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MSRA Content > Level 1 - Neonate, Infections, Haematology > Flashcards

Level 1 - Neonate, Infections, Haematology Flashcards

1
Q

What is jaundice?

A
  • Yellow colouration of skin and sclerae (whites of the eyes)
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2
Q

Jaundice is caused by?

A

o accumulation of bilirubin which is mainly produced from the breakdown of red blood cells
o Red blood cell breakdown creates unconjugated bilirubin which circulates mostly bound to albumin
o Unconjugated bilirubin is metabolised by the liver to produce conjugated bilirubin which is excreted in the stool

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3
Q

Why is there higher bilirubin levels in neonates?

A

o Higher bilirubin levels in neonates because they have a higher concentration of red blood cells, which also have a shorter lifespan (70 days) and liver less efficient

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4
Q

Epidemiology of neonatal jaundice?

A
  • 60% of term and 80% of preterm babies develop jaundice in the first week of life
  • 10% of breastfed babies are still jaundiced at 1 month
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5
Q

Risk factors for neonatal jaundice?

A
  • Low birth weight
  • Breast-fed babies
  • History of jaundice in family
  • Maternal diabetes
  • Males
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6
Q

What is physiological jaundice? When does it occur and disappear?

A
  • Increased erythrocyte breakdown and immature liver function.
  • Presents at 2 or 3 days of age, begins to disappear towards the end of the first week and has resolved by day 10
  • Baby remains well
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7
Q

What causes jaundice <24 hours (early) after birth?

A

Pathological

  • Sepsis
  • Haemolytic disorders
  • Congenital infections
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8
Q

What haemolytic disorders cause early neonatal jaundice?

A

Rhesus
ABO
G6PD deficiency
Spherocytosis

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9
Q

Describe rhesus incompatibility and how it presents?

A

 Usually identified antenatally and monitored
Only presents in Rh negative mother and Rh positive foetus
Antibodies against Rhesus D antigen are produced by mother and can then cross placenta
 Birth affected with anaemia, hydrops and hepatosplenomegaly
 Develop severe jaundice

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10
Q

Describe ABO incompatibility and how it presents?

A

 Now more common, some group O mothers have IgG anti-A haemolysin which crosses placenta (can have anti-B haemolysins)
 Can get severe jaundice but hepatosplenomegaly is absent
 Coombe’s test for antibody is positive

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11
Q

Describe G6PD deficiency and how it presents?

A

 X-linked disease
 Seen in Mediterranean, Middle and Far East
 Enzyme which prevents oxidative damage to RBCs
 List of drugs need to be avoided

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12
Q

Describe spherocytosis and how it presents?

A

 Recognised by spherocytes on blood film

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13
Q

What congenital infections cause early jaundice?

A

o TORCH infections

o Conjugated bilirubin

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14
Q

Definition of prolonged jaundice?

A

Longer than 2 weeks in term, 3 weeks in preterm baby

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15
Q

Name the causes of prolonged jaundice which causes unconjugated hyperbilirubinaemia?

A 
Breast milk jaundice (most common)
Infection
Hypothyroidism
Haemolytic Anaemia (G6PD deficiency)
Pyloric stenosis
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16
Q

Name the causes of prolonged jaundice which causes conjugated hyperbilirubinaemia?

A

o Bile Duct Obstruction
o Neonatal Hepatitis
o Biliary Atresia

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17
Q

What is breast milk jaundice?

A

 Mechanism unknown
 Common in healthy, term, breastfed babies. Weight gain, stools, urine output, and examination are normal and the neonate is well
 Usually presents within the first week of life (day 2-4) and peaks on day 7 to 15. In some cases, it can persist for up to 12 weeks

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18
Q

How does an infection cause jaundice?

A

 Results from poor fluid intake, haemolysis, reduced hepatic function, increase in entero-hepatic circulation
UTI especially

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19
Q

Symptoms of neonatal jaundice?

What is kernicterus?

A

Jaundice
- First becomes visible in the face and forehead
- Visible on the trunk and extremities
Drowsiness
May have Hepatosplenomegaly, petechiae and microcephaly
- Associated with haemolytic anaemia, sepsis and congenital infections
Jaundice and pale stools and dark urine
- Hepatitis (eg, congenital rubella, CMV, toxoplasmosis) and biliary atresia

Kernicterus

  • Encephalopathy resulting from deposition of neurotoxic unconjugated bilirubin in basal ganglia
  • Lethargy, poor feeding, irritability, increased muscle tone, seizures, coma
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20
Q

Investigations in neonatal jaundice?

A
  • Transcutaneous Bilirubinometer Reading
  • Bloods
    o Serum bilirubin (conjugated/unconjugated/total)
    o FBC, U&Es, LFTs
    o If sepsis suspected - septic screen
Other tests if prolonged/pathological
o	Blood type and Rhesus
o	Blood film
o	Coomb’s test (Rhesus)
o	TFTs
-	USS if obstruction suspected
-	MC&amp;S urine
-	G6PD levels
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21
Q

When to refer in neonatal jaundice?

A
  • Referral for urgent hospital assessment if jaundice presents in the first 24 hours of life, the baby is jaundiced and unwell, or for prolonged jaundice
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22
Q

Management of neonatal jaundice?

A
  • Treatment of any underlying illness (such as infection)
  • No treatment — for well neonates with physiological or breastmilk jaundice and a bilirubin level below the treatment threshold
  • Phototherapy — absorption of light through the skin converts unconjugated bilirubin into products that are more easily excretable in the stool and urine.
  • check bilirubin every 6-12 hours, stop phototherapy when 50 below treatment line
  • Exchange transfusion — indicated if the baby has signs of bilirubin encephalopathy and considered if the risk of kernicterus is high or jaundice is not responding to phototherapy.
  • Early surgical treatment — required for conditions such as biliary atresia
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23
Q

How to assess whether to treat neonatal jaundice?

A

Age adapted chart used to measure serum bilirubin and whether to start treatment

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24
Q

What is meningitis?

A
  • Inflammation of the meninges
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25
Q

Pathogenesis of meningitis?

A

o Colonization and invasion of the nasopharyngeal epithelium
o Invasion of the blood stream
o Attachment to and invasion of the meninges
o Induction of inflammation with leak of proteins leading to cerebral oedema (hydrocephalus)
o Alteration in cerebral blood flow and metabolism
o Cerebral vasculitis

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26
Q

What are considerations to take in infants with meningitis?

A
  • Infants do not get classical symptoms of meningism with meningitis
  • Perform lumbar puncture as part of septic screen in infants with unexplained fever or seizures
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27
Q

Epidemiology of meningitis?

A
  • UK around 5% incidence

- Viral Meningitis is most common

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28
Q

Which viruses most common and prognosis of meningitis?

A

o Enteroviruses = more common in autumn and winter

o 95% have complete recovery with no neurological complications

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29
Q

Epidemiology of bacterial meningitis?

A

o 80% of cases of bacterial meningitis occur in <16yr olds in UK
o 5-10% mortality

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30
Q

Risk factors for meningitis?

A

o Impaired Immunity
 Young age, complement defects, splenic defects from sickle-cell disease or asplenia (Strep pneumonia and Hib susceptibility)
o Factors associated with low socio-economic status

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31
Q

Most common viral causative agents in meningitis?

A

 Enteroviruses (80%)
 EBV, CMV, VZV, HSV
 Adenovirus
 Mumps (pre-MMR)

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32
Q

Most common bacterial causative agents in meningitis in neonates?

A
  • Group B Streptococcus
  • E. coli
  • Listeria monocytogenes
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33
Q

Most common bacterial causative agents in meningitis in 1m-6y?

A
  • Neisseria meningitidis (meningococcus) (mainly type b)
  • Haemophilus influenzae Type B (unvaccinated)
  • Streptococcal pneumoniae
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34
Q

Most common bacterial causative agents in meningitis in >6y?

A
  • Neisseria meningitidis (gram negative diplococci)

* Streptococcal pneumoniae

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35
Q

What other organism can cause meningitis in all ages?

A

 Mycobacterium Tuberculosis

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36
Q

Symptoms of meningitis in neonate?

A

Fever, irritability, lethargy, seizures
Crying, poor feedings
Rash may/may not be present (meningococcal septicaemia)

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37
Q

Symptoms of meningitis in infants/children?

A

 Fever, lethargy
 Headache, neck stiffness, photophobia Meningism
 Altered Consciousness, seizures
 Nausea & Vomiting, refusing food/drink
 Rash
 Focal cranial nerve signs common in tuberculous or cryptococcal meningi
tis

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38
Q

Signs of meningitis?

A

o Neck Stiffness – meningeal irritation prevents neck flexion
 Not always present in infants
o Rash – Purpuric or petechial:
 Usually non-blanching (but may initially be blanching)
 Characteristic of meningococcal infection
o Bulging fontanelle
o Signs of shock
o Signs of raised ICP

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39
Q

What special signs are present in meningitis?

A

o Brudzinski’s Sign
 Flexion of the neck with the child supine causes flexion of the knees and hips
o Kernig’s Sign
 In supine position, when knee and hip are flexed, extension of knee leads to pain

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40
Q

What are the signs of raised ICP in meningitis?

A 
	Papilledema (rare)
	↓ level of consciousness
	focal neurology
•	VI nerve palsy
•	Cushing reflex (High BP, Low HR)
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41
Q

Investigations in meningitis?

A
  • Bloods
    o FBC (High WCC, CRP), U&Es, LFTs, glucose, clotting studies
    o Cultures
    o VBG
  • Septic screen
    o Blood cultures, urine cultures, LP, CXR
    o CI to LP: raised ICP, shock, extensive purpura, abnormal clotting, infected LP site, seizures and respiratory insufficiency (stabilise)

Others can be done:
Throat swabs, stool
Viral PCR

42
Q

What tests to do in meningitis when TB suspected?

A

o Mantoux Test
o Chest X-ray
o Early Morning urine
o Consider CT/MRI

43
Q

Lumbar puncture characteristics in normal CSF?

A

Appearance - Clear
WBC - 0-5/mm3
Protein - 0.15-0.4g/L
Glucose - >50% of blood

44
Q

Lumbar puncture characteristics in bacterial meningitis CSF?

A

Appearance - Turbid
WBC - Very high, polymorphs (neutrophils)
Protein - Very high
Glucose - Very low

45
Q

Lumbar puncture characteristics in viral meningitis CSF?

A

Appearance - Clear
WBC - High lymphocytes
Protein - Normal/High
Glucose - Normal

46
Q

Lumbar puncture characteristics in tuberculosis meningitis CSF?

A

Appearance - Turbid/Clear
WBC - High lymphocytes
Protein - Extremely high
Glucose - Extremely low

47
Q

Management of meningococcal disease in primary care?

A

o If in community/GP then give IM Benzylpenicillin (single dose) before admission
 Children >10= 1.2g
 1-9yrs= 600mg
 <1yr= 300mg

48
Q

Management of bacterial meningitis in hospital?

A

 Abx following blood cultures and LP (if possible)
 If >3 months, give IV Ceftriaxone (80mg/kg, OD)
 If <3 months - ampicillin/amoxicillin + cefotaxime (50mg/kg, TDS)

49
Q

When to use steroids in meningitis?

A

o Do not use corticosteroids in <3mths
o Dexamethasone 0.15mg/kg QDS for 4 days to reduce neurological consequences
o Dexamethasone should be given before ABx or within 4hrs of starting Abx
o Do not start dexamethasone >12hrs after starting Abx

50
Q

Supportive management of meningitis?

A
  • Supportive care – analgesics, antipyretics, fluids
  • Notify relevant Health Authorities
  • Hearing tests following infection (6 weeks)
51
Q

Prophylactic management in meningitis?

A

o Rifampicin to all household contacts for meningococcal meningitis

If group B strep in labour - ABx

Vaccinations for HiB, MenB/C + strep pneumo

52
Q

Complications of meningitis?

A

Acute
- Septic shock, seizures, DIC, cerebral oedema
Chronic
- Hearing loss/deafness 10% (test at 6 weeks, most common strep pneumoniae ), seizures, CP

53
Q

Where is sepsis more common in neonates?

A

Premature babies

54
Q

How can sepsis be acquired in neonate?

A

Transplacentally, via ascent from vagina, during birth or from environment

55
Q

What is mortality of sepsis in neonate?

A

Up to 15%

56
Q

How is sepsis categorised?

A 
Early onset (<48 hours after birth)
Late onset (>48 hours after birth)
57
Q

Risk Factors for early onset sepsis?

A 
PROM >18h
Maternal infection/pyrexia
Mother carrier of group B strep
Preterm labour
Fetal distress
58
Q

Risk factors for late onset sepsis?

A 
Central line and catheters
Congenital malformations
Severe illness
Malnutrition
Immunodeficiency
59
Q

Causative agents in early onset sepsis?

A 
Usually acquired from mother
Group B strep
E.coli
Listeria
HSV, Chlamydia trachomatis, anaerobes and H.influenza
60
Q

Causative agents of late onset sepsis?

A 
Coagulase-negative staphylococci
S.aureus
E.coli
Group B strep
Fungal (candida) - especially if doesn't respond to standard therapy
61
Q

Presentation in neonatal sepsis?

A 
Labile temperature
Lethargy
Poor feeding
Respiratory distress
Collapse
DIC
Vomiting
Irritability, lethargy, drowsiness
62
Q

Management of neonatal sepsis?

A

ABC
Supportive - ventilation, IV fluids, inotropes
Take blood (FBC, U&Es, CRP, glucose, lactate)

Septic Screeen
Urine output measured and urinalysis
Blood cultures
CXR
Lumbar puncture for glucose, protein, WCC and Gram stain

If no response in 24 hours - virology, throat swab, urine culture

63
Q

Antibiotics in early neonatal sepsis?

A

<72h of life - IV benzylpenicillin + gentamicin
- stop if cultures negative
Continue for 7 days if cultures positive
If Listeria suspected - give ampicillin

64
Q

Antibiotics in late onset neonatal sepsis?

A

<3 months - IV ceftriaxone + Ampicillin/amoxicillin (cover listeria)
>3 months - IV ceftriaxone 80 mg/kg once a day

65
Q

What is idiopathic thrombocytopenic purpura?

A
  • Most common acquired childhood bleeding disorder
  • Caused by destruction of circulating platelets by anti-platelet IgG autoantibodies
  • Reduced platelets associated with compensatory increase in megakaryocytes
66
Q

Epidemiology of ITP?

A
  • Incidence 1 per 25,000 children per year

- Often presents between 2-10 years old

67
Q

When might ITP present?

A
  • May follow CMV, EBV, parvovirus, VZV or vaccination
68
Q

Symptoms and signs of ITP?

A
  • Onset after 1-2 weeks of viral infection
  • Develop petechial, purpuric rash and bruising
  • Can cause epistaxis or mucosal bleeding but usually not significant in ITP
  • Intracranial bleeding occurs in 0.1-0.5%
69
Q

DDx of ITP?

A
  • HSP, acute leukaemia, aplastic anaemia

- SLE

70
Q

Investigations of ITP?

A 
-	Blood film
o	Isolated thrombocytopenia
-	Blood tests
o	FBC, U&amp;E, LFTs
-	Bone marrow examination needed:
o	Unusual signs (lymphadenopathy, abnormal cells on blood film)
o	Platelet count not rising
-	CT if headache or CNS signs
71
Q

Management of ITP?

A
  • Gradual resolution over 3 months for 80%
  • Chronic form compatible with normal life but avoid contact sports
    If needed:
  • Oral prednisolone
  • Romiplostim (increases platelets)
72
Q

When to admit patient with ITP?

A

o Unusual features (bleeding excessively)
o Life threatening bleeding requires platelet transfusion
o Splenectomy for chronic ITP
o Rituximab reduces need for splenectomy

73
Q

What is anaemia defined as in neonates, 1-12 months and 1-12 years, 12-14 and over 15?

A 
o	Neonates - <14g/dl
o	1-12 months <10g/dl
o	1-12 years <11g/dl
o	12-14 years <12g/dl
o	15 and over <13g/dl
74
Q

Pathology of iron deficiency anaemia?

A
  • Due to ineffective erythropoiesis which is a reduced red cell production
75
Q

Epidemiology of iron deficiency anaemia?

A
  • Commonest nutritional deficiency

- 25% of infants with peak at 18 months

76
Q

Causes of iron deficiency anaemia?

A

Dietary
Malabsorption
Blood Loss
Intestinal parasites

77
Q

Describe causes of dietary iron def anaemia?

A

o COMMONEST
o e.g. prolonged and exclusive consumption of cow or breast milk with late introduction of iron containing solids >6 months
o Low level of dietary iron e.g. high milk intake (low iron), vegan, poverty
o GI blood loss e.g. cow’s milk protein enteropathy
o Increased demand due to rapid growth

78
Q

Describe causes of malabsorption iron def anaemia?

A

o e.g. Coeliac disease, IBD

79
Q

Describe causes of blood loss iron def anaemia?

A 
o	e.g.  Meckel’s diverticulum, oesophagitis. Bleeding may be occult into cysts, tumours or secondary to drugs e.g. NSAIDs
o	Females (growth spurts and menstruation)
80
Q

Describe causes of parasites iron def anaemia?

A

e.g. hookworm (less developed world)

81
Q

Symptoms of iron deficiency anaemia? In severe? Other?

A

Mostly asymptomatic
Pallor, lethargy, poor feeding, breathlessness (only in severe anaemia)
May develop neuro effects of lethargy and irritability (infants), mood changes, reduced cognitive and psychomotor performance and rarely pica (eating unusual items e.g. soil, chewing on pencils etc)

82
Q

DDx of iron deficiency anaemia?

A

Beta-thalassaemia (usually Asian, Arabic, Mediterranean origin)
Alpha-thalassaemia (usually African, Far Eastern)
Anaemia of chronic disease (Renal failure)

83
Q

Investigations of iron deficiency anaemia?

A

Bloods
- FBC (low Hb, MCV, MCH), low ferritin
Blood film
- Small, pale red cells

84
Q

Management of iron deficiency anaemia? Dietary advice? Supplementation?

A

Address underlying cause if apparent
Dietary Advice
- Increase level of iron in food
- e.g. iron fortified formulas and breakfast cereals, meat, liver, oily fish (sardines, pilchards), green veg, beans, egg, yolk, foods rich in vit C (inc iron absorption)
Supplementation
- Oral iron supplements (ferrous fumerate) or other preparations (Sytron/Niferex) continued until Hb is normal and for a further 3 months
- Check Hb levels every 2-4 weeks once started and then every 3 months for 1 year after normalised
- Level starts to rise within a week so failure to do so indicates non-compliance
- Stools turn black and iron is dangerous in overdose

85
Q

Causes of sepsis?

A

Acquired transplacentally, via ascent from vagina, during birth or from environment

86
Q

Mortality of sepsis?

A

15%

87
Q

Characterised depending on what in sepsis?

A 
Early onset (<48h)
Late onset (>48h)
88
Q

Presentation of sepsis in neonate?

A

Non-specific, subtle

Labile temp, lethargy, poor feeding, respiratory distress, collapse, DIC

89
Q

Management of sepsis in neonates?

A

ABCDE

BUFALO
Bloods - FBC, CRP, glucose, U&amp;Es, ABG
Urine output measured
Fluids -IV fluids (0.9% saline 20mls/kg)
Abx
Lactate
Oxygen if needed

Septic screen
CXR, Blood cultures, urinalysis (clean catch) (M,S and C), lumbar puncture

May require ventilation, inotropes

90
Q

What antibiotics needed in sepsis of neonate (72h), children under 3 months and children over 3 months?

A

<72h of life - IV benzylpenicillin + gentamicin
<3 months - IV ceftriaxone + Ampicillin/amoxicillin (cover listeria)
>3 months - IV ceftriaxone 80 mg/kg once a day

91
Q

Meningococcal septicaemia causes

A

Neiseria meningitidis (gram negative diplococci)

Groups ABCWY

Most cases <5

92
Q

Symptoms and signs of meningococcal septicaemia

A

Early
Leg pain, skin mottling, cold peripheries, breathing problems

Late
Haemorrhagic non-blanching rash (tends to present after 12h), confusion, seizures, coma

93
Q

Complications of meningococcal sepsis

A 
Early
DIC, AKI, adrenal haemorrhage, circulatory collapse
Late
Deafness
Scarring
Renal failure
Limb amputations
94
Q

Define a household contact in meningitis prophylaxis?

A

Prolonged close contact in a household-type setting during the 7 days before onset of illness (for example, living or sleeping in the same household, pupils in the same dormitory, boy/girlfriends, or university students sharing a kitchen in a hall of residence).
Transient close contact only if they have been directly exposed to large particle droplets/secretions from the respiratory tract around the time of admission to hospital

95
Q

What is TTP?

A

Thrombotic thrombocytopenic purpura

Microangiopathic haemolysis, thrombocytopenia, neurological abnormalities, fever and renal dysfunction

96
Q

Mortality of TTP without treatment?

A

90% but reduced with prompt platelet transfusion

97
Q

Pathology of TTP?

A

Due to deficiency of von Willebrand factors cleaving protein (ADAMTS1)

98
Q

Risk factors for TTP?

A

Pregnancy

HIV

99
Q

Symptoms of TTP/

A

Prodromal flu like illness (fever, fatigue, arthralgia)
Epistaxis, bruising, petechiae, haematuria)
Confusion, headache, paresis
Fever, anaemia, jaundice

100
Q

Signs of TTP?

A

Fever
Purpura - non-palpable small purpuric spots and petechiae
Thrombocytopenia (<50)
Jaundice

101
Q

Investigations in TTP?

A

Blood film - fragmented erythrocytes (schistocytes)
U&E - creatinine elevated
LDH highly elevated
Reticulocyte and indirect bilirubin elevated
ADAMTS13 and ADAMTS13 antibodies measured

102
Q

Management of TTP?

A

IV plasma exchange (plasmapheresis) - within 4-8 hours
Infusion of FFP until patient transferred to plasma exchange
Glucocorticoid steroid
Splenectomy for chronic relapses

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