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Year 4 - Paediatrics > Neonatal Medicine > Flashcards

Neonatal Medicine Flashcards

1
Q

What are the different types of neonatal jaundice? And their causes?

A

Early jaundice

  • Usually pathological
  • Blood: ABO incompatability, rhesus incompatability, maternal blood group

Jaundice 24h to 14 days: usually physiological

  • Physiological (usually unconjugated) RBC breakdown, immature liver, breastfeeding
  • Pathological:
    • Cephalohaematoma
    • TPN
    • Hypothyroidism
    • Haemaglobinopathoes
    • Infection
    • Metabolic (hypo/hyperthyroidism
    • Galactosaemia, choledactal cyst
    • BILIARY ATRESIA

Prolonged

  • Unconjugated: UTI, gilbert syndrome
  • Conjugated: hypothyroidism, biliary atresia, choledocal abnormalities, galactosaemia, tyrosinaemia, neonatal haemachromatosis, CF
  • Obstructive jaundice with hepatomegaly:
    • Extra hepatic biliary atresia
    • Alagille syndrome
    • Endocrine and metabolic: panhypopituitarism, galactosaemia, tyrosinaemia
    • Structural: choledochal cyst
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2
Q

What are some of the RFs for neonatal jaundice?

A
  • SMALL BABY: LBW/ prematurity
  • SUGAR MAMA: diabetic mother, exclusively breast fed
  • Jaundice in <24h
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3
Q

How is neonatal jaundice assessed

A
  • Serum bilirubin
    • <35/40,
  • Transcutaneous bilirubinometer
    • If >35 weeks, gestation >24h
  • Further Ix: : serum bilirubin, blood group, FBC, UE, LFTs, infection screen, Microbiological cultures if infection suspected: blood, urine, CSF. Consider TORCH screen, Glucose-6-phosphate dehydrogenase,
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4
Q

How does a baby with neonatal jaundice present?

A
  • Eyes: yellowing sclera, skin, gums
  • Drowsy: off feeds, short feeds, difficult to rouse
  • Neurologically: altered muscle tones, seizures
  • Other: abdo mass, organomegaly, dark stool pale urine
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5
Q

How is neonatal jaundice managed?

A

Phototherapy

IV immunoglobulin

Exchange tranfusion

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6
Q

What are some of the complications of neonatal jaundice?

A
  • Kernectirus
  • Unconjugated bilirubin can cross BBB
  • Low IQ, CP, deafness
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7
Q

What is biliary atresia?

A
  • Congenital condition causing the narrowing or absence of common bile duct
  • This can result in cholestasis
  • It causes an increase in conjugated bilirubin: dark stools and pale urine
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8
Q

What are some of the associations of biliary atresia?

A
  • Cardiac abnormalities
  • Situs intervsus ​
  • Polysplenia
  • Preterm births
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9
Q

What are some of the signs of biliary atresia?

A
  • Hepato/splenomegaly
  • Jaundice
  • Abnormal growth
  • Cardiac murmurs
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10
Q

What are some of Ix used for biliary atresia?

A
  • Serum bilirubin: conjugated (abnormally high)
  • LFTs: serum bile acids and aminotransferases
  • Serum alpha 1 anti trypsin
  • Sweat chloride test
  • USS of liver tree and biopsy
  • Perc. liver biopsy with intraoperative cholangioscopy : bile plugs and bile duct proliferation
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11
Q

How is biliary atresia managed?

A

Surgery: Kasai portoenterostomy and (roux en y)

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12
Q

What are some of the complications of biliary atresia?

A
  • Cirrhosis -> liver transplant ->> increased risk of HCC
  • Faulty anastomosis
  • Liver disease
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13
Q
A
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14
Q

What is pyloric stenosis?

A
  • Present 2nd-4th week of life with vomiting
  • Caused by a hypertrophy of the circular muscle of the pylorus resulting in a narrowing of pylorus
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15
Q

What factors affect pyloris stenosis?

A
  • +ve FH
  • More common in males
  • First borns
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16
Q

What are some the features of pyloris stenosis?

A
  • Projectile (non bilious) vomiting usually 30mins after eating
  • Constipation and dehydration
  • Failure to thrive
  • Palpable olive sized mass in the upper abdomen
  • Metabolic alkalosis (hypochloraemic, hypokalaemia)
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17
Q

How is pyloric stenosis diagnosed?

A

USS

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18
Q

How is pylorus stenosis managed?

A
  • Wide bore NGT - to correct the electrolye disturbances
  • Ramstedt pyloromyotomy
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19
Q

What is gastroschisis

A

Congenital defects in the anterior abdominal wall resulting in the intestines being outside the abdo cavity

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20
Q

How is gastroschisis managed?

A
  • Can attempt vaginal delivery
  • Surgery: post birth no more than 4 hours
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21
Q

What is omphalocoele?

A

Gastrointestinal congenital condition where there is a defect in the anterior abdominal wall resulting in the abdominal contents protruding outwards (but covered by the amniotic sac formed by the amniotic membrane and peritoneum

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22
Q

How is omphalocoele managed

A
  • Delivery by C section
  • Surgery: A staged repair
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23
Q
A
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24
Q

What are some of the associations of omphaloceoele?

A

DS

Cardiac and kidney malformation

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25
Q

What is hirschsprungs disease?

A
  • Congenital GI condition where the nerve cells of the myenterix plexus are absent
  • Pathophysiology: thought to occur due to the absence of parasynmpathetic ganglion cells when they dont travel down the colon
  • Can result in total colonic agangliosis
  • This results in constriction of some parts of the colon and distension of others, and absent peristalsis
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26
Q

What are some of the associations of Hirshsprungs disease?

A

DS

Neurofibromatosis

Wardenburgs Syndrome

Multiple Endocrine Neoplasia II

27
Q

How can Hirshsprungs disease present itself?

A
  • Delay in the passage of meconium in the first 24h
  • Chronic constipation
  • Abdominal distension and pain (due to obstruction)
  • Vomiting
  • Poor weight gain/ failure to thrive
28
Q

How is Hirschsprungs disease investigated

A

Gold standard: Rectal biopsy

AXR

29
Q

How is Hirshsprungs disease managed?

A

Conservative: rectal washouts, bowel irrigation

Surgical: definitive: surgical resection of the aganglionic section of bowel

30
Q

What are some of the complications of Hirshsprungs disease?

How is it managed?

A

Hirshsprungs associated enterocolitis

  • Inflammation and obstruction of the intestine (20% of neonates w/ the condition)
  • 2-4 weeks: diarrhoea, N+V, abdominal distension, maybe fx of sepsis
  • Complications: toxic megacolon + bowel perforation
  • Mx: IV fluids, NG tube, urgent abx, decompression of the obstructed bowel.
31
Q

What is necrotizing enterocolitis?

A
  • Bowel becomes necrotic which increases the risk of perforation causing potention peritonitis and shock
32
Q

What are the cardinal features of NEC?

A
  • Abdominal distension
  • Bilious aspirates
  • Bloody stools
33
Q

What are some of the RFs for NEC?

A
  • Enteral feeding: formula milk (not breastfeeding),
  • Gut ischaemia: IUGR, perinatal asphyxia, placental abruption, PDA, cyanotic HD, umbilical arterial cathetarisation, anaemia
  • Fetal echogenic bowel
  • Abnormal blood flow
34
Q

When/ where/ how does NEC present?

A
  • Presents in 2nd to 3rd week of age in preterms
  • Sites: terminal ileum, caecum and ascending colon
  • Sx: feeding intolerance, abdominal distension and bloody stools, which can quickly progress to abdominal discolouration, perforation and peritonitis.
35
Q

What are some of the signs of NEC?

A
  • GI: persistent GI bleeding, marked abdo distension, ascites, palpable distended bowel loops, tender abdomen, abdo discolouation
36
Q

What are some of the AXR signs of NEC?

A
  • dilated bowel loops (often asymmetrical in distribution)
  • bowel wall oedema
  • pneumatosis intestinalis (intramural gas)
  • portal venous gas
  • pneumoperitoneum resulting from perforation
  • air both inside and outside of the bowel wall (Rigler sign)
  • air outlining the falciform ligament (football sign)
37
Q

How is NEC ixd?

A
  • Ix: WCC, CRP (up), reduced Hg, platelets (up then down), deranged U+E
    • ABG: metabolic acidosis
  • AXR: dilated bowel loops (often asymmetrical in distribution)
  • USS: bowel wall thickening, intramural gas, free peritoneal fluid, blood culture
  • Test: for occult blood ins aspirates and stool (rule out anal fissure)
38
Q

How is NEC managed?

A

STAIN

  • S: SURGICAL EMERGENCY
  • TPN
  • Abx: gentamycin, amoxicillin and metronidazole
  • IV fluids
  • NBM/ NGT
39
Q

What are the most common organisms for neonatal sepsis?

A

GBS E. Coli, Listeria. Others: Klebsiella, Staphylococcus aureus

40
Q

What are the RFs for neonatal sepsis?

A
  • Vaginal GBS colonisation
  • GBS sepsis in a previous baby
  • Maternal sepsis, chorioamnionitis or fever > 38ºC
  • Preterm birth following spontaneous labour (before 37 weeks)
  • Early (premature) rupture of membrane
  • Prolonged rupture of membranes (PROM) – over 18 hours in a pre term birth
41
Q

What are the signs + sx of neonatal sepsis?

A
  • Fever/ but also being cold: (<36 or >38)
  • Reduced tone and activity (floppiness)
  • Poor feeding
  • Respiratory distress or apnoea
  • Vomiting
  • Tachycardia or bradycardia
  • Hypoxia
  • Jaundice within 24 hours
  • Seizures
  • Hypoglycaemia
  • Need for mechanical ventilation in a pre term baby
42
Q

What are the main differentials for neonatal sepsis?

A

CHD, metabolic problems, TTN

43
Q

How is neonatal sepsis Ixd?

A
  • Bloods: FBC, UE, CRP, Blood cultures (before abx are given)
  • CXR only if clinical signs suggestive of pneumonia
  • LP before abx if safe, strong clinical suspicion of infection, or there are clinical sx or signs suggesting meningitis.
    • Perform If: -has a CRP of >10 mg/litre OR -has a +ve blood culture, OR does not respond satisfactorily to antibiotic treatment
    • After 48h of treatment to document whether the treatment is working
    • If deterioration occurs during abx course
  • Ix: ABG – also includes glucose
  • Eye swab: Chlamydia and Gonococcus (purulent eye discharge)
44
Q

How is neonatal sepsis mxd?

A
  • Supportive care: A-E, ventilation, ionotropic support, anticonvulsants
  • Blood cultures should be taken before antibiotics are given: Check baseline FBC and CRP, + LP
  • Choice of antibiotics (in 1h)
  • Empirical therapy if the organism is unknown: benzylpenicillin + gentamycin (neonatal to cover bacteria in the mother genitalia
    • 1st line (if the baby has gone home and come back): cefotaxime
    • Gram negative: infection either by CSF gram stain or culture: cefotaxime (can penetrate BBB/ CSF)
    • CSF gram stain +ve :IV amoxicillin + cefotaxime
    • GBS: benzylpenicillin least 14 days (Max 21 days)
    • Listeria: (rare): amoxicillin + according to NICE gentamycin (cannot cross BBB)
    • HS:+ Aciclovir – if HS detected
45
Q

What is Chronic Lung Disease?

A
  • Also known as bronchopulmonary dysplasia
  • Requirement for ventilator support with supplementary oxygen +/- mechanical ventilation for >28 days with typical CXR changes
46
Q

What are some of the RFs for CLD?

A
  • pre-term birth, maternal chorioamnionitis, severe RD
  • hyperoxia, pulmonary air leak (pneumothorax and PIE), PDA, post natal sepsis
47
Q

How does CLD present?

A
  • Chronic ventilator and oxygen dependence
  • Increased work of breathing
  • Increased respiratory secretions and bronchospasm
  • Apnoea, bradycardia, de-sat episodes
  • Feeding difficulties and growth failure
  • Crackles and wheeze on auscultation
48
Q

How is CLD prevented?

A

Corticosteroids – PO dexamethasone to mothers that show signs of premature labour at less than 36 weeks gestation

49
Q

How is CLD mxd?

A
  • Caffeine
  • CPAP (aim for o2 sats of 90-95)
  • NOT over oxygenating with supplementary oxygen
  • Salbutamol and ipratropium bromide, Diuretics,Systemic steroids
  • Further mx: RSV prophylaxis
50
Q

What is surfactant deficienct lung disease?

A
  • Surfactant deficient lung disease (SDLD, also known as RDS) is a condition seen in premature infants.
  • Caused by insufficient surfactant production and structural immaturity of the lungs
51
Q

What are the main RFs for surfactant deficient LD?

A
  • male sex
  • diabetic mothers
  • Caesarean section
  • second born of premature twins
  • Others: maternal hypertension, IUGR in babies born < 29 weeks, FH, MAS, Congenital pneumonia, severe HDN
52
Q

What are the sx/ signs of surfactant deficient LD?

A
  • tachypnoea, intercostal recession, expiratory grunting and cyanosis
  • Nasal flaring
  • Head bobbing
  • Poor feeding/ lethargy
  • CXR: ‘ground-glass’ appearance with an indistinct heart border
53
Q

How is Surfactant deficient lung disease mxd?

A

Prevention during pregnancy: maternal corticosteroids to induce fetal lung maturation

Post natal

  • oxygen
  • assisted ventilation
  • exogenous surfactant (curosurf/ survanta) given via endotracheal tube
54
Q

What is Transient tachypnoea of the newborn (TTN)?

A
  • Transient tachypnoea of the newborn (TTN) is the commonest cause of respiratory distress in the newborn period.
  • It is caused by delayed resorption of fluid in the lungs
55
Q

What are the RFs for TTN?

A

C section: possibly due to the lung fluid not being ‘squeezed out’ during the passage through the birth canal

56
Q

How does TTN present?

A
  • tachypnoea +/- other signs of respiratory distress
  • Raised RR
57
Q

What does TTN show on x ray?

A
  • Signs of pulmonary overload:
    • Wet looking lung fields with fluid in fissures, hyperinflation of the lungs,
    • Prominent perihilar interstitial markings
58
Q

How is TTN mxd?

A
  • May require supplemental oxygen, rare: PPV (+ve pressure ventilation), maintain body temperature
  • Prognosis: usually resolves in 24h
59
Q

What is meconium aspiration syndrome (MAS)?

A
  • Meconium aspiration syndrome refers to respiratory distress in the newborn as a result of meconium in the trachea.
  • It occurs in the immediate neonatal period.
60
Q

What are the RFs for MAS?

A
  • Post-term deliveries: 44% in babies born after 42 weeks.
  • Foetal distress: tachy/bradycardia
  • Hx of maternal hypertension, pre-eclampsia, chorioamnionitis, smoking or substance abuse.
  • Intrapartum hypoxia, IUGR
61
Q

How does MAS present?

A
  • Respiratory distress
    • Total or partial airway obstruction
    • Foetal hypoxia
    • Infection
    • Persistent pulmonary hypertension of the newborn
62
Q

How is MAS ixd?

A
  • CXR: increased lung volumes, assymetrical patchy, pulmonary opacities , pleural effusions, pneumothorax
  • Infection markers: FBC, CRP, blood stools
  • Other standard neonatal investigations: ABG, dual pulse oximetry, echo, cranial USS
63
Q

How is MAS mxd?

A
  • Surfactant, inhaled NO, abx, chest drain
  • Ventilation: early intubation and PPV: Aim for sats of ?98%’ High PEEP: risk of a pneumothorax

Year 4 - Paediatrics (4 decks)

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