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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
What is hirschsprungs disease?
* 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**
26
What are some of the associations of Hirshsprungs disease?
DS Neurofibromatosis Wardenburgs Syndrome Multiple Endocrine Neoplasia II
27
How can Hirshsprungs disease present itself?
* 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
How is Hirschsprungs disease investigated
Gold standard: Rectal biopsy AXR
29
How is Hirshsprungs disease managed?
Conservative: rectal washouts, bowel irrigation Surgical: definitive: surgical resection of the aganglionic section of bowel
30
What are some of the complications of Hirshsprungs disease? How is it managed?
**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
What is necrotizing enterocolitis?
* Bowel becomes necrotic which increases the risk of perforation causing potention peritonitis and shock
32
What are the cardinal features of NEC?
* A*bdominal distension* * *Bilious aspirates* * *Bloody stools*
33
What are some of the RFs for NEC?
* **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
When/ where/ how does NEC present?
* 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
What are some of the signs of NEC?
* GI: persistent GI bleeding, marked abdo distension, ascites, palpable distended bowel loops, tender abdomen, abdo discolouation
36
What are some of the AXR signs of NEC?
* 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
How is NEC ixd?
* 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
How is NEC managed?
STAIN * S: SURGICAL EMERGENCY * TPN * Abx: gentamycin, amoxicillin and metronidazole * IV fluids * NBM/ NGT
39
What are the most common organisms for neonatal sepsis?
GBS E. Coli, Listeria. Others: Klebsiella, Staphylococcus aureus
40
What are the RFs for neonatal sepsis?
* 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
What are the signs + sx of neonatal sepsis?
* 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
What are the main differentials for neonatal sepsis?
CHD, metabolic problems, TTN
43
How is neonatal sepsis Ixd?
* 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
How is neonatal sepsis mxd?
* **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
What is Chronic Lung Disease?
* Also known as bronchopulmonary dysplasia * Requirement for ventilator support with supplementary oxygen +/- mechanical ventilation for \>28 days with typical CXR changes
46
What are some of the RFs for CLD?
* pre-term birth, maternal chorioamnionitis, severe RD * hyperoxia, pulmonary air leak (pneumothorax and PIE), PDA, post natal sepsis
47
How does CLD present?
* 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
How is CLD prevented?
Corticosteroids – PO **dexamethasone** to mothers that show signs of premature labour at less than 36 weeks gestation
49
How is CLD mxd?
* **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
What is surfactant deficienct lung disease?
* 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
What are the main RFs for surfactant deficient LD?
* **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
What are the sx/ signs of surfactant deficient LD?
* tachypnoea, intercostal recession, expiratory grunting and cyanosis * Nasal flaring * Head bobbing * Poor feeding/ lethargy * CXR: ***'ground-glass'*** appearance with an indistinct heart border
53
How is Surfactant deficient lung disease mxd?
Prevention during pregnancy: maternal **corticosteroids** to induce fetal lung maturation Post natal * oxygen * assisted ventilation * **exogenous** **surfactant** (curosurf/ survanta) given via endotracheal tube
54
What is Transient tachypnoea of the newborn (TTN)?
* 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
What are the RFs for TTN?
**C section:** possibly due to the lung fluid not being 'squeezed out' during the passage through the birth canal
56
How does TTN present?
* tachypnoea +/- other signs of respiratory distress * Raised RR
57
What does TTN show on x ray?
* Signs of pulmonary overload: * Wet looking lung fields with *fluid in fissures, hyperinflation of the lungs,* * *Prominent perihilar interstitial markings*
58
How is TTN mxd?
* May require **supplemental** **oxygen**, rare: **PPV** (+ve pressure ventilation), maintain body temperature * Prognosis: usually resolves in **24h**
59
What is meconium aspiration syndrome (MAS)?
* 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
What are the RFs for MAS?
* **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
How does MAS present?
* **Respiratory distress** * Total or partial airway obstruction * Foetal hypoxia * Infection * Persistent pulmonary hypertension of the newborn
62
How is MAS ixd?
* **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
How is MAS mxd?
* 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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