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Phase 3a AW > Paeds ILAs > Flashcards

Paeds ILAs Flashcards

1
Q

What is sepsis?

A

An infection that leads to organ dysfunction- a systemic infective response

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2
Q

What is involved in the septic screen?

A

FBC (inc differential WCC)
Blood cultures
Acute phase reactant e.g. CRP
Urine MC&S

Consider if indicated- CXR, LP, rapid antigen screen on blood/CSF/fluid, meningococcal and pneumococcal PCR
LP contraindicated for meningococcal septicaemia

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3
Q

What would a gram film show for meningococcal septicaemia?

A

Gram negative diplococci

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4
Q

What are the CSF findings of meningococcal septicaemia?

A

Turbid, WCC raised (neutrophils), glucose decreased, protein increased

“the neutrophils eat the glucose to become strong and build muscle (protein)”

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5
Q

What is the management of meningococcal septicaemia?

A 
ABC
IV access
Get bloods
Fluid bolus
Abx- if <3 months- cefotaxime 200mg/kg/24hr and IV amoxicillin to cover for listeria
If >3 months, ceftriaxone or cefotaxime
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6
Q

What is the management of H.Influenzae causing bacterial meningitis?

A

Cefotaxime for at least 10 days
Dexamethasone may also be required

Rifampicin prophylaxis

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7
Q

What is further management of meningococcal septicaemia in PICU?

A 
O2
Protect airway
IVI
Monitor obs and GCS
Alert haematology that blood may be required
Continuously monitor ECG
Inotropes if needed: dobutamine or DA
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8
Q

How is Neisseria meningitidis spread?

A

Air e.g. sneezing, coughing, kissing

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9
Q

How are close contacts for meningococcal septicaemia patients treated?

A

Rifampicin or Ciprofloxacin (new guidelines)

Dose: 600mg every 12 hours for 2 days. Children under 1- 5mg/kg every 12 hours. Children 1-12 years- 10mg/kg every 12 hours.

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10
Q

What is a close contact?

A

Anyone that lives in same house, halls of residence or is in a relationship with the person.

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11
Q

What are common causes of bacterial meningitis in:

a) neonate- 3 months
b) 1 month- 6 years
c) >6 years

A

Neonatal-3 months
Group B streptococcus
E.Coli and other organisms
Listeria monocytogenes

1 month- 6 years Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae

> 6 years
Neisseria meningitidis
Streptococcus pneumoniae

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12
Q

What is Brudinski sign? (bacterial meningitis)

A

flexion of the neck with the child supine causes flexion of the knees and hips.

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13
Q

What is Kernig sign? (bacterial meningitis)

A

With the child lying supine and with the hips and knees flexed, there is back pain on extension of the knee

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14
Q

Name some side effects of rifampicin

A

Interacts with the OCP, can stain contact lenses and turn urine red, N&D&V, headache.

Neonatal bleeding in 3rd trimester if pregnant.

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15
Q

Name some conditions where rifampicin prophylaxis contraindicated

A

Jaundice, liver failure, abnormal LFTs, alcoholism, polyphyria, diabetes.

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16
Q

What is Juvenile Idiopathic arthritis?

A

An autoimmune disease that affects a single ankle or knee

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17
Q

What are some signs and symptoms of JIA?

A

High fever
Salmon coloured rash
Eye inflammation

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18
Q

What physical examinations would you do for suspected JIA?

A

MSK exam
Abdo exam
Lymph nodes
Rash exam

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19
Q

Name some differential diagnoses of JIA.

A 
Reactive arthritis
Lyphoma
Leukaemia
Septic arthritis
Transient synovitis
Osteomyelitis
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20
Q

Investigations for JIA?

A 
Bloods- FBC, U&amp;E, LFTs, albumin, ESR/CRP
Blood cultures
Ultrasound/ Xrays
CT/MRI
ECHO
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21
Q

Management of JIA?

A

NSAIDS (acute)
Corticosteroids for quick symptoms relief and systemic disease
Methotrexate- if multiple joint involvement or steroid injections needed more than 3 times
Sulfasalazine and leflunomide
Etanercept (TNFa inhibitor)- for polyarticular JIA
Tocilizumab

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22
Q

Which professionals would be involved in the management of JIA?

A

Paediatrician. PT, Nurses, OT, School rep, Rheumatologist, Social Worker, GP, dietician

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23
Q

What is the criteria for Kawasaki’s disease?

A

Fever >5 days plus 4/5 of:

  • Conjunctival infection- non-purulent
  • Mucous membrane changes- red, strawberry tongue
  • Cervical lymphadenopathy
  • Rash
  • Red and oedematous palms and soles or bleeding of fingers and toes
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24
Q

Differential diagnoses of Kawasaki’s disease?

A 
Scarlett fever
Measles
Scalded skin syndrome
JIA
Strep infection
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25
Q

What is the management of Kawasaki’s?

A

Prompt treatment with IVIG within the 1st 10 days lowers the risk of coronary artery aneurysms.
Aspirin- reduces the risk of thrombosis- high dose at first (anti-inflammatory) followed by low-dose (anti-platelet)

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26
Q

What are the risks of using Aspirin in childhood?

A

-Reye’s syndrome- damaged mitochondria- liver damage- septicaemia, coma, seizures, vomiting
Renal complications- reduced GFR from decreased blood flow due to inhibition of renal prostaglandin synthesis
- GI- epigastric distress

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27
Q

What is a cardiac complication of Kawasaki’s?

A

Coronary artery aneurysms (do ECHO +/- cardiac catheterisation with angiography)

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28
Q

What is a common presentation of DKA?

A

Confusion, vomiting, polyuria, polydipsia, weight loss, abdominal pain, coma

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29
Q

How do you diagnose DKA?

A

Hyperglycaemia (>11mmol/L)
Acidosis (venous pH <7.3 and bicarb <15mmol/L)
Ketones in blood and urine

Level of acidosis categorises severity

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30
Q

What is the management of DKA?

A

1) ABC and give fluid bolus 10mls/kg
2) Rapidly confirm diagnosis- finger prick glucose, venous blood gas, urine dip
3) Formal investigation- bloods, weight, blood gas, ECG, lab urine
4) Use clinical signs to asses dehydration
5) Start IV fluids- calculate deficit and subtract bolus (use 0.9% saline with 20mmol KCl/500ml until blood glucose is lower than 14, then change to 0.9% saline with 5% dextrose 20mmol KCl/500ml)
6) Start IV insulin only after 1 hour of IV fluids (1 unit/ml solution of fast acting insulin e.g. Actrapid)
7) Stop IV insulin once blood ketone level <1mmol/L and patient is able to tolerate food

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31
Q

What are the 2 categories of causes of hypothyroidism?

A

Congenital and acquired

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32
Q

What are the causes of congenital hypothyroidism?

A
  • Maldescent of the thyroid and athyrosis
  • Dyshormonogenesis- common in consanguineous families
  • Iodine deficiency (commonest cause worldwide)
  • Hypothyroidism due to TSH deficiency
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33
Q

What are the clinical features of congenital hypothyroidism?

A

Usually asymptomatic and picked up on screening (Guthrie test- shows raised TSH)
Otherwise- failure to thrive, feeding problems, jaundice, constipation, pale, cold, mottled skin, goitre, coarse facies, large tongue, hoarse cry, delayed development

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34
Q

What are the clinical features of acquired hypothyroidism?

A 
Females >males (similar to normal hypothyroid symptoms)
Short stature
Cold intolerance, cold peripheries
Dry skin/ hair
Bradycardia 
Delayed puberty
Constipation
Obesity
SUFE
Leaning difficulties
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35
Q

What is the treatment of hypothyroidism?

A

Levothyroxine
Neonates approx 15mcg/kg/day
Adjust by 5mcg every 2 weeks to a typical dose of 20-50mcg/kg/day

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36
Q

What are the 4 main differentials for an unwell neonate?

A

Sepsis
Congenital heart disease
Metabolic
Trauma/ NAI

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37
Q

What is congenital adrenal hyperplasia?

A

AR disorder of adrenal steroid biosynthesis- defect in gene for 21-hydroxylase enzyme

Leads to decreased glucocorticoids (cortisol) and mineralocorticoids (aldosterone) and increased androgens (ACTH increase due to reduced -ve feedback from cortisol)

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38
Q

How do patients with decreased mineralocorticoids present?

A

Salt-losing crisis: metabolic acidosis (low pH, low HCO3, low CO2)

Vomiting, dehydration, weight loss, floppiness, collapse

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39
Q

What is the management of a salt-losing crisis?

A

IV sodium chloride
IV dextrose
IV Hydrocortisone (synthetic glucocorticoid)
Fludrocortisone (synthetic mineralocorticoid)

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40
Q

How do patients with low glucocorticoids present?

A

Hypoglycaemia

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41
Q

How do males and females present different with increased androgens?

A

Females- virilisation of external genitalia (more masculine)
Males- Tall structure, muscular build, acne, precocious puberty

80% males present with salt-losing crisis, the other 20% present with precocious puberty

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42
Q

What is the long term treatment of CAH?

A

Fludrocortisone
Hydrocortisone
Surgery for females
Monitor growth, skeletal maturity and plasma androgens

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43
Q

What can high risk women be given in pregnancy to suppress androgen secretion?

A

Dexamethasone

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44
Q

What is stridor?

A

Harsh musical sound on inspiration due to partial obstruction of the lower portion of the upper airway

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45
Q

What are the symptoms of croup?

A 
Preceded by fever
Barking cough
Stridor
Recession
Worse at night
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46
Q

What must you not do when examining the child with suspected croup?

A

Examine the throat or lie the child down- can precipitate airway obstruction if it is acute epiglottitis

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47
Q

What is the causative organism of croup?

A

Parainfluenza virus

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48
Q

What age group is croup most common?

A

6 months-6 years (most common aged 2)

More common in autumn months

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49
Q

What is 1st line treatment for croup?

A

Dexamethasone 150mg/kg

If they don’t improve, give high flow O2 and nebulised adrenaline

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50
Q

Signs and symptoms of bronchiolitis?

A

Coryzal, breathlessness, poor feeding

Signs- nasal flaring, head bobbing, subcostal recessions, intercostal recessions, tracheal tug, grunting

Fine end inspiratory crackles, high pitched wheeze, cyanosis (on feeding)

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51
Q

What is the most likely causative organism for bronchiolitis?

A

RSV (respiratory syncytial virus)

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52
Q

What factors increase the risk of developing bronchiolitis?

A

Immunocompromised
Prematurity <32 weeks/ poor lung development
Congenital heart disease

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53
Q

What are the investigations for bronchiolitis?

A

PCR analysis of nasal secretions

CXR- hyperinflation

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54
Q

What is the management of bronchiolitis?

A

Supportive- humidified O2, NG feeds, fluids

Palivizumab- monoclonal antibody, IM once a month through autumn and winter. Used in CF, immunocompromised, congenital heart disease, downs

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55
Q

In ILA- turns out patient has CF

Does a diagnosis of cystic fibrosis change the management of the respiratory infection?

A

Children with CF are at risk of recurrent and persistent bacterial infections due to thick mucus in lower airways- this damages bronchial walls- causes bronchiectasis and abscess formation.

Therefore antibiotics would be needed in this case, as well as physiotherapy for airway clearance, nebulised DNase or hypertonic saline may decrease the viscosity of the sputum and aid clearance.

56
Q

What are the other presenting features of CF?

A

Neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice (due to pancreatic ducts blocked by thick secretions- maldigestion, malabsorption and steatorrhoea)

Recurrent chest infections (40%) (due to reduction in air surface liquid layer and impaired ciliary function retention of secretions)

Malabsorption (30%): steatorrhea (due to fat malabsorption from pancreatic enzymes failing to be secreted), failure to thrive

Other features (10%): liver disease

57
Q

What are some other features of CF?

A 
• Short stature
	• Diabetes mellitus
	• Delayed puberty
	• Rectal prolapse (due to bulky stools)
	• Nasal polyps
Male infertility, female subfertility
58
Q

How is CF diagnosed?

A

• Guthrie heel prick screening test- 6-9 days of life
• Sweat test (Cl ions markedly)
• Faecal elastase (low levels)
Gene abnormalities in CFTR protein

59
Q

What are the signs and symptoms of heart failure?

A

Symptoms- breathlessness, sweating, poor feeding, recurrent chest infections

Signs- Poor weight gain, tachypnoea, tachycardia, heart murmur, hepatomegaly, cool peripheries, chest crackles, oedema

60
Q

How are the causes of HF different for neonates, infants and children/adolescents?

A

Neonates- R to L shunt (cyanotic)- severe coarctation of the aorta, hypoplastic left heart syndrome

Infants- L to right shunts (breathlessness)- ASD, VSD, PDA

Older children- Eisenmenger syndrome (reversal of shunt causing R to L shunt), rheumatic heart disease, cardiomyopathy

61
Q

What are the investigations for HF?

A

Echo- shows shunt
CXR- 5 signs (ABCDE)
ECG
Bloods- FBC, thyroid, LFTs, anaemia, blood gases

62
Q

What is the management of HF?

A

Medical: Diuretics, ACEi (captopril), calories
Surgical: at 3-6 months to manage HF and failure to thrive. To prevent permanent lung damage from pulmonary hypertension and high blood flow

63
Q

What are the different classifications of faltering growth?

A

1) Inadequate intake
2) Inadequate retention
3) Malabsorption
4) Failure to utilise nutrients
5) Increased requirements

64
Q

Faltering growth: What are the organic and non-organic causes of inadequate intake?

A

Organic:
- impaired suck-swallow- cleft palate, CP
- chronic disease leading to anorexia
- CF, Crohn’s, liver disease, chronic renal failure
Non-organic:
- Inadequate availability of food
- Psychosocial deprivation- post-natal depression
- Neglect

65
Q

Faltering growth: What are the causes of inadequate retention?

A

Vomiting, severe GORD

66
Q

Faltering growth: What are the causes of malabsorption?

A

Coeliac, CF, Cow’s milk protein intolerance, cholestatic liver disease

67
Q

Faltering growth: What are the causes of failure to utilise nutrients?

A

Chromosomal disorders
Extreme prematurity
Down’s syndrome

68
Q

Faltering growth: What are the causes of increased requirements?

A 
Thyrotoxicosis
CF
Malignancy
Chronic infection
CHD
69
Q

What investigations would you do for a child failing to thrive?

A

Bloods- FBC, U&E, LFT, TFT, Ig, IgA TTG
Urine- MC&S
Stool- MC&S
CXR and sweat test (CF)

70
Q

A urinalysis shows increased nitrites and leucocytes, what is the diagnosis?

A

UTI

71
Q

What are the most common causative organisms of a UTI?

A

E.coli

Followed by klebsiella, proteus, pseudomonas and strep faecalis

72
Q

Is a UTI more common in boys or girls, and why?

A

Boys, shorter urethra for bowel flora to enter and colonise

73
Q

What are the predisposing factors for a UTI?

A

Incomplete bladder emptying
Constipation
Vesicoureteric reflex

74
Q

What are the common presentations of a UTI?

A

Infants- Poor feeding, vomiting, irritability
Younger children- abdo pain, fever, dysuria

Features that suggest an upper UTI- loin pain/tenderness, temp >38 degrees

75
Q

What is the management for a UTI?

A
  • children aged more than 3 months old with a lower UTI should be treated with oral antibiotics for 3 days according to local guidelines, usually trimethoprim, nitrofurantoin, cephalosporin or amoxicillin. Parents should be asked to bring the children back if they remain unwell after 24-48 hours
    • antibiotic prophylaxis is not given after the first UTI but should be considered with recurrent UTIs

<3years- refer to paediatrician

76
Q

What further investigations could be done if complications of a UTI are suspected?

A

USS of kidneys and urinary tract
DMSA to check for renal scars 3 months after UTI
MAG3 or MCUG to detect obstruction and vesicoureteric reflux

77
Q

What are the possible causes of diarrhoea in children?

A
  • Toddler’s diarrhoea
  • Coeliac disease or cow’s milk protein intolerance
  • GE
  • Chronic constipation- overflow
  • Lactose intolerance
  • IBD
  • Cholestatic liver disease
78
Q

What happen in overflow diarrhoea?

A

Chronic constipation causes the rectum to be distended and cause a loss of feeling of needing to defecate
Involuntary soiling occurs as contractions of the full rectum inhibit the internal sphincter- causing overflow
Recovery of normal rectal size and sensation may take a long time

79
Q

What is the management of constipation?

A
  • Constipation arising acutely in young children e.g. acute febrile illness, usually resolves spontaneously or with the use of mild laxatives and extra fluids. Encourage a balanced diet
    • In more long-standing constipation, the rectum becomes overdistended, with a subsequent loss of the feeling of needing to defecate, leading to involuntary soiling.
    • Macrogol laxative e.g. polyethylene glycol and electrolytes (Movicol paediatric plain)- 2 weeks 1st line (osmotic laxative)
    • Stimulant laxatives are the next step (e.g. senna or picosulphate) +/- osmotic laxative (e.g. lactulose) 2nd line
      If there is no success, consider enema (+/- sedation) or manual evacuation under GA
80
Q

What is a red flag for Hirschprung’s disease?

A

Failure to pass meconium <24 hours after birth

81
Q

What is Hirschprung’s disease?

A

The absence of ganglion cells from the myenteric and submucosal plexuses in part of the large bowel results in a narrow, contracted segment. The abnormal bowel extends from the rectum for a variable distance proximally, ending in a normally inverted, dilated colon.
More common in boys, and is associated with Downs syndrome.

82
Q

How does Hirschprung’s disease present?

A

Usually in the neonatal period with intestinal obstruction heralded by failure to pass meconium within the first 24 hours of life.
Abdominal distension and later bile-stained vomiting develop. Occasionally, infants present with severe life-threatening Hirschsprung enterocolitis during the first few weeks of life, sometime due to Clostridium Difficile infection.

In later childhood, presentation is with chronic constipation, usually profound, and associated with abdominal distension but usually without soiling. Growth failure may also be present.

83
Q

How can you diagnose Hirschprung’s disease?

A

Suction rectal biopsy

84
Q

What is the management of Hirschprung’s disease?

A

Whole bowel irrigation for symptomatic relief.
Enemas.
Surgical and usually involves an initial colostomy followed by anastomosing normally innervated bowel to the anus.

85
Q

What are the differentials for proteinuria in children?

A 
Orthostatic proteinuria
Glomerular abnormalities- minimal change disease, glomerulonephritis
Reduced renal mass
Hypertension
Tubular proteinuria
86
Q

What is the triad of findings for nephrotic syndrome?

A

Hypoalbuminaemia- <25g/L
Proteinuria- urine protein >1mg/m2/24 hours
Oedema- peripheral, scrotal/vulval, periorbital, ascites

87
Q

What are the complications of nephrotic disease?

A

Hypovolaemia
Thrombosis
Infection
Hyperlipidaemia

88
Q

What is the management of nephrotic syndrome (steroid-sensitive vs steroid resistant)?

A 
- Steroid sensitive 85-90%
		○ Prednisolone oral 60mg/m2/day
	- Steroid resistant
		○ Diuretics, salt restriction, ACE-I, NSAIDs
		○ Cyclophosphamide +/- ciclosporin
89
Q

What is the prognosis for nephrotic syndrome?

A

1/3 resolve directly
1/3 infrequent relapses
1/3 frequent relapses

90
Q

What developmental milestones would you expect a child to have by 6 months?

A

Gross motor- sits without support
Fine motor and vision- palmar grasp, transfers hand-to-hand
HS&L- babbles, turns head to loud sounds
Social- Puts objects to mouth, shakes rattle, reaches for bottle/breast

91
Q

What developmental milestones would you expect a child to have by 12 months?

A

GM- walking (18 months= threshold for worry)
FM&V- neat pincer grip, points
HS&L- 1-2 words, understands nouns/names
Social- Waves bye-bye, drink for beaker, claps

92
Q

What is the Moro reflex?

A

Response to sudden loss of support- arms extend and adduct

Normally disappears by 6 months. It is remains, suggests UMN lesions such as cerebral palsy

93
Q

What is cerebral palsy?

A

A permanent disorder of movement and posture to a non-progressive lesion of motor pathways in the developing brain

94
Q

What are the causes of CP?

A

80% antenatal- CV haemorrhage or ischaemia, structural maldevelopment of the brain during development or congenital infection
10% hypoxic- ischaemic injury before or during birth
10% post-natal- periventricular leukomalacia secondary to ischaemia/haemorrhage

95
Q

What are the different types of CP?

A
  1. Spastic (70%)- UMN signs- rigidity, hyperreflexia/tonia
  2. Athetoid- Basal ganglia due to bilirubin encephalopathy or hypoxic-ischaemic injury- extrapyramidal and fluctuating hyper/hypotonia
  3. Ataxic- poor coordination, cerebellar lesions, ataxic gait, intention tremor
  4. Mixed
96
Q

How do you diagnose CP?

A

MRI

97
Q

Which healthcare professionals are involved in the care of a CP patient?

A 
Orthopaedic paediatrician, gastro paediatrician
GP
PT
OT
salt
dietician
social worker
school
psychologist
98
Q

What medications can be given to a CP patient?

A
  • treatments for spasticity include oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopaedic surgery and selective dorsal rhizotomy
  • anticonvulsants, analgesia as required

Botox works by preventing release of ACh causing flaccid paralysis, can treat muscle spasms and hypertonia

99
Q

What are the differential diagnoses for a child presenting with recurrent daydreaming?

A 
Absence seizures
ADHD
Hypoglycaemic attacks
Visual/hearing problems
Narcolepsy
100
Q

What are the investigations for epilepsy?

A

EEG- shows spike and wave discharges 3-4 Hz
12-lead ECG
24 ambulatory ECG

101
Q

Could a delay in treatment for epilepsy be dangerous?

A

Yes, SUDEP- sudden unexpected death in epilepsy

102
Q

What is the treatment for absence seizures?

What are the side effects?

A

Ethosuxamide

SE: Anorexia, diarrhoea, weight loss, abdo pain, vomiting

103
Q

3 years later, the patient presents with generalised tonic-clonic seizures and clumsiness. Why is the clumsiness relevant?

A

Classic history of juvenile myoclonic epilepsy is throwing drinks or cornflakes about in the morning as myoclonus occurs at this time

104
Q

What are the characteristic features of JME?

A
  1. Infrequent generalized seizures, often in morning
  2. Daytime absences
  3. Sudden, shock like myoclonic seizure
105
Q

What is the treatment for JME?

A

Sodium valproate or lamotrigine

106
Q

Do the 2 separate presentations at different ages have any relation?

A

Yes, absence seizures can lead to other seizure disorders in 10-15% of cases

107
Q

What are the different types of squint?

A

Paralytic and non-paralytic

Paralytic- Due to paralysis of extraocular muscles. Can’t move eye at all.

Non- paralytic- Due to imbalance in extraocular muscles. Convergent is more common than divergent

108
Q

What is an exotropia?

A 
Exo= looking out (opposite is ezo)
Tropia= malalignment always present (only present when the synchronisation of eyes is broken= phoria)
109
Q

What are the causes of non-paralytic squint?

A

Refractive errors
Cataracts
Retinoblastoma

110
Q

What are the causes of paralytic squint?

A 
Intraocular causes
Downs
CP
Measles
Requires imaging as could be a space-occupying lesion
111
Q

What is the investigation test and what are the treatments for squint?

A

Cover test

Glasses, eye match, surgery on appropriate muscles

112
Q

What is the most likely cause of a premature neonate struggling to breathe and why?

A

Respiratory distress syndrome. There is a deficiency of surfactant which lowers surface tension. This leads to widespread alveolar collapse and inadequate gas exchange.

The more premature, the worse it is.

More common in boys than girls.

113
Q

What are the clinical signs of RDS?

A

tachypnoea, intercostal recession, expiratory grunting and cyanosis

114
Q

What are the differentials for RDS?

A 
Sepsis
CHD
Transient tachypnoea of the newborn
Pneumothorax
Apnoea and bradycardia
115
Q

What would a CXR show for RDS?

A

Ground-glass appearance

116
Q

What is the treatment for RDS?

A
  • prevention during pregnancy: maternal corticosteroids to induce fetal lung maturation
  • oxygen
  • assisted ventilation - CPAP
  • exogenous surfactant given via endotracheal tube
  • Prophylactic Abx- benzylpenicillin (25mg/kg) and gentamycin (5mg/kg). Add cefotaxime if gram -ve sepsis.
117
Q

The blood glucose in a neonate with RDS has dropped to 2.1. Why is this likely to have happened?

A

Increased work of breathing and decreased feeds means blood sugar decreases.
Also preterms already have deficiency of glycogen stores.
Give 2.5mls/kg of 10% dextrose IV and check BG after 30 mins

118
Q

Would you management be different of the blood glucose in the RDS baby if it were a term baby?

A

Normal term babies commonly have BG <2.6mmool/L but because they can use ketones and lactate, this is not a long term problem.

119
Q

How would you feed a preterm baby with RDS?

A

OG/ NG tube, or PIC line if very immature
Enteral feeds, preferably breast milk supplemented with calories, phosphate and protein are introduced early (150-180ml/kg/day by 2 weeks in babies <1000g or by 2 weeks if 1000-1500kg. Start low at 15-20mls/kg/day)
If it is increased too early= NEC risk

Trophic feeds from 24 hours of life- 10-15ml/kg/day

120
Q

How do you monitor adequacy of nutrition in a newborn?

A

Growth e.g. weight, length, head circumference

Urine output

121
Q

How is an intraventricular haemorrhage in a neonate investigated? (complication of RDS)

A

USS through the anterior fontanelle

122
Q

What are some long-term complications of RDS?

A 
EYES- retinopathy of prematurity, blindness
LUNGS- Pneumothorax
Hearing problems
Cerebral palsy
20% have intraventricular haemorrhages
123
Q

How is jaundice assessed clinically?

A

Inspect skin, sclerae, gums

Assess by blanching the skin with your finger

124
Q

What investigations would you perform for jaundice?

A 
Serum bilirubin
FBC, U&amp;E, CRP, TFTs
TORCH screening
DAT test (Coomb's test)- tests for Ig (rhesus disease of the newborn)
USS- biliary atresia
125
Q

How is jaundice treated in the newborn?

A

Measure serum bilirubin every 6 hours
Phototherapy
Exchange transfusion
IVIG (if rhesus haemolytic disease)

126
Q

What are the different causes of jaundice?

A

• <24 hours- SERIOUS

  • Haemolytic disorders- rhesus incompatibility, ABO incompatibility, G6PD deficiency, spherocytosis, pyruvate kinase deficiency
  • Congenital infection- toxoplasmosis, CMV, syphilis, rubella, herpes, hepatitis

• 24 hours- 2 weeks

  • Physiological jaundice, breast milk jaundice
  • Infection, haemolytic disorders, bruising, crigler-najjar syndrome

• >2 weeks- SERIOUS
As above and hypothyroidism, pyloric stenosis
Conjugated- biliary atresia, neonatal hepatitis

127
Q

What is a complication of unconjugated bilirubin?

A

Kernicterus
Encephalopathy with seizures and coma
Can cause choreoathetoid cerebral palsy
(unconjugated bilirubin can cross the BBB causing neurotoxic effects)

128
Q

What are some worrying clinical features for jaundice?

A

Dark urine and pale stools

129
Q

How common is jaundice in ‘healthy infants’?

A

Very, it is seen in 60% of term babies in the first week of life but only 1% need treatment

130
Q

What causes osteogenesis imperfecta?

A

AD inheritance, mostly caused by defects in Type I collagen genes

131
Q

What are the signs and symptoms of OI?

A

bone fragility, fractures and deformity, bone pain, impaired mobility, poor growth, deafness, blue sclera

132
Q

What investigations should be carried out for suspected OI?

A 
Bloods- FBC, U&amp;E, CRP, Vit D, Ca, PTH
X-Rays of possible fractures
ECHO
Skeletal survey- if suspected NAI
MRI- rule out malignancy
133
Q

What is appropriate analgesia for a fracture in a newborn?

A

Intranasal diamorphine

splint/immobilise

134
Q

What is the management plan for a patient with OI?

A

MDT involvement
○ Physician- bone-targeted drugs, pain, associated medical problems
○ Surgeon- long bones, spine
Therapists/nurses- muscle strength/mobility, social and education

135
Q

What is the sepsis 6 for children?

A
  1. O2
  2. IV access and bloods- Lactate, CRP, BG, ABG
  3. IV or IO antibiotics
  4. Fluid resuscitation
  5. Get senior help
  6. Inotropes e.g. DA

Phase 3a AW (7 decks)

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