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
Pathogenesis of meningitis?
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
26
What are considerations to take in infants with meningitis?
- 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
27
Epidemiology of meningitis?
- UK around 5% incidence | - Viral Meningitis is most common
28
Which viruses most common and prognosis of meningitis?
o Enteroviruses = more common in autumn and winter | o 95% have complete recovery with no neurological complications
29
Epidemiology of bacterial meningitis?
o 80% of cases of bacterial meningitis occur in <16yr olds in UK o 5-10% mortality
30
Risk factors for meningitis?
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
31
Most common viral causative agents in meningitis?
 Enteroviruses (80%)  EBV, CMV, VZV, HSV  Adenovirus  Mumps (pre-MMR)
32
Most common bacterial causative agents in meningitis in neonates?
* Group B Streptococcus * E. coli * Listeria monocytogenes
33
Most common bacterial causative agents in meningitis in 1m-6y?
* Neisseria meningitidis (meningococcus) (mainly type b) * Haemophilus influenzae Type B (unvaccinated) * Streptococcal pneumoniae
34
Most common bacterial causative agents in meningitis in >6y?
* Neisseria meningitidis (gram negative diplococci) | * Streptococcal pneumoniae
35
What other organism can cause meningitis in all ages?
 Mycobacterium Tuberculosis
36
Symptoms of meningitis in neonate?
Fever, irritability, lethargy, seizures Crying, poor feedings Rash may/may not be present (meningococcal septicaemia)
37
Symptoms of meningitis in infants/children?
 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
38
Signs of meningitis?
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
39
What special signs are present in meningitis?
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
40
What are the signs of raised ICP in meningitis?
```  Papilledema (rare)  ↓ level of consciousness  focal neurology • VI nerve palsy • Cushing reflex (High BP, Low HR) ```
41
Investigations in meningitis?
- 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
What tests to do in meningitis when TB suspected?
o Mantoux Test o Chest X-ray o Early Morning urine o Consider CT/MRI
43
Lumbar puncture characteristics in normal CSF?
Appearance - Clear WBC - 0-5/mm3 Protein - 0.15-0.4g/L Glucose - >50% of blood
44
Lumbar puncture characteristics in bacterial meningitis CSF?
Appearance - Turbid WBC - Very high, polymorphs (neutrophils) Protein - Very high Glucose - Very low
45
Lumbar puncture characteristics in viral meningitis CSF?
Appearance - Clear WBC - High lymphocytes Protein - Normal/High Glucose - Normal
46
Lumbar puncture characteristics in tuberculosis meningitis CSF?
Appearance - Turbid/Clear WBC - High lymphocytes Protein - Extremely high Glucose - Extremely low
47
Management of meningococcal disease in primary care?
o If in community/GP then give IM Benzylpenicillin (single dose) before admission  Children >10= 1.2g  1-9yrs= 600mg  <1yr= 300mg
48
Management of bacterial meningitis in hospital?
 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
When to use steroids in meningitis?
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
Supportive management of meningitis?
- Supportive care – analgesics, antipyretics, fluids - Notify relevant Health Authorities - Hearing tests following infection (6 weeks)
51
Prophylactic management in meningitis?
o Rifampicin to all household contacts for meningococcal meningitis If group B strep in labour - ABx Vaccinations for HiB, MenB/C + strep pneumo
52
Complications of meningitis?
Acute - Septic shock, seizures, DIC, cerebral oedema Chronic - Hearing loss/deafness 10% (test at 6 weeks, most common strep pneumoniae ), seizures, CP
53
Where is sepsis more common in neonates?
Premature babies
54
How can sepsis be acquired in neonate?
Transplacentally, via ascent from vagina, during birth or from environment
55
What is mortality of sepsis in neonate?
Up to 15%
56
How is sepsis categorised?
``` Early onset (<48 hours after birth) Late onset (>48 hours after birth) ```
57
Risk Factors for early onset sepsis?
``` PROM >18h Maternal infection/pyrexia Mother carrier of group B strep Preterm labour Fetal distress ```
58
Risk factors for late onset sepsis?
``` Central line and catheters Congenital malformations Severe illness Malnutrition Immunodeficiency ```
59
Causative agents in early onset sepsis?
``` Usually acquired from mother Group B strep E.coli Listeria HSV, Chlamydia trachomatis, anaerobes and H.influenza ```
60
Causative agents of late onset sepsis?
``` Coagulase-negative staphylococci S.aureus E.coli Group B strep Fungal (candida) - especially if doesn't respond to standard therapy ```
61
Presentation in neonatal sepsis?
``` Labile temperature Lethargy Poor feeding Respiratory distress Collapse DIC Vomiting Irritability, lethargy, drowsiness ```
62
Management of neonatal sepsis?
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
Antibiotics in early neonatal sepsis?
<72h of life - IV benzylpenicillin + gentamicin - stop if cultures negative Continue for 7 days if cultures positive If Listeria suspected - give ampicillin
64
Antibiotics in late onset neonatal sepsis?
<3 months - IV ceftriaxone + Ampicillin/amoxicillin (cover listeria) >3 months - IV ceftriaxone 80 mg/kg once a day
65
What is idiopathic thrombocytopenic purpura?
- 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
Epidemiology of ITP?
- Incidence 1 per 25,000 children per year | - Often presents between 2-10 years old
67
When might ITP present?
- May follow CMV, EBV, parvovirus, VZV or vaccination
68
Symptoms and signs of ITP?
- 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
DDx of ITP?
- HSP, acute leukaemia, aplastic anaemia | - SLE
70
Investigations of ITP?
``` - Blood film o Isolated thrombocytopenia - Blood tests o FBC, U&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
Management of ITP?
- 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
When to admit patient with ITP?
o Unusual features (bleeding excessively) o Life threatening bleeding requires platelet transfusion o Splenectomy for chronic ITP o Rituximab reduces need for splenectomy
73
What is anaemia defined as in neonates, 1-12 months and 1-12 years, 12-14 and over 15?
``` 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
Pathology of iron deficiency anaemia?
- Due to ineffective erythropoiesis which is a reduced red cell production
75
Epidemiology of iron deficiency anaemia?
- Commonest nutritional deficiency | - 25% of infants with peak at 18 months
76
Causes of iron deficiency anaemia?
Dietary Malabsorption Blood Loss Intestinal parasites
77
Describe causes of dietary iron def anaemia?
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
Describe causes of malabsorption iron def anaemia?
o e.g. Coeliac disease, IBD
79
Describe causes of blood loss iron def anaemia?
``` 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
Describe causes of parasites iron def anaemia?
e.g. hookworm (less developed world)
81
Symptoms of iron deficiency anaemia? In severe? Other?
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
DDx of iron deficiency anaemia?
Beta-thalassaemia (usually Asian, Arabic, Mediterranean origin) Alpha-thalassaemia (usually African, Far Eastern) Anaemia of chronic disease (Renal failure)
83
Investigations of iron deficiency anaemia?
Bloods - FBC (low Hb, MCV, MCH), low ferritin Blood film - Small, pale red cells
84
Management of iron deficiency anaemia? Dietary advice? Supplementation?
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
Causes of sepsis?
Acquired transplacentally, via ascent from vagina, during birth or from environment
86
Mortality of sepsis?
15%
87
Characterised depending on what in sepsis?
``` Early onset (<48h) Late onset (>48h) ```
88
Presentation of sepsis in neonate?
Non-specific, subtle | Labile temp, lethargy, poor feeding, respiratory distress, collapse, DIC
89
Management of sepsis in neonates?
ABCDE ``` BUFALO Bloods - FBC, CRP, glucose, U&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
What antibiotics needed in sepsis of neonate (72h), children under 3 months and children over 3 months?
<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
Meningococcal septicaemia causes
Neiseria meningitidis (gram negative diplococci) Groups ABCWY Most cases <5
92
Symptoms and signs of meningococcal septicaemia
Early Leg pain, skin mottling, cold peripheries, breathing problems Late Haemorrhagic non-blanching rash (tends to present after 12h), confusion, seizures, coma
93
Complications of meningococcal sepsis
``` Early DIC, AKI, adrenal haemorrhage, circulatory collapse Late Deafness Scarring Renal failure Limb amputations ```
94
Define a household contact in meningitis prophylaxis?
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
What is TTP?
Thrombotic thrombocytopenic purpura | Microangiopathic haemolysis, thrombocytopenia, neurological abnormalities, fever and renal dysfunction
96
Mortality of TTP without treatment?
90% but reduced with prompt platelet transfusion
97
Pathology of TTP?
Due to deficiency of von Willebrand factors cleaving protein (ADAMTS1)
98
Risk factors for TTP?
Pregnancy | HIV
99
Symptoms of TTP/
Prodromal flu like illness (fever, fatigue, arthralgia) Epistaxis, bruising, petechiae, haematuria) Confusion, headache, paresis Fever, anaemia, jaundice
100
Signs of TTP?
Fever Purpura - non-palpable small purpuric spots and petechiae Thrombocytopenia (<50) Jaundice
101
Investigations in TTP?
Blood film - fragmented erythrocytes (schistocytes) U&E - creatinine elevated LDH highly elevated Reticulocyte and indirect bilirubin elevated ADAMTS13 and ADAMTS13 antibodies measured
102
Management of TTP?
IV plasma exchange (plasmapheresis) - within 4-8 hours Infusion of FFP until patient transferred to plasma exchange Glucocorticoid steroid Splenectomy for chronic relapses