serology = endoscopic duodenal bx
82
How would you mx coeliac disease?
gluten free diet
diet supplements if malabsorption e.g. iron
annual f/u for sx, development, growth, long term complications
83
How does GORD differ from gastro-oesophageal reflux?
reflux is the passage of gastric contents into the oesophagus, which is normal in infants if asymptomatic
GORD is the symptoms and complications which arise as a result of reflux
84
Risk factors for GORD
prematurity, parental hx heartburn/acid reflux, obesity, hiatus hernia, hx congenital diaphragmatic hernia/oesophageal atresia (whether repaired or not), neurodisability e.g. CP
85
Differentiating GORD from reflux in the history
Distressed behaviour - excessive crying, unusual neck postures or back arching
Unexplained feeding difficulties
Faltering growth
Pneumonia
Check volume and frequency of feeds and vomits, relationship between feeding and vomiting.
Child - persistent cough, hoarseness, stomach pain
86
Mx of GORD in infants
Breastfed - after feed give alginate mixed with water
Bottlefed - ensure not overfeeding, decrease feed volume by increasing frequency (e.g. 2-3hrly), use feed thickener, if that doesn't work add alginate to formula instead.
2wks of alginate without improvement = PPI
87
How would you expect pyloric stenosis to present and when?
2nd-4th week of life
projectile non-bilious vomiting after feeds, palpable olive shaped mass in upper R abdo, constipation/dehydration
vomiting -> hypochloraemic, hypokalaemia metabolic alkalosis
88
How would you investigate and mx ?pyloric stenosis
Ultrasound scan pyloric mass
| Correct metabolic alkalosis and pyloromyotomy surgery
89
What is intussusception and in what anatomical region is intussusception most common?
Invagination of one portion of the small bowel into the lumen of the adjacent bowel causing 'telescoping'
Ileocaecal
90
How does intussusception present?
Most commonly 6-18 months old boys
Paroxysmal abdo pain (colicky pain in which they draw knees up and turn pale), vomiting, bloody stool (redcurrant jelly is late sign)
O/E Sausage shaped mass RUQ
91
How would you ix and mx intussusception?
Ultrasound - target sign
| Mx - reduction by air insufflation under radiological control; if this fails or peritonism then surgery
92
Most common causative organisms of UTI
E. coli, proteus, pseudomonas, klebsiella, s.saprophyticus
93
Risk factors for UTI
<1 y/o, female (though more common in boys under 3m), previous UTI, vesicoureteric reflux (33% cases), voiding dysfunction, spinal abnormalities, constipation, immunosuppression
94
Clinical features of a UTI in an infant not yet talking
vomiting, pyrexia, malaise/lethargy, poor feeding, failure to thrive
95
Clinical features of a UTI in a child able to talk
Dysuria and frequency, may also report dysfunctional voiding, changes in continence, abdo/loin pain
96
How would you investigate ?UTI
Observations
| Urine dipstick and MC&S from clean catch sample ideally
97
How would you manage UTI in an infant under 3months old?
Refer to paeds and urgent urine MC&S, screen for sepsis
98
How would you manage UTI in an infant over 3m/child?
Upper UTI - ?admission, PO cefalexin for 7-10d
| Lower UTI - PO cefalexin 3d
99
What are the indications for USS in a child with UTI?
<6 m with a lower UTI - scan within 6wks
>6m - Recurrent UTIs (scan in 6/52) or atypical UTI (voiding abnormality, ?sepsis, not responding to rx, mass or raised creatinine) (scan in acute illness) and follow up with DMSA scan in 4-6m
100
What triad characterises haemolytic uraemic syndrome?
AKI + microangiopathic haemaolytic anaemia + thrombocytopenia
101
What is the most common cancer of childhood
Acute Lymphoblastic Leukaemia
102
At what age is peak incidence of ALL?
2-5y/o
103
Describe the underlying pathophysiology of ALL
Dysregulation and disturbed proliferation of lymphoid precursor cells in bone marrow leading to excessive production of immature blast cells and subsequent decline in the number of functional WBC, RBC, plt
104
Clinical features of ALL
UEW, anorexia, poor growth
Anaemia - pallor, lethargy
Thrombocytopenia - bleeding, bruising, petechial rash
Leukopenia - recurrent infections and fever
Lymphadenopathy and hepatosplenomegaly
(CNS involvement, orchidomegaly from testicular involvement, bone pain from hyper plastic marrow)
105
Ddx for brusiing
ITP, ALL, trauma/NAI
106
List investigations for ?ALL
```
FBC - pancytopenia or anaemia, thrombocytopenia and a leukocytosis
Blood film - blasts
BM aspirate/trephine to confirm dx
CXR to exclude mediastinal masses
LP to exclude CNS involvement
```
107
Poor prognostic factors in ALL
Age <1 or >10, male, CNS involvement, cytogenetics/morphological aspects of WBC, WCC>50
108
Management of ALL
Resuscitate and stabilise - marked lymphocytosis requires hyper hydration to prevent hyper viscosity, mediastinal mass = give steroids to prevent airway compromise, abx if infection
Chemotherapy - intravascular and intrathecal, support with blood products, prophylactic anti-fungals. Mx for 2yrs in girls, 3yrs in boys.
Follow up regularly for relapse/side effects chemo for 5 years after completing treatment, then annual follow up for late s/e chemo
109
Clinical features of lymphoma in kids
Lymphadenopathy, hepatosplenomegaly
B sx - nightsweats, fever, weightloss
Lethargy/anorexia
110
How would you ix ?lymphoma
FBC, U+Es, LDH, USS LN ± bx, full body staging CT, CXR if ?mediastinal mass
111
Mx of lymphoma
Resuscitate and stabilise, rx TLS/SVCO etc
| Chemotherapy ± radiotherapy
112
What is henoch-schonlein purpura?
IgA-mediated small vessel vasculitis
113
How does Henoch-Schonlein purpura present?
Purpuric rash on the extensor surfaces of arms and legs, buttocks with localised oedema
Abdo pain
Polyarthritis
Features IgA nephropathy (haematuria, renal failure)
Recent hx infection
114
How would you ix ?HSP and how would you mx HSP.
Urine dipstick - protein
BP
Bloods - U&Es, ESR, IgA and ASO titres
Supportive rx - analgesia for arthralgia, mx nephropathy, self limiting condition with good prognosis though around a third do relapse
115
Causes of raised ICP in child
```
Infection - meningoencephalitis
Vascular - haemorrhage, VST
Trauma
Metabolic - ketoacidosis, hypoxia, toxic ingestion
Tumour
```
116
Sx of raised ICP in child
irritable, drowsy, listless, headache, diplopia, vomiting, tense fontanelle, reduced GCS/responsiveness, unequal pupils, abnormal posturing, Cushings triad (htn, bradycardia, abn breathing)
Chronic - papilloedema, hydrocephalus
117
Mx of raised ICP in child
A to E assessment
Aim to prevent ischaemia
Keep head 25 degrees elevated in midline to promote venous drainage, avoid hyperthermia, treat hypotension seizures and hypoglycaemia.
IV mannitol or hypertonic saline
118
Sx of encephalitis?
Flu-like prodrome, reduced consciousness, behavioural change, vomiting, fits, pyrexia, meningism
119
Causes of encephalitis
HSV (temporal lobe sx, IV acyclovir), mumps (recent parotiditis or testicular pain), VZV (chickenpox), rabies, parvovirus (slapped cheek synd), immunocompromised, influenza, toxoplasmosis, Lyme disease
Non-infective - DKA, hypoglycaemia, kernicterus, poisoning, SAH, malignancy, SLE
120
Rx encephalitis
IV aciclovir + ceftriaxone (+ amoxicillin if under 3m)
121
Sx of meningitis
```
Infant = lethargy, irritability, poor deeding, vomiting, seizures, temp instability, rash, shock, tense fontanelle
Child = + photophobia, neck stiffness, headache, papilloedema, CN palsy, confusion, altered GCS
```
122
Mx meningitis
A-E assessment for sx shock and raised ICP
Sepsis 6 bundle
LP unless CI - sx raised ICP, coagulation disorder, uncontrolled seizures, ?meningococcla sepsis
Abx - <28d = IV cefotaxime + gentamicin + amoxicillin, 1-3m = IV ceftriaxone + amoxicillin, 3m+ = IV ceftriaxone (only add amoxicillin if ?listeria)
LP shows bacteria on gram stain/frank purulent CSF/protein >1g/l and its less than 12h since abx initiated add IV dexamethasone.
123
Follow up after discharge for meningitis
6-8 weeks, with a hearing test up to 6 weeks after presentation
124
What is epilepsy?
Neurological syndrome characterised by recurrent seizures, episodes of abnormal electrical discharge by neurones in the brain. Presents as a variety of changes in behaviour, movement, LOC.
125
A 7 year old girl is brought to the GP as her mother is concerned about strange episodes the child has 20-30 times times a day. During the episodes her daughter stares blankly to the side, sometimes smacking her lips as she does so. She comes to within 20 seconds not aware of what has just happened, usually only knowing due to being told off by teachers for day dreaming. What is the most likely dx and how would you manage this?
Absence seizures
| Ethosuximide
126
A 10 year old boy presents to the GP after a 2nd seizure (the first was a few weeks before). Both times the boys limbs have stiffened and started jerking. What type of seizure is this and what medication is appropriate?
Tonic-clonic
| Valproate/lamotrigine
127
What type of AED is used to rx tonic or atonic seizures?
valproate/lamotrigine
128
What AED is used to treat myoclonic seizures?
Valproate/levitiracetam
129
What EEG finding and seizure would you expect to see in an infant with West syndrome (infantile spasm)?
```
Hypsarrythmia
Salaam attacks (head nodding and arms jerking every 3-30s)
```
130
What AED is used to treat focal seizures?
lamotrigine/carbamazepine
131
Ddx for epilepsy in kids
```
Febrile convulsions
Hypo-glycaemia/natraemia/calcaemia
Epilepsy
Migraine
Intracranial SOL or infection (meningitis/encephalitis) or intoxication or injury to head
```
132
What is a febrile convulsion?
Single seizure provoked by fever in otherwise normal child, usually aged 6m-5yr
133
Clinical presentation of febrile convulsion?
Usually occur early in viral infection as temperature rises rapidly, seizures usually <5mins and tonic-clonic.
134
Classification of febrile convulsions
Simple - <15mins, generalised tonic-clonic, typically no recurrence in 24h and should be complete recovery within 1h
Complex - 15-30mins, focal seizures, recurrence within 24h
Febrile status - >30mins
135
Mx of febrile convulsions?
Note the time seizure starts, remove harmful objects in vicinity and cushion head.
>5mins and tonic-clonic = 999 ?status; rectal diazepam/buccal midazolam (2nd dose 10 mins later)
Seizure stopped = check airway and place in recovery position, observe inc for injury and rx.
Admit to hospital if - 1st episode, under 18months, complex, diagnostic uncertainty surrounding cause
After-care - may consider emergency benzodiazepine rescue medications for parents if recurrence, advice parents 1 in 3 risk recurrence
136
What is enuresis?
Involuntary discharge of urine by day and/or night in a child aged 5+, in the absence of congenital or acquired defects of the nervous system/urinary tract. Can be primary (child never achieved continence) or 2ndary (prev 6months of continence)
137
What might you want to rule out in enuresis?
UTI, diabetes, constipation
138
Mx of enuresis
Healthy diet and encourage non-sugary non-caffeinated fluids.
Toilet regularly during the day and before bed (4-7x)
Rewards system for assoc behaviour (e.g. drinking water, going before bed) NOT dryness
Still not dry and 7+ (younger if mature) can offer enuresis alarm, or desmopressin for short term/as 2nd line
139
When would you refer to a specialist in the case of delayed speech?
18 months if not achieved 2-6 words (usually 12-15m)
140
Causes of delayed speech
Familial (parents language delay), hearing impairment (chronic OM), environmental (poor social interaction, deprivation, abuse), neuropsychological (global developmental delay, ASD)
141
Causes global developmental delay?
Genetic - chromosomal disorder e.g. T21, DMD, fragile X)
Congenital brain abnormalities (hydro/micro-cephaly)
Antenatal - infection (CMV, rubella, toxoplasmosis), teratogenic drugs or alcohol, hypothyroidism
Perinatal - extreme prematurity -> IVH/PVL, metabolic disorder e.g. hypoglycaemia, brain injury.
142
Causes of delayed walking?
```
Benign variant
Cerebral palsy
DMD in boys (creatine kinase)
Global delay
Chronic illness
```
143
What is cerebral palsy?
Disorder of movement and posture caused by a non-progressive lesion of the motor pathways in the developing brain sustained in early childhood, usually presents by the 2nd/3rd year of life. Most common cause of major motor impairment
144
Causes of cerebral palsy
Antenatal - congenital infection (rubella, CMV, toxoplasmosis), cerebral malformation, PVL
Intrapartum - birth asphyxia/trauma, prematurity, kernicterus
Postpartum - brain injury, IVH, meningitis, severe hypoglycaemia
145
Sx of cerebral palsy
first 2/3 yrs of life
Motor = delayed motor development, abnormal posture, hypotonia, random uncontrolled movements, jerky or clumsy movements, muscle spasm, tiptoe walking, handedness before 1y/o.
Other = feeding difficulties, learning disability, urinary incontinence, epilepsy, hearing loss, visual loss/squint/nystagmus
146
Classes of cerebral palsy
Spastic - increased muscle tone and reduced ROM, difficult to move
Dyskinetic - muscles switch between spasticity + hypotonia, uncontrolled movement/posture
Ataxic - clumsy, uncoordinated movements, balance problems, tremors
Mixed
147
Classification of learning disability
Mild - 50-69
Moderate - 35-49
Severe - 20-34
Profound - <20
148
List factors differentiating viral-induced wheeze and asthma
VIW only during a cold, asthma will have other triggers e.g. exercise, cold weather, pollen
VIW only SAB2A salbutamol as rx when required, not preventative rx
VIW more likely than asthma in a pre-school aged child
149
Mx of anaphylaxis
```
Call resus team
A to E assessment
IM adrenaline - 1:1,000 <6 0.15ml (150mcg), 6-11 0.3ml (300mcg), 12+ 0.5ml (500mcg), repeat in 5mins
High flow O2
IV fluids 20ml/kg
IVI/IM chlorphenamine, IV hydrocortisone
```
150
Jaundice which appears within the first 24h of life can be physiological true or false
False - always pathological
151
What are the 2 main causes of neonatal jaundice within the first 24h of life?
haemolytic disease - ABO or rhesus incompatibility, G6PD deficiency, spherocytosis
Sepsis - congenital infection
152
Ddx for jaundice seen in a neonate between 1-14 days old?
Physiological + breastmilk jaundice
Infection
Bruising
Crigler Najjar synd
153
Ddx prolonged jaundice (persisting >14d)?
Conjugated - biliary atresia, neonatal hepatitis, galactosaemia
Unconjugated - Breastmilk jaundice; Infection (UTI, TORCH, congenital CMV/toxoplasmosis); hypothyroidism; pyloric stenosis, bile duct obstruction
154
Describe the process by which bilirubin is handled in the body normally
Hb breakdown leads to production of bilirubin pigment, which binds to albumin for transport in blood to be conjugated in the liver, making it water-soluble and able to be excreted in urine.
155
Describe the pathophysiological basis of unconjugated hyperbilirubinaemia
In unconjugated hyperbilirubinaemia the production of bilirubin outstrips the livers capacity to conjugate it and excrete it in the gut.
156
Describe the pathophysiological basis of conjugated hyperbilirubinaemia
In conjugated hyperbilirubinaemia there is an obstruction between the liver and duodenum which prevents excretion of bilirubin in bile.
157
Describe the pathophysiological basis of Kernicterus
Bilirubin is usually conjugated in the liver, rendering it water-soluble for excretion. When bilirubin is not conjugated, levels increase in the blood causing an unconjugated hyperbilirubinaemia - which if severe and prolonged leads to lipid soluble unconjugated bilirubin crossing the blood brain barrier and depositing in the basal ganglia and brainstem nucleus, to cause encephalopathy known as kernicterus.
158
How would you investigate neonatal jaundice
Transcutaneous bilirubin monitor - if >35/40 + >24h
Serum bilirubin - if <35/40, <24h, or TCB >250umol/l - need total and conjugated bilirubin
FBC, blood group mom and baby, DCT
± U+Es, LFTs, TFTs, sepsis screen, G-6-p dehydrogenase
159
How would you manage neonatal jaundice
Plot total serum bilirubin on gestation-specific treatment threshold graph to determine need for phototherapy
<50umol/l below phototherapy line repeat level within 18h (risk factors) /24h (no risk factors).
During - bilirubin 4-6h after starting to ensure it is not still rising, then 6-12hourly once level is stable/reducing; maximum skin coverage and eye protection
Stop phototherapy - >50umol/l below treatment line, check for rebound hyperbilirubinaemia 12-18h later.
Exchange transfusion via umbilical a/v - if over threshold or sx of encephalopathy
160
Risk factors for neonatal jaundice
```
prematurity, LBW, SFD
previous sibling required phototherapy
exclusively breastfed
jaundice <24h
infant of diabetic mother
```
161
when does screening for developmental dysplasia of the hip take place, how is it screened for?
At the NIPE (within 72h birth) + 6 week check - asymmetry of skin folds/knee height/abduction/leg length. Perform Barlows test (dislocate femoral head from acetabulum) and Ortolanis test (relocate)
If these tests are positive USS hip within 2wks or the infant was breech at 36, 1st degree fam hx DDH, multiple pregnancy - USS within 6wks corrected age
162
How do you investigate ?DDH
USS or if infant >4.5m XR hip
163
Mx of DDH and complication
many will spontaneously stabilise by wk 3-6, if <4-5/12 Pavlik harness, older = surgery. Complication = AVN of femoral head
164
What is perthes disease? How does it present?
AVN of femoral head (more specifically of the epiphyses) in 4-8y/o, progressive hip pain, limp, and stiffness/reduced ROM.
165
How would perthes disease look on XR hip and how would you manage it?
widened joint space, reduced size of femoral head/flattening
<6 = observe - many will resolve with early diagnosis and casts/braces to keep femoral head in acetabulum, >6 = surgical correction
166
which congenital heart defects are cyanotic?
TGA and tetralogy of fallot
167
What defects characterise Tetralogy of Fallot
overriding aorta, RV hypertrophy, pulmonary stenosis and a large VSD
168
what features are typical of an 'innocent' murmur?
soft blowing, systolic murmur, heard at least sternal edge which is asymptomatic
169
how does heart failure present in an infant
breathlessness on exertion/feeding, sweating, poor feeding, recurrent chest infections, faltering growth, tachycardia-cardia/pnoea, heart murmur/galloping rhythm, cardiomegaly, hepatomegaly and cold peripheries.
170
in first week of life what class of heart defects are more likely to be the cause of a heart failure presentation
left heart obstruction - hypo plastic left heart, severe coarctation of aorta, critical aortic valve stenosis
171
presentation and treatment of TGA
day 2 (when PDA closes) get cyanosis, circulatory shock. mx - PG infusion and immediate surgical correction
172
presentation and treatment of TOF CHD
pick up antenatally or 1-2 months old - hypercyanotic episodes and ESM at LLSE (VSD)
mx cyanotic ep - self-limiting rx >15min with IV propranolol. Surgical correction at 6-9 months.
173
presentation and treatment of PDA
continuous machinery murmur under left clavicle which radiates to back and bounding pulse, large shunt can get heart failure/recurrent chest infections; PG inhibitors or cardiac catheterisation for closure at 1y/o
174
presentation and treatment of a large VSD
heart failure 4-6wks, tachypnoea, hepatomegaly, breathless/sweaty feeding, faltering growth/recurrent chest infection, soft PSM at LLSE, left parasternal heave. Mx diuretics, captopril, calories and surgery at 3-6/12
175
presentation and treatment of aortic coarctation
severe - circulatory collapse when PDA closes/later = htn/heart failure, absent femoral pulses, radio-femoral delay, arm BP>leg BP, systolic murmur over back. Mx A to E resus, PG infusion
176
define hyperkinetic disorder
early onset, persistent pattern of inattention, hyperactivity and impulsivity that is more frequent and severe than that seen in an individual of comparable stage of development, it must be present in more than one situation, e.g. present at school and at home
177
risk factors for hyperkinetic disorder
male, family hx, social deprivation, family conflict, parental cannabis and alcohol exposire
178
clinical features of hyperkinetic disorder
onset <7y/o with duration 6m+ in 2+ settings
inattention - forgetful, distractible, finds it difficult to sustain/organise tasks, reluctant to engage in mentally strenuous task
hyperactivity - excessively talkative, running/climbing/jumping inappropriately, fidgets
impulsivity - can't wait turn, interrupts, runs into the road, temper tantrums
that does not fulfil the dx'ic criteria for a pervasive developmental disorder, mania, depression, anxiety
179
Ix in hyperkinetic disorder
collateral reports from parents and school, hearing tests, rating scales, ?blood tests inc thyroid
180
Mx of hyperkinetic disorder
10wk watch + wait to see if sx resolve before referral to secondary care
pre-school - parental education and training to reinforce positive behaviour and mx disruptive behaviour
school-age - psychoeducation + CBT (± social skills training), if severe then rx 6 wk trial methylphenidate 1st line, lisdexamfetamine 2nd line.
181
counsel methylphenidate prescription
```
Take OM (bedtime dose can result in sleep disturbance)
S/E headache, insomnia, appetite suppression and weightloss. Often see rebound hyperactivity as dose wears off in evening. Potentially cardiotoxic so baseline ECG. 6-monthly height, weight, BP + HR.
```
182
what is autism spectrum disorder?
a pervasive developmental disorder characterised by impaired social interaction, impaired communication and repetitive/stereotyped behaviour and interests.
183
clinical features of autism spectrum disorder?
onset <3y/o
asocial - few social gestures (waving, nodding, pointing), lack of eye contact/social smile (6wk)/response to name (12m)/interest in others/emotional expression/sustained relationships/awareness of social rules
Behaviour - repetitive restricted and stereotyped (twisting, rocking), upset by changes in routine, may prefer the same food/clothes/games, obsessively pursed interests
Communication - delayed + distorted speech, echolalia
may also have intellectual disability, temper tantrums, impulsivity, cognitive impairment. conditions assoc with autism = epilepsy, visual/hearing impairment, pica, constipation, infection, sleep disorder, underlying conditions (PKU, fragile X, TS, congenital rubella, hyperkinetic disorder, MDD, BPAD, anxiety, OCD)
184
Ix Autism spectrum disorder
diagnosis by a specialist, full developmental assessment (family hx, obstetric hx, milestones, medical hx, daily living skills, assessment communication/social interaction/behaviour) ?hearing test, screening tools inc CHAT and ASSQ
185
Ddx for ASD
Aspergers syndrome, rests syndrome, childhood disintegrative disorder, learning disability, deafness
186
how does Aspergers syndrome differ to ASD?
NO impairment in language/cognition/intelligence
187
what is childhood disintegrative disorder?
2yrs of normal development followed by regression in motor/language/social skills, repetitive and stereotyped interests and behaviours, decline in cognition
188
mx of ASD
Dx by specialist at age 3+ (reliable), local autism team provide key worker to manage and coordinate care
- Bio = little role for it, rx comorbidities, if v severe challenging behaviour that does not respond to psychosocial intervention ?haloperidol, sleeping disorder ?melatonin
- Psych - psychoeducation for families and carers, full assessment of functions of behaviour, CBT if verbal + cognitive ability to engage and is motivated
- Social - support groups and self-help groups (national autistic society), ?special schooling, social communication intervention (play based), modification of environment that reinforces challenging behaviour, intervention for life skills, coping strategies,
189
What is a learning disability
state of arrested/incomplete development of the mind, characterised by intellectual performance <70, onset at birth/early childhood and wide range of functional impairment inc social handicap due to reduced ability to acquire adaptive skills
190
causes of learning disability
commonly not known if mild LD
T21, ASD, CP, APH, pre-eclampsia, birth asphyxia/IVH, angel man synd, fragile X, neonatal hypothyroidism, alcohol/cocaine exposure in-utero, socioeconomic deprivation
191
clinical features of learning disability
mild - picked up at school struggle with academic work, adequate language/social/self-care ability
moderate - can communicate but limited language, may require some supervision but can do simple work
severe - marked motor impairment, little/no speech in early childhood but may eventually use simple communication, supervision for simple tasks
profound - severe motor impairment and difficulty communicating, little-no self care, mostly require residential care
192
how does fragile x syndrome present?
large protruding ears, long face, high arched palate, flat feet, lax joints, macro-orchidism, mitral valve prolapse
193
why are preemies more at risk of PDA?
immature lungs - where PG usually broken down for closure of PDA
heart less sensitive to falling PG levels at birth
hypoxia more common in preterm - promotes duct staying open
194
how does Kawasaki disease present?
```
5 days fever + 4 of CLEAR
Conjunctivitis
Lymphadenopathy and lips (cracked, red) + strawberry tongue
Extremities involved
Aneurysm
Rash
```
195
iv fluid bolus in child with shock quantity and time
20ml/kg over less than 10mins
196
iv fluid quantity in kids maintenance fluid
100ml/kg/24h first 10kg
50ml/kg/24h 10-20
20ml/kg/24h remaining
(4/2/1 rule hourly rate)
197
kids fluid replacement equation
% dehydration (<7.1 10%; 7.1+ 5%) x weight (kg) x 10(ml) over 24-48h
198
presentation of measles and what is back to school advice?
prodrome - irritable, fever, conjunctivitis and harsh cough, Koplik spots, maculopapular 'morbiliform' rash spreads from behind ears to face and trunk. School exclusion for 4d from rash onset
199
complications of measles
otitis media, pneumonia, encephalitis, febrile convulsions, very rare late - subacute sclerosing panencephalitis
200
presentation of mumps and complications, back to school advice?
uni->bilateral parotitis, fever, myalgia, malaise
| viral meningitis, orchitis, unilateral transient hearing loss, pancreatitis; 5d after onset of gland swelling
201
presentation of rubella and back to school advice
low grade fever, maculopapular rash spreads from face to whole body fades day 3-5, lymphadenopathy
School exclusion for 4d from rash onset
202
presentation of chickenpox and management and complications
fever with itchy, rash - macular -> papular -> vesicles; calamine lotion, don't scratch, stay off school until lesions have dried out and crusted over (~5d after rash onset). complications - pneumonia, encephalitis, secondary bacterial skin infection
203
slapped cheek syndrome presentation
fever -> rose red rash on cheeks, fine lace-like rash which may spread to trunk and limbs; caused by parvovirus B19 - can cause aplastic crisis in SCA, foetal anaemia heart failure and death in pregnancy (can affect erythroblasts in BM)
204
scarlet fever aetiology, presentation, management and complications
reaction to erythrogenic toxins produced by group a b-haemolytic strep. P/C high fever, sore throat, 'sandpaper' texture rash, strawberry tongue, flushed cheeks with circumoral pallor. PO penicillin V for 10d back to school 24h after starting. Complications - OM, rheumatic fever, acute glomerulonephritis
205
risk factors for respiratory distress syndrome?
```
Prematurity
Male
diabetic mom
C-section
younger of premature twins
```
206
how does respiratory distress syndrome present?
In first 24h life - increased rate and work of breathing, tachypnoea, intercostal and subcostal recessions, grunting, increased oxygen requirement, CXR ground glass shadowing and air bronchograms
207
management of resp distress syndrome?
IM corticosteroids to moms in premature labour to advance fetal lung maturation
resp support - O2, assisted ventilation, CPAP
surfactant via ET tube
208
presentation of necrotising enterocolitis inc AXR findings
pre-term baby with feed intolerance, abdo distension, bloody stool; pneumatosis intestinalis (air in the intestinal wall), bowel wall oedema, Riglers sign (air inside and outside wall), dilated bowel loops often asymmetrical
209
complications and management of necrotising enterocolitis
bowel ischaemia, inflammation, necrosis and perforation
Mx - bowel rest (NBM with TPN), antibiotics - benzylpenicillin gentamicin and metronidazole, surgery to remove perforated or necrotic bowel
210
differential diagnosis of neonatal constipation
```
imperforate anus
duodenal/oesophageal atresia
meconium ileus/plug inc CF
hypothyroidism
Hirschsprungs disease
```
211
differential diagnosis of constipation in an infant/child
```
idiopathic
hypothyroidism
obstruction/intusussception
coeliac disease
CMPI
Hirschsprungs
pain on defecation - fissures
metabolic - hypercalcaemia, hypokalaemia, dehydration
```
