Paediatrics 10 Flashcards
1
Q
Management of gastroenteritis
A
- usually managed conservatively with fluid replacement or roal rehydration sachets, if severe antibiotics can be used in bacterial.
- May need hospitalisation for IV fluids
- Dont return to work in hospitals, schools or care homes till >48hrs after vomiting and diarrhoea have stopped
- Wash clothes regularly and disinfect surfaces
Indications for antibiotics: systemically unwell, immunosuppressed, elderly
2
Q
Specific antibiotics for gastroenteritis
A
- Salmonella and shigella are treated with ciprofloxacin.
- Campylobacter is treatment with a macrolide, such as erythromycin.
- Cholera is treated with tetracycline, to reduce transmission.
- Food poisoning is a notifiable disease in the UK.
3
Q
Visual field defects
A
- Different causes like glaucoma, stroke, brain tumour and retinal detachment
- Bitemporal hemianopia: associated with pituitary adenomas compressing the optic chiasm. Homonymous hemianopia may be caused by stroke. Central scotoma is often seen in macular degeneration and optic neuritis
- Investigations: Automated perimetry (assessment of visual fields), MRI of brain and orbit and OCT
4
Q
Volvulus
A
- Twisting of the GI tract causing obstruction and possible strangulation or infarction
- Paediatric causes: Meckels diverticulum, Hirschsprungs disease
- Tend to get midgut or small bowel volvulus
- Clinical features: severe, crampy abdo pain, associated with nausea, vomiting and constipation
- Examination: distended abdomen which is tympanic to percussion with decreased or absent bowel sounds
5
Q
Volvulus investigations and management
A
- Investigation: AXR shows a ‘coffee bean sign’, CT, Sigmoid/colonoscopy (can be diagnostic and therapeutic), Barium enema (birds beak sign)
- Management: IV fluids and analgesia, decompress the twisted segments either endoscopically or surgically
- Sigmoid volvulus can be managed initially with flexible sigmoidoscopy but has high recurrent rate so should recieve definitive surgery
- Complications: ischaemic bowel, peritonitis, sepsis
6
Q
Whooping cough
A
- Whooping cough is caused by the gram negative Bordetella pertussis and typically presents in children
- Vaccinated at 2, 3, 4 months and 3-5 years
- Newborn infants are particularly vulnerable which is why pregnant woman are vaccinated at 16-32 weeks gestation
- Neither infection or immunisation results in lifelong protection
7
Q
Whooping cough features
A
- Prodrome: viral URTI like symptoms
- Cough which is worse at night and after feeding, can cause vomiting and central cynaosis
- Inspiratory whoop
- Infants may have apnoea spell
- Lasts between 2-8 weeks
- Complications: subconjunctival haemorrhage, pneumonia, bronchiectasis, seizure
8
Q
Whooping cough investigations and management
A
- Investigations: nasal swab with PCR and serology
- Management: Notifiable disease, infants under 6 months with the condition should be admitted
- Give an oral Macrolide (Clarithromycin, azithromycin) if cough onset is within 21 days
- Household contacts should get antibiotic prophylaxis
- School exclusion:48 hoursafter commencing antibiotics (or 21 days from onset of symptoms if no antibiotics )
9
Q
Jaundice overview
A
- Yellow discolouration of skin and sclera of newborn babies
- Accumulation of bilirubin in the skin and mucous membranes (hyperbilirubinaemia).
- Very common- 60% of term babies and 80% of preterm
- Can be due to an underlying condition but is usually physiological
10
Q
Physiological jaundice
A
- Causes= High haemoglobin in utero, Immature liver, HbF- short BC lifespan (70-80 days), Bruising
- Appears after 24 hours, peaks day 4-5, not detectable after 14 days, disappears without any treatment
- Well and thriving
- Baby should be watched for worsening jaundice
- Jaundice related to breastfeeding: inadequate feeding causing dehydration, increased enterohepatic circulation, glucuronyl transferase inhibitor
11
Q
Pathological causes of jaundice
A
- Haemolytic disease of the newborn: Rhesus incompatibility, ABO incompatibility
- Infection
- Hypothyroidism
- Neonatal hepatitis
- Biliary atresia
12
Q
Why do we worry about Hyperbilirubinaemia- Kernicterus
A
- Unconjugated bilirubin (fat soluble) can cross blood brain barrier and penetrate brain cells, causing irreversible neuronal dysfunction or death
- Bilirubin causes staining and necrosis of neurons in the basal ganglia, hippocampal cortex, subthalamic nuclei, and cerebellum
- Complications: Chorioathetoid cerebral palsy, Sensorineural hearing loss, Dental enamel dysplasia, Cognitive impairment
13
Q
Why do we worry about Hyperbilirubinaemia: Acute Bilirubin Encephalopathy
A
- Phase 1 - reduced alertness, hypotonia and poor feeding
- Phase 2 - fever and hypertonia or opisthotonos
- Phase 3 - hypotonia, high pitched cry, hearing and visual abnormalities and athetosis
- Opisthotonos: a prolonged severe spasm of the muscles causing the back to arch acutely, the head to bend back on the neck, the heels to bend back on the legs and the arms and hands to flex rigidly at the joints
14
Q
Why do we worry about Hyperbilirubinaemia: Rhesus incompatibility
A
- When blood from a Rh+ baby enters the Rh- mums blood stream and antibodies develop which cross the placenta and destroy the infants red blood cells
- Increased destruction of red blood cells leads to increased bilirubin in the blood
- Anti Rh D immunoglobulin given to pregnant women at 28 weeks of pregnancy and within 72 hours of delivering an infant who is born Rh positive. If mother is already sensitised the injection doesn’t work
15
Q
ABO incompatibility
A
- Haemolytic disease caused by reaction of maternal anti-A or anti-B antibodies with foetal A or B antigens
- Usually milder than Rh, almost exclusively in type O mothers, jaundice appears at 24 hours
