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
16
Q
Why do we worry about Hyperbilirubinaemia: biliary atresia
A
- CBD is blocked or absent
- Condition leads to liver failure and deat
- Cause is unknown
- Needs surgical intervention: kasai procedure or liver transplantation
- Signs and symptoms: Clay coloured stool, dark urine, distended abdomen, hepatomegaly, prolonged jaundice resistant to phototherapy and/or exchange transfusion
17
Q
Investigations: day 3 jaundice
A
- FBC: platelets (viral infection), anaemia (haemolysis), Neutrophils (infection), blood film
- Split bilirubin: total and conjugated (<20%)
- Group and Coombs: ABO/ Rhesus incompatibility
18
Q
Prolonged jaundice investigations
A
- Split bilirubin
- Thyroid function
- LFT (increased ALT suggests hepatitis)
- Septic screen- urine culture
- If conjugated: TORCH screen, Urine metabolic screen, Liver USS (assess biliary tract), Liver isotope scan (biliary atresia), Coagulation (obstructive jaundice -> vitamin K deficiency)
Direct Coombs test: measures the amount of maternal antibody coating the infants red blood cell. If the antibody is present the test is positive
19
Q
Phototherapy and Exchange transfusion
A
Phototherapy
- Photoisomerization of unconjugated bilirubin so it can be excreted without conjugation (bile and urine)
- Use blue light phototherapy
- Make sure skin is exposed as possible and light isn’t too far away, protect the eyes
Exchange transfusion: approximately 85% of electrolytes will be replaced, serum bilirubin levels should decrease by 50%
20
Q
Causes of prolonged jaundice
A
- biliary atresia
- hypothyroidism
- galactosaemia
- urinary tract infection
- breast milk jaundice: thought to be due to high concentrations of beta-glucuronidase → increase in intestinal absorption of unconjugated bilirubin
- prematurity: due to immature liver function, increased risk of kernicterus
- congenital infections e.g. CMV, toxoplasmosis
21
Q
Management in the delivery room for premature babies
A
- Senior staff presence
- Temperature Control: roasting bags can be used to maintain the temperature of babies born <32 weeks gestation. There are manufactured thermal bags for preterm infants on the market but a lot more expensive. Also hats
- Respiratory support
- Surfactant
- Usually in presence of parents
- Once stabilised – transfer to NICU, usually at 10-15 minutes of age
- Usually stabilisation rather than rescusitation
22
Q
Premature babies: temperature control and fluid balance
A
- Preterm babies susceptible to heat and fluid loss
- At birth placed in plastic bag with direct heat
- Nursed in humidified incubators to prevent fluid loss
23
Q
Preterm babies: neonatal care
A
- Temperature/Fluid loss
- Skin Care- preterm babies have very friable skin which is prone to breaking which can lead to infection.
- Pain
- Optimal Environment/ Minimal Handling
- Respiratory Support- most preterm infants have respiratory failure due to weak respiratory muscles, immature respiratory centre and surfactant deficiency
- Cardiovascular Support
- Prevention of Infection
- Feeding
24
Q
Respiratory distress syndrome
A
- Deficiency of pulmonary surfactant
- Surfactant: reduces surface tension, maintains alveolar stability. Mainly produced at 30-32 weeks onwards. Antenatal steroids increase cortisol levels which stimulate surfactant production
- CXR: ground glass appearance, limited expansion, air bronchogram
25
Preterm: cardiovascular problems
- Patent ductus arteriosus
- Cardiac failure
- Careful fluid management and ionotropic (support cardiac muscle contractility) support
26
Preterm: feeding/nutrition
- Fewer nutrient reserves- fat and glycogen are only deposited in the third trimester
- Increased physiological and metabolic stresses
- <34 weeks oral feeding may not be safe/possible
- Feeds slowly established over a few days, preterm babies have a lack of suckling reflex
- Babies fed with breast milk/ EBM/ Preterm formula. May need formula for adequate growth
27
Preterm: providing nutrition
- Fine feeding tube passed via nose/mouth into stomach (orogastric/nasogastric feeding tube). If unable to tolerate sucking/swallowing/breathing
- Very preterm infants: slow to tolerate feeds (takes 7-10 days), fed by Total Parenteral nutrition (TPN), expressed breast milk
- Prevention of Necrotising Enterocolitis
- Feeding slowly introduced at <32 weeks gestation and takes several days to build up
28
Necrotising enterocolitis
- Inflammation and necrosis of the bowel wall
- Increased risk with lower gestational age
- High morbidity and mortality
- Breast milk protective
- AXR: intestinal pneumatosis and perforation
29
Preterm: neurological problems
- Premature brain- highly vascular
- Intraventricular haemorrhage- prone to bleeding in the first 7-10 days of life, can be mild in ventricles or severe in brain tissue. Graded 1-4, with 4 being severe. Diagnosed by cranial US
- Prognosis related to severity: motor problems, developmental delay
- Promote normal development in NICU: environment i.e. reducing noise and light
30
Preterm: long term issues
- Preparation for discharge
- Chronic lung disease/ home oxygen
- Risk of different development- Neurodisability input
- Allied health professionals-Physio, SAKT, Dietician
- Opthalmology follow up- if significant retinopathy of prematurity
- Audiology follow up- risk of hearing loss
31
Chronic lung disease of prematurity
- Need for ventilatory support/oxygen at 36 weeks after gestation
- Majority of babies born <28 weeks gestation will go home on oxygen
- More at risk of respiratory conditions i.e. bronchiolitis
- Home oxygen: have small portable cylinder which carer wears as a backpack for short visits out which is discreet and can fit in the bottom of the pram
32
Reasons for admission to NICU
- Respiratory distress
- Neurological: Hypoxic-ischaemic Encephalopathy, seizures
- Infection
- Feeding intolerance: congenital anomaly
33
Respiratory distress- clinical signs
- Worsening respiratory distress at/soon after birth
- Tachypnoea (>60/minute)
- Recession – intercostal, subcostal, sternal)
- Tracheal tug
- Expiratory grunting
- Cyanosis
- Decreased breath sounds
- Differentials: RDS, Transient Tachypnoea of Newborn, Infection, Meconium Aspiration Syndrome, Congenital anomaly (Congenital Diaphragmatic Hernia, Abnormalities of airway/lungs)
34
Respiratory distress: CXR findings
- TTN: Fluid level in right lung in horizontal fissure
- Meconium aspiration – bilateral patchy changes
- Congenital diaphragmatic hernia – bowel in left side of chest
35
Causes of Hypotonic infant at birth
- Antenatal/perinatal insult: Hypoxic ischaemic encephalopathy
- Genetic/syndromes: Trisomy 21, prader Willi, muscular dystrophy
- Infection, metabolic, congenital brain abnormalities
36
Hypoxic ischaemic enchalopathy
- Oxygen shortage around the time of and during birth
- Can lead to brain injury resulting in disability or death
- Some babies can benefit from therapeutic hypothermia, where the baby’s temperature is lowered to 33.5 degrees for 72 hours by cooling mat. Slows down/prevents inflammatory cascade that can cause brain injury. Not all babies are suitable. Only done on term, near-term babies, has to be after 6-8 hours after birth
37
Infection in term infants
- Usually onset within 48 hours of birth
- Risk factors- prelabour rupture of membranes, maternal infection
- Common organisms: Group B streptococcus, E.coli
38
Congenital abnormalities: GIT
- Feeding intolerance: upper GI atresia, malrotation. Duodenal atresia has a classic bubble sign
- Abdominal distension: Hirschsprung, volvulus/malrotation, meconium plug (associated with CF), lower GI atresia
