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Phase 3a > Paeds > Flashcards

Paeds Flashcards

1
Q

What are the 3 core behaviours of ADHD?

A

Hyperactivity
Inattention
Impulsivity
(HII behaviours) extreme where it is causing

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2
Q

What are the DSM criteria for ADHD?

A

at least 6 inattentive symptoms + 6 hyperactive or impulsive symptoms

Present in a primary setting
Developmentally inappropriate
Interferes in life and function
Symptoms in multiple settings

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3
Q

What comorbidities are often found with ADHD and autism?

A 
Tics 
Tourette's 
Asperger's 
Developmental/ Learning difficulties 
Sensory difficulties 
Sleep difficulties

In older people:
- Depression/ anxiety

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4
Q

What investigations should be conducted in ADHD?

A

Clinical interview
Classroom (behavioural) observation
Information from third parties
Quantitive behaviour testing (QB)

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5
Q

What is the aetiology of ADHD?

A
  • GENETIC
  • Abnormal dopamine pathways (neurochemical or neuroanatomical)
  • Environmental factors
  • CNS insults
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6
Q

What are the risk factors of ADHD?

A
  • prematurity
  • foetal alcohol syndromes
  • abuse
  • substance abuse
  • mental health issues
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7
Q

What is the management of ADHD?

A

Lifestyle advice:

  • education!!! and associated lifestyle management (emotional age of ADHD children are 1/3 less than they should be, e.g. 12y/o has emotional maturity of 9y/o)
  • Parenting and school information courses
  • balanced diet/ exercise
Medication: Stimulants (2)
            - Methylphenidate 
            - Dexamfetamine
Medication: Non-stimulants 
- Atomoxetine
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8
Q

What is the presentation of autism?

A

2-4 y/o, boys ++

Issues with:

  • COMMUNICATION (abnormal language development, abnormal accents or speech patterns, repetition, poor non-verbal communications- eye contact)
  • SOCIAL INTERACTION (2-way relationships) (no desire to interact with others or don’t understand how to navigate social rules- comes across as rude, personal space issues)
  • SOCIAL IMAGINATION (inability to play or write imaginatively, rule based play, resists change, positive obsessions/rituals (unlike negative in OCD))
  • SENSORY ISSUES
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9
Q

What is the management of autism?

A

Social Managements:

  • Education
  • Applied behavioural analysis
  • Learning/ playing tools (visual)
  • Communication tools
  • Visual planners
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10
Q

What are signs of dehydration in children?

A 
skin turgor 
moist mucosal membranes 
reduced urine output 
sunken eyes/ fontanel 
lethargic/ unconscious
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11
Q

What is normal fluid requirement for a neonate?

A

1st day: 60ml/kg
2nd day: 90ml/kg
3rd day: 120ml/kg
4th day- 1 month: 150ml/kg

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12
Q

What different fluids would you give to a 0-48hr baby, 48hr-1 month baby, 1 month onwards child?

A

0-48hr–> 10% dextrose
48hr-1month–> dextrose, sodium, potassium
1 month onwards–> 0.9% sodium chloride + 5% glucose

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13
Q

What is maintenance fluid requirements for children?

A

First 10kg: 100ml/kg
Next 10kg: 50ml/kg
Every other kg: 20ml/kg

if dehydrated; +50ml/kg
if shocked: +100ml/kg + bolus

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14
Q

What are symptoms of inattention? (ADHD)

A
  • easily distracted
  • does not appear to be listening
  • difficulty sustaining attention
  • forgetful in ADL and loses things
  • fails to complete tasks
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15
Q

What are symptoms of impulsivity? (ADHD)

A
  • interrupts in conversation
  • difficulty waiting
  • adolescents: risky behaviours- sex, alcohol, drugs, car accidents etc.
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16
Q

What are symptoms of hyperactivity? (ADHD)

A
  • squirmy/ fidgeting
  • runs or climbs excessively/ inappropriately
  • excessive talking (girls)
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17
Q

Measles:

  • Cause
  • Presentation
  • Complications
  • Management
A

Cause
- Viral

Presentation:

  • CCCK; cough, coryza, conjunctivitis, Koplick spots
  • Fever, malaise
  • Rash- discrete maculopapular rash from behind ears/ forehead—> down, to blotchy rash

Complications:

  • Pneumonia
  • Encephalitis

Management:
MMR vaccine, ribavirin, Vitamin A

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18
Q

Mumps:

  • Cause
  • Presentation
  • Complications
  • Management
A

Cause
- Virus, accesses parotid glands before disseminating

Presentation:

  • Fever, malaise
  • Pain swallowing
  • PAROTITIS

Complications:

  • Orchitis + infertility
  • Encephalitis

Management:
- Symptomatic

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19
Q

Rubella:

  • Cause
  • Presentation
  • Complications
  • Management
A

Cause:
- Virus

Presentation:

  • Maculopapular rash- face then to body, not itchy in children
  • Insignificant fever
  • Lymphadenopathy

Complications:
- Microcephaly in foetus if pregnant lady infected

Management:
- self limiting

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20
Q

Herpes Simplex Virus:

  • Cause
  • Presentation
  • Complications
  • Management
A

Cause:
- Virus

Presentation:

  • Gingivostomatitis (lesions in mouth)
  • Cold sores
  • Eczema herpeticum (can lead to septicaemia)
  • Herpetic whitlow

Management:
- Acyclovir

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21
Q

Varicella Zoster Virus:

  • Cause
  • Presentation
  • Complications
  • Management
A

Cause:
- Chickenpox virus (is a HSV), very contagious

Presentation: (1-5 y/o)

  • initial fever
  • vesicular rash (itchy+++)

Complications:

  • Shingles in the adult
  • Dangerous in immunocompromised- haemorrhagic lesions, DIC

Management:
- Calamine lotion

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22
Q

Epstein- Barr Virus:

  • Cause
  • Presentation
  • Investigations
  • Complications
  • Management
A

Cause:
- Virus (HSV)

Presentation:

  • Glandular fever;
    • fever, malaise
    • extreme fatigue
    • severe tonsillopharyngitis, lymphadenopathy
    • palatal petechiae

Investigations:

  • Positive Monospot test
  • Atypical lymphocytes

Complications:
- linked to Burkitt’s lymphoma + nasopharyngeal cancer,

Management:
- Symptomatic

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23
Q

Cytomegalovirus:

  • Cause
  • Presentation
  • Complications
  • Management
A

Cause:
- Virus (HSV)

Presentation:

  • Asymptomatic
  • like EBV (severe tonsillopharyngitis)
  • like acute hepatitis

Complications:
- congenital CMV

Management:

  • symptomatic or
  • ganciclovir
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24
Q

Roseola Infantum:

  • Cause
  • Presentation
  • Management
A

Cause:
- Virus (HSV, HHV6)

Presentation:

  • sudden high fever
  • after fever rash

Management:

  • Symptomatic
  • Ganciclovir
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25
Q

Parvovirus B19:

  • Cause
  • Presentation
  • Complications
  • Management
A

Cause:

  • Virus, resp transmission
  • infects erythroblastoid red cell precursors in bone marrow

Presentation:

  • SLAPPED CHEEK
  • fever, malaise
  • headache

Complications:

  • Aplastic crisis in haemolytic anaemias
  • Hydrops fetalis

Management:
- symptomatic

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26
Q

Hand-Foot-and-Mouth:

  • Cause
  • Presentation
  • Management
A

Cause:
- Coxsackie virus, hand-foot and mouth

Presentation:

  • vesicular rash on hands and feet
  • ulcers in and around mouth
  • mild systemic features

Management:
- resolves itself

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27
Q

What common infections are caused by Staph A?

A

Gram +ve, in clumps
Scalded skin syndrome (flucloxacillin)
Cellulitis! Abscess, osteomyelitis

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28
Q

What common infections are caused by Strep B?

A

Septicaemia (GBS+ve), UTI, Pneumonia

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29
Q

What common infections are caused by Strep A?

A

Sore throat- pharyngitis and tonsillitis

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30
Q

What are the causes of CAP?

+ Management

A

Strep Pneumoniae
Haemophius Influenzae
Atypical- legionella, chlamydophila, mycoplasma
Staph A

Management: oral amoxicillin, clarithromycin, doxycycline

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31
Q

What are the causes of HAP?

+ Management

A

Gram -ve bacilli
Pseudonomas

Aminoglycoside IV, cephalosporin, antipseudonomal penicillin

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32
Q

Meningitis/ Encephalitis

- Causes

A

Inflammation of the meninges/ the brain

Causes
- Viral (most common)- enterovirus, EBV, adenovirus
- Bacterial- Neonates- Strep B
Older- Neisseria Meningitides, Strep Pneumoniae
- HSV for encephalitis

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33
Q

What findings would you see in LP of meningitis or encephalitis

A
  • Raised Lymphocytes
  • Raised Protein
  • Decreased Glucose
  • Cloudy colour if bacterial
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34
Q

What is the presentation of meningitis

A

Presentation

  • fever
  • headache
  • neck stiffness
  • photophobia
  • Meningococcal purpural rash
  • Bulging fontanel
  • Kernig’s sign (pain on leg extension)
  • Brudzinski’s sign (hip + knee flexion when flexing neck)
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35
Q

What investigations would you carry out for meningitis

A

Investigation
- Lumbar puncture- raised lymphocytes/ polymorphs,
raised protein, decreased glucose
+ culture
- FBC with differential count
- Blood culture, throat swabs, urine culture
- Rapid antigen screens or PCR of any samples

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36
Q

What is the management of meningitis?

A

Viral: Supportive

Bacterial: Ceftriaxone/cefataxime + dexamethasone

Prophylactic rifampicin given to contacts

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37
Q

Meningococcal Septicaemia

A

Any febrile child with purpuric rash is considered meningococcal septicaemia until proven otherwise!!!!!

  • IM BENZYLPENICILLIN in community
  • IV cefotaxime or ceftriaxone
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38
Q

What are the complications of meningitis?

A
  • Developmental delay
  • Hearing impairment
  • Vasculitis/ Infarction–> focal lesions/ CN palsies, seizures
  • Subdural effusion/ hydrocephalus
  • Cerebral abscess
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39
Q

Kawasaki Disease

  • What is it
  • Who does it effect
  • Presentation
  • Differentials
  • Investigations
  • Complications
  • Management
A
  • systemic vasculitis of small-medium arteries, diagnosis made on clinical features alone
  • 6 months- 4 years old

Presentation

  • irritability + malaise
  • prolonged fever
  • conjunctivitis
  • red and peeling extremities
  • red mucous membranes
  • strawberry tongue
  • high CRP, ESR, and WCC

Differentials

  • Scarlet fever
  • Measles
  • Toxic shock syndrome
  • JIA

Investigations

  • Bloods- FBC, CRP, WCC, BNP (cardiac stress)
  • Urine dip + culture
  • ECG
  • Echocardiogram

Complications
- Coronary artery aneurysm!!!!!

Management

  • Gammaglobulins
  • High anti-inflammatory dose of aspirin
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40
Q

What are the 2 stages of allergic response?

A

Early: within minutes; sneezing, urticaria, angioedema, vomiting, bronchospasm, CV shock

Late: 4-6 hours; nasal congestion, cough and bronchospasm in the lower airway

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41
Q

What is eczema?

  • exacerbations
  • complications
A

Atopic dermatitis, very itchy
Erythematous, weeping, crusted

Exacerbated by infection, ingestion of allergen, medication, change in environment, stress

Complications are skin infections (staph a or strep) as a result of damaged skin barrier

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42
Q

What is the management of eczema?

A
  • Avoid irritants/ triggers
  • Emollients
  • Topical corticosteroids (e.g. 1% hydrocortisone creams)
  • Immunomodulators- tacrolimus
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43
Q

What are warts, causes and managements?

A

Viral- HPV or Poxvirus

Usually disappear naturally, can be treated with salicylic acid, over the counter, or cryotherapy

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44
Q

What is the management of scabies?

A

benzyl benzoate to patient and all close contacts

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45
Q

What is the presentation of TB in children?

A
  • Persistent fever
  • Persistent cough
  • Malaise
  • Night sweats
  • Weight loss

Signs

  • CXR- Gohn Complex, calcifications, bilateral lymphadenopathy
  • Histopathology: caseous granuloma
  • Positive mantoux test or interferon gamma release assays
  • positive sputum culture/ gastric washing (ziehl nielson)
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46
Q

What is the management of TB?

A

Rifampicin (red urine) 6 MONTHS

Isoniazid (burning feet) 6 MONTHS

Pyrazinamide (hepatitis) 2 MONTHS

Ethambutol (optic neuritis) 2 MONTHS

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47
Q

What is whooping cough?

  • causes
  • symptoms/ presentation
  • investigations
  • complications
  • management
A

Bordatella Pertussis

Presentation

  • coryzal symptoms (catarrh to begin with)
  • paroxysmal cough followed by distinctive whoop
  • worse at night
  • apnoea (child goes blue/ red between coughs)
  • epistaxis/ subconjunctival haemorrhage (from coughing)

Investigations

  • Pernasal swab culture/ PCR
  • FBC- lymphocytosis

Complications

  • Pneumonia
  • Bronchiectasis
  • Seizures

Management

  • Macrolides
  • prophylaxis for parents
  • immunisation!
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48
Q

What are the causes of wheeze in preschool children?

A
  • Recurrent viral wheeze (during viral infections) (up until age 3)
  • Multiple trigger wheeze (such as cold, dust, foods -can lead to asthma) (ages 3-6)
  • Asthma (continues throughout childhood)
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49
Q

What is asthma?

What is the pathophysiology of asthma?

A

Chronic inflammatory condition in the lungs caused by a genetic predisposition + atopy + environmental triggers causing;

REVERSIBLE OBSTRUCTED AIRFLOW

Trigger–>
Bronchial inflammation (oedema, mucus production, WC infiltration (mast cells, neutrophils, eosinophils, lymphocytes))–>
Bronchial hyperresponsive–>
Airway narrowing (airflow restriction)–>
Symptoms (wheeze, cough, breathlessness, chest tightness)

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50
Q

What are the symptoms and signs of asthma?

+ investigations

A

Wheeze (polyphonic)
Cough
Breathlessness
Chest tightness

Diurnal variation- worse at night and morning
Relief between episodes
Positive response to therapy

Investigations

  • commonly diagnosed on history and examination
  • peak flow (with bronchodilators)
  • spirometry (with bronchodilators)
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51
Q

What causes acne?

A

androgenic stimulation of sebaceous glands and increased sebum
inflammation

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52
Q

What is the management for acne?

A

Hygiene advice- not to over clean
Lifestyle- healthy diet, don’t pick spots, make up cleansers

Topical retinoid ± benzoyl peroxide
Topical antibiotic

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53
Q

What is the management for asthma?

A

1st Line: Short Acting Beta 2 Agonist e.g. salbutamol, terbutaline

2nd Line: SABA + Inhaled Corticosteroids (e.g. beclametasone, budesonide)

3rd Line: SABA + ICS + Leukotriene receptor antagonist (e.g. Montelukast SE MENTAL HEALTH)

4th Line: SABA + ICS + LABA (e.g. Salmeterol)

Avoid exacerbators

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54
Q

What is the management of acute asthma?

A

O SHIMIE

Oxygen 
Salbutamol 
Hydrocortisone/ prednisolone 
Ipratropium 
Magnesium 
IV Salbutamol/Aminophylline
Escalate care (intubation, ventilaiton etc.)

CO2:
Low- good as they’re compensating
Normal- not good, they’re not offloading enough CO2 for their resp rate
High- Life threatening

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55
Q

Respiratory Syncytial Virus

  • what is it
  • presentation
  • management
A

Common viral RTI

  • cold like symptoms
  • mucus
  • wheeze

management: conservative

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56
Q

Who is at risk of respiratory failure?

A
  • Preterm/ ex-preterm
  • Bronchopulmonary dysplasia!
  • Haemodynamicall significant congenital heart disease
  • Congenital causes of muscle weakness
  • Cystic fibrosis
  • Immunodeficiency
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57
Q

What is bronchopulmonary dysplasia?

A

Chronic lung disease that effects newborns and infants (usually preterm)
From damage caused by mechanical ventilation effect on immature lungs

Manage with oxygen

More susceptible to lung infection

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58
Q

What pathogens commonly cause pharyngitis and tonsilitis?

A
  • Strep A

- EBV

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59
Q

What is otitis media?

  • Presentation
  • Causative agents
  • Management
A

Inflammation of the middle ear

Common in children due to short eustachian tubes

Presents with ear pain and fever
+ red and bulging tympanic membrane
± pus in the external canal

Recurrent infections in an ear without a patent Eustachian tube, can cause effusion (glue ear) which causes reduced hearing

Caused by: Viruses (RSV, rhinovirus) Bacteria (Pneumococcus, Hib)

Management:

  • analgaesia (paracetamol and ibuprofen)
  • Amoxicillin if persists
  • Grommits for effusion
  • Hearing aids
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60
Q

What is ALL?

How does Leukaemia present?

(inc. investigations)

A

ALL- Acute Lymphoblastic Leukaemia, malignancy of lymphocytic cells (that develop into T cells, B cells, NK cells)
- Aged 2-5

Symptoms caused by disseminated disease;

  • fatigue/ malaise/ anorexia
  • pallor (anaemia)
  • infection
  • easy bruising/ petechiae/ nose bleeds
  • bone pain
  • hepatosplenomegaly
  • lymphadenopathy
  • mediastinal mass
  • headaches/nausea/vomiting
  • nerve palsies and enlarged testicles

Investigations:

  • Blood film: Low Hb, Thrombocytopenia (low platelets), evidence of leukemic blast cells
  • Clotting screen: looking for DIC (low fibrinogen, prolonged prothrombin time (PT/PTT), raised D-dimer)
  • Lumbar puncture
  • Chest x-ray
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61
Q

What are risk factors of malignancy in children?

A
  • Down’s syndrome
  • Immunocompromised (e.g. HIV)
  • Family history (retinoblastoma)
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62
Q

What is the management of ALL?

A

Correct anaemia with blood transfusion
Reduce haemorrhage risk with platelet transfusion
Hydration + allopurinol for renal protection

  1. Induction- prep (above) + chemotherapy inc steroids until 95% remission
  2. Intensification/ Consolidation- high intensity chemotherapy
  3. Continuation/ interim maintenance- moderate dose chemotherapy for 3 years (with prophylactic Ab)
  4. High dose chemotherapy + bone marrow transplant for relapse
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63
Q

What indicates prognosis of ALL?

A
  • cytogenetics of leukemic cells
  • white cell count at presentation (tumour load)
  • response to treatment
  • patient age (poor is <1 or >10)
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64
Q

What are the types of brain tumours in children?

A

Astrocytoma- originate from glial cells in the CNS (sometimes benign) ~40%

Medulloblastoma- from the cerebellum (MOST COMMON MALIGNANT) ~20%

Ependymoma- posterior fossa ~8%

Brainstem glioma

Craniopharyngioma

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65
Q

How do CNS tumours present?

A

Raised ICP: headache, nausea, vomiting, confusion, dizziness, visual disturbances, nystagmus, ataxia

Focal neurological signs (personality change, nerve palsies)

Back pains, limb weakness, bowel/ bladder dysfunction

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66
Q

What is the management of CNS malignancies?

A

Surgery for most- managing hydrocephaly/ removing lesion

Radio/chemotherapy

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67
Q

What is Lymphoma?

A

Tumour of Lymphocytic cells (T cells, B cells, NK cells) aggregating within the lymph nodes

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68
Q

What is the most common lymphoma in children vs adolescent?

A

Children: Non-Hodgkins Lymphoma
Adolescent: Hodgkins Lymphoma

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69
Q

What is the clinical presentation of Hodgkin’s and Non-Hodgkin’s Lymphoma? + whats the difference

A

h- painless lymphadenopathy, hepatosplenomegaly, ±systemic features (fatigue, sweating, fever, anorexia, pruritus, recurrent infections, anaemia- pallor)

Reed-Sternberg cells on lymph node biopsy in Hodgkin’s

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70
Q

What investigations would you do for ?lymphoma or leukaemia?

A
  • FBC (WCC, Hb, MCV, platelets)
  • Clotting screen (?DIC)
  • Ferritin
  • Blood film (?Leukaemic blast cells)
  • LDH
  • Lymph node biopsy (?reed sternberg cells)
  • Lumbar puncture
  • CXR- ?mediastinal lymph node enlargement
  • CT scan to assess extent of disease
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71
Q

What is the management of Lymphoma?

A
  • Stage the disease (Ann Arbor)
  • Chemotherapy
  • Stem cell transplants
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72
Q

Where does a Neuroblastoma arise?

A

Neural crest cells, classically from adrenal medulla

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73
Q

What is the presentation of a neuroblastoma?

A

Classically; abdominal mass, but can be wider spread along Sympathetic Nervous System

Abdominal symptoms:

  • mass
  • pain
  • haematuria
  • constipation
  • htn
  • weight loss
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74
Q

What is the presentation of a neuroblastoma?

A

Classically; abdominal mass, but can be wider spread along Sympathetic Nervous System

Abdominal symptoms:

  • mass/ hepatomegaly
  • pain
  • haematuria
  • constipation
  • htn
  • weight loss

Other symptoms:

  • cervical lymphadenopathy
  • periorbital bruising
  • proptosis
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75
Q

What is Wilm’s tumour and how does it present?

A

Tumour of embryonic renal tissue (nephroblastoma), common in <5yo

Presents:

  • abdominal mass with haematuria
  • symptoms of abdominal mass/ general symptoms of malignancy
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76
Q

What is the management of Wilm’s tumour?

A

Chemotherapy and then resection
±more chemo ± radiotherapy

80% survival

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77
Q

What causes retinoblastoma?

A

RB1 gene mutation

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78
Q

How does a retinoblastoma present?

A
  • LOSS OF RED REFLEX
  • strabismus (cross eyed)
  • Visual changes
  • eye pain
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79
Q

What are the characteristics or an acute upper airway restriction?

A
  • stridor (rasping sound)
  • hoarseness in voice
  • barking cough
  • dyspnoea
  • cyanosis
  • chest recessions (subcostal, intercostal, sternal)
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80
Q

What is croup?

A

Laryngotracheobronchitis

Mucosal inflammation, and increased secretions
+ subglottic oedema causing narrowing of the trachea

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81
Q

What are the causes of croup?

Symptoms?

A

Viral- Parainfluenza

Symptoms:

  • Coryza + fever
  • Hoarseness
  • barking cough
  • stridor
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82
Q

What is the management of laryngotracheobronchitis? (croup)

A 
- Inhalation of warm air
STEROIDS++
- dexamethasone 
- prednisolone 
- nebulised steroids budesonide
  • adrenaline + oxygen if severe
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83
Q

What is croup+ thick airway secretions?

A

Staph A infection!!!

Manage with IV antibiotics (cefuroxime) and intubation

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84
Q

What is epiglottitis caused by?

How does it present?

What is the management?

A

Hib, commonly associated with septicaemia

  • minimal or no cough
  • saliva drooling++
  • toxic appearance
  • quick onset
  • reluctant to speak or swallow

Management

  • intubation/ ventilation
  • ENT + anaesthetist referral urgent
  • Ab
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85
Q

What is the presentation of bronchiolitis?

A
  • Coryzal symptoms
  • dry cough
  • dyspnoea
  • APNOEA
  • subcostal/ intercostal recession
  • hyperinflation of the chest (prominent sternum
  • ## fine inspiratory crackles
86
Q

What is the presentation of bronchiolitis?

A
  • Coryzal symptoms, inc low grade fever
  • dry cough
  • dyspnoea
  • APNOEA
  • subcostal/ intercostal recession
  • hyperinflation of the chest (prominent sternum, liver displaced downwards)
  • fine inspiratory crackles
  • tachycardia
  • cyanosis
  • pallor
87
Q

What are the risk factors of bronchiolitis?

A
  • Prematurity
  • bronchopulmonary dysplasia
  • underlying lung disease
  • congenital heart disease
88
Q

What is the management of bronchiolitis?

A
  • Supportive
  • Humidified oxygen
  • Fluids
  • beta agonists not given as no beta receptors <6 months
89
Q

What is the most common causative agent of pneumonia in;

Newborns
Infants
Children

A

Newborns; organisms from maternal GU tract- Strep B or Gram -ve enterococci

Infants: RSV, Strep Pneumonia (lobar) , Haemophilus Influenza

Children: Mycoplasma/ Strep/ Chlamydia Pneumoniae

90
Q

What is the presentation of pneumonia in children?

A
  • high fever
  • cough
  • tachypnoea +
  • coryzal symptoms
  • bronchial breathing, unilateral coarse crackles
    ± wheeze
  • nasal flaring, chest indrawing
  • Bacterial infection- neck/ abdo pain (pleural irritation)
91
Q

What is the management for Pneumonia?

A
  • Oxygen
  • analgesia
  • fluids
  • IV benpen
  • oral amoxicillin or co-amoxiclav
92
Q

What is the presentation of a UTI in young children?

A

Non-specific

  • fever
  • malaise
93
Q

What investigations would you do for ?pneumonia?

A
  • Blood culture

- CXR

94
Q

What are the associated risks of steroid use in children (e.g. asthmatics)?

A
  • adrenal suppression
  • growth suppression
  • osteoporosis
95
Q

What is the pathophysiology and management of bronchiectasis ?

A
  • inflammation –> airway damage –> mucocilliary clearance impaired–> increased infection–> inflammation etc.

Management:

  • physiotherapy to clear
  • management of infection
  • fluids/ oxygen
96
Q

What is the pathophysiology of cystic fibrosis?

A
  • autosomal recessive disorder

Mutation of the Cystic Fibrosis Transmembrane conductance Regulator gene

Causes impaired chloride transport into mucus (which thins it)

CF:
Thick mucus–> impaired ciliary function + retention of mucopurulent secretions

—> multisystem pathology

97
Q

How is cystic fibrosis diagnosed?

A
  • Newborn screening test
  • clinical presentation with recurrent chest infections, faltering growth, malabsorption , meconium ileus

On examination: finger clubbing, hyperinflated chest, expiratory wheeze, inspiratory crepitation

Sweat test:
- increased Cl in the sweat

98
Q

How does CF effect the lungs + management?

A

Viscous mucus causes trapping of bacteria+ recurrent infections (Staph A, H. Influenzae)

Recurrent infections leads to damaged airways (can cause bronchiectasis and abscesses)

+ persistent loose cough and producing purulent sputum

Management:

  • physiotherapy to clear sputum
  • prophylactic antibiotics (Fluclox)
  • Nebulised DNase or hypertonic saline to decrease viscosity of sputum
  • lung transplant
99
Q

How does CF effect the pancreas + management?

A

Thick mucus blocks the exocrine pancreatic duct, therefore products (lipase, amylase and proteases) can’t flow through.
There is pancreatic exocrine insufficiency. Therefore there is failure to thrive, maldigestion, malabsorption.

Patients pass frequent large, pale, greasy and offensive stools.
Low elastase in faeces.

Managed with oral pancreatic enzyme replacement, ursodeoxycholic acid to improve bile flow

Also develop diabetes mellitus

100
Q

What are the causes of a Left–>Right shunt?

A

atrial septal defects (secundum ASD or partial AVSD)

ventricular septal defect

persistant ductus arteriosus

101
Q

What signs would you see in a child with an atrial septal defect?

A

ejection systolic murmur (heard over pulmonary valve- upper left sternal edge- due to increased blood flow)

split second heart sound

102
Q

What are the cyanotic heart conditions?

A
  • deoxygenated blood being circulated
    (Bypass the lungs) (Right–> Left shunt)
  1. One big trunk–> Truncus Arteriosus
  2. Two interchanged vessels–> Transposition of the great vessels
  3. Tricuspid atresia
  4. Tetralogy of Fallot
  5. Five words- Total Anomalous Pulmonary Venous Return
103
Q

What is the tetralogy of fallot?

A
  1. Pulmonary Stenosis
  2. Right ventricular hypertrophy
  3. Overriding aorta
  4. Ventricular septal defect
104
Q

What are the acyanotic heart conditions?

A
  • Less oxygenated blood being circulated

Left–> Right shunt

  • ASD
  • VSD
  • AVSD
  • PDA
105
Q

What are the signs of a ventricular septal defect?

A

Small: asymptomatic

  • loud pansystolic murmur and lower left sternal edge
  • quiet pulmonary second sound

Large:
- heart failure, breathlessness and failure to thrive after 1 week
- soft pansystolic/ no murmur
- mid-diastolic murmur
CXR findings: cardiomegaly, enlarged pulmonary arteries, pulmonary oedema, increased pulmonary vascular markings

106
Q

What investigations do you do for ?congenital cardiac abnormality?

A
  • CXR
  • cardio echogram

In cyanosis:
- hyperoxia test

107
Q

What diseases cause clubbing in children?

A
  • CF
  • Tetralogy of Fallot
  • Chronic IBD
108
Q

How does heart failure present in neonates+ infants?

A
  • breathlessness
  • sweating
  • poor feeding + failure to thrive
  • recurrent chest infections
  • tachypnoea/ tachycardia
  • heart murmurs
  • cardiomegaly
  • hepatomegaly
109
Q

What are the causes of heart failure in neonates?

A

OBSTRUCTIVE OF FLOW (duct dependant circulation)

  • severe aortic stenosis
  • coarctation of the aorta
  • interruption of the aortic arch
  • hypoplastic left heart syndrome
110
Q

What are the causes of heart failure in infants?

A

HIGH PULMONARY BLOOD FLOW leading to uncompensated pulmonary oedema (due to left to right shunt)

  • AVSD
  • VSD
  • Large persistant ductus arteriosus
111
Q

What are the causes of heart failure in older children?

A
  • After initially compensated left to right shunt: Eisenmenger’s syndrome (increased pulmonary resistance, causing a right to left shunt- cyanosis)
  • rheumatic heart disease
  • cardiomyopathy
112
Q

What are the causes of cyanosis in the neonate?

A

Cardiac:
- cyanotic congenital heart conditions

Respiratory:

  • RDS (surfactant deficiency)
  • Meconium aspiration
  • Pulmonary hypoplasia

Persistant pulmonary hypertension of the newborn (failure of the pulmonary vascular resistance to fall)

Infection: GBS, TORCH

Inborn error of metabolism- acidosis and shock

113
Q

What are the clinical features of a persistant ductus arteriosus?

A

small- asymptomatic
continuous murmur
bounding pulse

114
Q

How do you manage a large patent ductus arteriosus?

A

closure with a coil or occlusion device

surgical ligation

115
Q

What is the management of a cyanotic heart disease?

A

ABCDE–> stabilise airways and ventilate

Prostaglandin infusion

Manage underlying cause

116
Q

What is the management of tetralogy of fallot?

A
  • surgery at 6 months

medical management before:
- propanolol

117
Q

What are the causes of being cyanotic and breathless?

A

Complete mixing-

  • complete ASVD
  • tricuspic atresia
118
Q

What is the management of heart failure in children?

A

ABCDE
Prostaglandins in the neonate
Medical: - digoxin, ACEi (captopril), diuretics (furosemide)

  • Surgical repair of the cause
119
Q

What is the presentation of infective endocarditis?

+causative agents

+ investigations

+ management

A
  • fever malaise
  • raised ESR
  • anaemia
  • haematuria

+ viral or staph A

  • anaemia and pallor
  • splinter haemorrhages
  • splenomegaly

Investigations:

  • blood cultures
  • echo (vegitations)
120
Q

What is cerebral palsy?

A

Non-progressive lesion on motor pathways in the developing brain, leading to abnormalities in movement and posture

121
Q

What is the presentation of cerebral palsy?

A

symptoms develop over time

  • Abnormal motor development (e.g. can’t sit up/ support own head)
  • abnormal posture
  • feeding difficulties
  • abnormal gait
  • asymmetric hand function <12m
  • persisting primitive reflexes

Other:

  • Learning difficulties
  • Epilepsy
  • Squints/ visual impairment
  • hearing impairment
  • speech and language disorders
  • joint disorders- e.g. scoliosis, contractures, subluxation
122
Q

What is the aetiology of cerebral palsy?

A

Antenatal (80%):

  • vascular occlusion
  • gene deletions/ chromosomal abnormalities
  • antenatal infection

During birth:
- hypoxic brain injury

Post natal:

  • Periventricular Leukomalacia- death of tissue around ventricles (secondary to ischaemia or haemorrhage- ?haem problems)
  • Meningitis
  • Encephalitis
  • Hypoglycaemia
  • Trauma
123
Q

What are the types of Cerebral Palsy?

A
  1. Spastic - hemiplegia, tetraplegia, diplegia
  2. Ataxic- cerebellar dysfunction- hypotonia, poor balance and coordination
  3. Dyskinetic- involuntary muscle movements e.g. chorea
124
Q

What is the management for Cerebral Palsy?

A

MDT- physio, occupational, speech and language, dietician

Botox injections for spasticity

125
Q

How do you OBJECTIVELY assess hearing loss in children?

A 
Otoacoustic emissions ( babies screening)
Auditory brainstem response (in older children)
126
Q

How do you SUBJECTIVELY assess hearing loss in children?

A 
distraction testing (6-18m)
visual reinforcement audiometry (10m-3y)
performence testing
127
Q

What is intussuseption?

+ where is it most common?

A

Invagination of the proximal bowel into the distal bowel.

Most commonly ileum passing into the caecum through the ileocaecal valve,

128
Q

What is periorbital cellulitis?

  • presentation
  • management
A

** medical emergency **
URTI followed by painful swollen eye

  • proptosis
  • red colour vison
Management:
- URGENT ENT AND OPTHALM INVOLVEMENT 
- Imaging 
- Incision and drainage 
IV Abx
129
Q

What are the causes of prematurity?

A

Multiple gestation
Polyhydramnios

Uterine abruption
Antepartum haemorrhage

Intrauterine infection: 
Chorioamnionitis 
CV 
Preterm prolonged rupture of membranes 
Maternal UTI

IUGR
Congenital malformations

Pre-eclampsia
Maternal hypertension
Maternal chronic disease

Cervical weakness

130
Q

What are the foetal problems associated with maternal diabetes mellitus?

A

increased risk of:

congenital malformations- e.g. cardiac
IUGR- microvascular disease
Macrosomia- maternal hyperglycaemia

131
Q

What are the neonatal problems associated with maternal diabetes mellitus?

A

Hypoglycaemia- hyperinsulinism (give early feeding)

Respiratory distress syndrome- delayed lung maturation

Hypertrophic cardiomyopathy

Polycythaemia

132
Q

What does use of SSRIs during pregnancy cause for the newborn?

A

Persistant pulmonary hypertension

133
Q

What are the features of foetal alcohol syndrome?

A

Face: Eyes: small palpebral fissure, epicanthal folds
Nose: low nasal bridge (saddle), short, upturned nose
Lips: absent philtrum, thin upper lip
Micrognathia

Growth restriction
Mental retardation
Cardiac defects- VSD

134
Q

What abnormalities does maternal rubella infection cause?

A

Deafness
Cataracts
Growth restriction

135
Q

What abnormalities does maternal CMV infection cause?

A

sensorineural hearing loss

Hepatosplenomegaly and petechiae

136
Q

What abnormalities does maternal Varicella zoster infection cause?

A

skin scarring
ocular + neurological damages
digital dysplasia

neonatal infection

137
Q

What abnormalities does maternal rubella, CMV, toxoplasmosis and syphilis cause?

A 
Congenital heart disease- patent DA 
Hepatosplenomegaly 
Petechiae 
anaemia 
deafness 
intracerebral calcification
138
Q

What is included in the APGAR score?

A
  1. Heart rate (/2) (absent, <100bpm or >100bpm)
  2. Respiratory effort (/2) (absent, gasping/irregular or regular/strong cry)
  3. Muscle tone (/2) (flaccid, some flexion, good flexion/ active)
  4. Reflex irritability (/2) (none, grimace, cry/cough)
  5. Colour (/2) (blue, blue extremities only, pink)
139
Q

How do you resuscitate the neonate?

A
  • ——-temperature control throughout——–
    1. Airway in neutral positioning (level)
    2. Ventilation Breaths (repeat and then intubate if necessary)
    3. Chest compressions
    4. Drugs: adrenaline (for poor HR). Sodium bicarb (if lactic acidosis). Dextrose+ NaCl fluids (volume)
140
Q

How do you thermally control the neonate?

A

Skin to skin
Blankets
Under the heat lamp (resus)
In a plastic bag (preterm)

141
Q

What is assessed in a NIPE?

A

Birthweight
Gestational age
Head circumference
General inspection: movements, colour (plethoric, pale, jaundice)

Fontanelle: sutures, tense or soft

Face: any deformities

Eyes: red reflex, retinal vessels

Palate: cleft palate

Heart, lungs, abdomen

Femoral pulses

Genitalia, anus

Developmental dysplasia of the hip (barlow and ortolani)

142
Q

What are the complications in macrosomia?

A 
Birth trauma 
Shoulder dystocia + Erb's palsy 
Difficult delivery (asphyxiation) 
Hypoglycaemia (due to hyperinsulinaemia)
polycythaemia
143
Q

Why is IM vitamin K given to newborns?

A

to prevent haemorrhagic disease of the newborn

144
Q

What causes GORD in the neonate?

A

Inappropriate relaxation of the lower oesophageal sphincter due to functional immaturity

+fluid diet, horizontal posture, short oesophagus

145
Q

What are the complications of GORD?

A

Failure to thrive
Iron deficiency anaemia
Recurrent pneumonia (pulmonary aspiration)
Oesophagitis- haematemesis

146
Q

What is the presentation of GORD in infants?

A

Recurrent vomitting episodes

± poor weight gain

147
Q

What is the management of GORD?

A
  • Food thickeners
  • head prone up position after feeds
  • Proton pump inhibitor (e.g. omeprazole, lansoprazole)
  • H2- receptor antagonist (e.g. ranitidine)

Surgery

148
Q

Who is at increased risk of GORD?

A 
CF 
Neuromuscular problems 
Previous oesophageal or diaphragm surgery 
Preterm infants 
Bronchopulmonary dysplasia
149
Q

What is the pathophysiology of pyloric stenosis?

A

Hypertrophy or the pyloric muscle resulting in gastric outlet obstruction

150
Q

What is the presentation of pyloric stenosis?

A

2-7 weeks
Projectile vomiting !!

Hunger after vomiting
weight loss if delayed presentation
dehydration

151
Q

What pH imbalance is noted in pyloric stenosis?

A

Hypochloraemic metabolic acidosis with low sodium and potassium

Everything reduced!! Due to vomiting

152
Q

How do you diagnose pyloric stenosis?

A

Give feed and observe

  • gastric peristalsis
  • examine “olive” in RUQ

USS if necessary

153
Q

What is the management of pyloric stenosis?

A

Correct fluid balance (0.45% saline with dextrose and potassium)

Surgical correction: pyloromyotomy

154
Q

What are common causes of acute abdominal pain?

A 
Appendicitis 
Intussusception 
Intestinal obstruction 
Peritonitis 
Hernias- inguinal or umbillical 
Trauma 
Diabetic ketoacidosis 
Hepatitis 
Pyelonephritis 
UTI 
IBS 
IBD 
Crohn's 
Peptic ulcer 
GORD 
Gastroenteritis 
Gynae
155
Q

What is the presentation and management of appendicitis?

A

Presentation:

  • Abdominal pain: initially central and then localises to the right iliac fossa (aggravated by movement)
  • vomiting
  • anorexia

Signs:

  • Low grade fever
  • Flushed face
  • Tenderness with guarding in RIF

Investigation:

  • Bloods (FBC (WCC), U+Es)
  • Abdominal X-ray if needed

Management:

  • Regular clinical review
  • Appendicectomy
156
Q

What is intussusception?

A

Invagination of proximal bowel loop into a distal segment

Commonly: ileum–> caecum (through iliocaecal valve)

157
Q

What is the presentation of intussusception?

+ investigations

A

Peak presentation: 3m-2y

Paroxysmal, severe, colicky pain with pallor 
Anorexia and vomiting 
Palpable abdominal mass 
**Redcurrant jelly stool** 
Distention, shock

Abdo Xray: dilated small bowel, absence of air in large bowel

158
Q

What is the complications of intussusception?

A

Mesenteric venous occlusion–> fluid aggregation, bleeding–> perforation + gut necrosis–> sepsis

159
Q

What is the management of intussusceptions?

A

Fluid resus
Air enema- Rectal air insufflation
Surgical correction if peritonitic/ suspect perforation

160
Q

Meckel’s diverticulum:

  • What is it
  • Complications
  • Management
A

Ileal duct remnant which contains gastric mucosa or pancreatic tissue

Usually asymptomatic
Can present as: rectal bleeding, intussusception, volvulus, diverticulitis

Management:
Surgical resection

161
Q

What does bilious vomiting indicate?

A

Bowel obstruction!

162
Q

What is malrotation?

A

No dudodenojejunal flexure or ileocaecal region fixture of mesentery, so bowel can rotate on itself, causing volvulus and obstruction ± necrosis

163
Q

What is the management of peptic ulcers?

A

H. pylori investigation: stool sample, biopsy, 13C breath test

H. pylori +ve: amoxicillin and metronidazole

164
Q

What is the presentation of gastroenteritis?

A

Watery stools
Vomiting
Dehydration: reduced urine output, pale/mottled skin, hypotension, cold, tachycardic, tachypnoeic, reduced tissue turgor, increased capillary refill, dry mucous membranes, sunken fontanelle,

165
Q

What is coeliac disease?

A

Immunological response against gliadin in gluten

Causes damaging inflammation of the proximal small intestine.
Results in lost villi and flattened mucosa

166
Q

What is the classical presentation of coeliac disease?

A

8-24 months
Depends on when gluten is introduced into diet

Failure to thrive
Non-specific GI symptoms (pain, discomfort)
Anaemia (iron-deficiency)
Abdominal distention

Or identified in screening of at risk groups (T1DM, autoimmune thyroid disease, Down’s, Family Hx)

167
Q

How do you diagnose coeliac disease?

A

Serology screening: IgA tissue transglutaminase antibodies + endomysial antibodies

Endoscopic small intestinal biopsy: increased intraepithelial lymphocytes + villous atrophy, crypt hypertrophy

168
Q

What is the management of coeliac disease?

A

Removal of gluten from diet

169
Q

What is the cause of an inguinal hernia?

+ management

A

Patent processus vaginalis ( peritoneum that descends with testes embryologically) allows herniation of bowel loop through inguinal canal

± hydrocoele from peritoneal fluid

Management: surgical correction

170
Q

What is the management of gastroenteritis?

A

oral fluid rehydration solution

- increases fluid reabsorption so child stays hydrated until organism is flushed out

171
Q

How do you manage toddler’s diarrhoea?

A
  • assess for coeliacs
  • assess cow’s milk allergy and trial without

Will improve with age

172
Q

What is Crohn’s disease?

A

transmural, focal subacute or chronic inflammatory disease
Commonly affects the distal ileam and proximal colon

Diagnosed with endoscopy and histology of biopsy

173
Q

What is the histological landmark of Crohn’s disease?

A

Non-caseating epithelioid cell granulomata

174
Q

What is the presentation of Crohn’s?

A

Growth failure
Delayed puberty

Abdo pain, weight loss and diarrhoea

Fever, lethargy and weight loss

Mouth ulcers, perianal tags, uveitis, arthralgia, erythema nodosum

175
Q

What is the managemetn for Crohn’s in children?

A

whole protein modular feeds
oral steroids
immunosuppression (e.g. azathioprine)
monoclonal antibodies

176
Q

What is the management of constipation in children?

A

Often self resolve
advise on hydration and good fibre intake
laxatives (e.g. Movicol Paediatric Plain)

177
Q

What is Hirschsprung Disease?

A

no ganglion cells in parts of the large bowel (myenteric and submucosal plexus)
Results in a narrow, contracted section of the colon

178
Q

How does Hirschsprung present?

A 
Neonatal period: 
Intestinal obstruction:
Failure to pass meconium 
Abdominal distention 
Bile stained vomit
179
Q

What is the management of Hirschsprung disease?

180
Q

Causes of not passing meconium?

A 
Hirschsprung's 
Cystic Fibrosis (meconium ileus) 
Small bowel syndrome 
Foetal distress (already passed)
Anorectal malformation
181
Q

What causes jaundice in the first 24 hours?

A

ALWAYS PATHOLOGICAL
Rhesus disease or ABO incompatibility
Other enzyme or haem problems: G6PD, spherocytosis, polycythaemia
TORCH

182
Q

What causes jaundice from 2-14 days?

A

Physiological:
Increased RBC breakdown (foetal Hb has a shorter half life)
Immature enzymes- slower conjugation
Increased conjugated bilirubin being absorbed into enterohepatic circulation
Breastfeeding jaundice (most common)- continue feeding, increases enterohepatic circulation

OR early presentation of prolonged jaundice…

183
Q

What causes prolonged neonatal jaundice after 2 weeks?

A 
Congenital hypothyroidism 
Biliary atresia 
Prolonged breastfeeding jaundice
Pyloric stenosis 
Bile duct obstruction 
Hepatitis
184
Q

What is the complication (and presentation) of neonatal jaundice?

A

KERNICTERUS
in the basal ganglia
- neurological signs- seizures, coma, lethargy, poor feeding, death, deafness

185
Q

What investigations are done in neonatal jaundice?

A 
FBC, Blood film, and blood group 
LFTs (deranged in biliary atresia)
TFTs 
Blood cultures 
Urine dip (sepsis)
Abdo/ biliary USS
186
Q

What is the management of neonatal jaundice?

A

Phototherapy (slow)

Exchange transfusion

187
Q

What is bronchopulmonary dysplasia?

A

Infants with oxygen therapy requirements for at post-menstrual age of 36 weeks

188
Q

What is the pathophysiology of bronchopulmonary dysplasia?

A

Lung damage due delayed lung maturation

189
Q

What are the chest X-ray findings in bronchopulmonary dysplasia?

A

Widespread consolidation

Cystic changes

190
Q

What is the management of bronchopulmonary dysplasia?

A

Continued oxygen therapy;
mechanical ventilation
CPAP
high-flow nasal cannula

±low dose corticosteroid therapy

191
Q

What are the risk factors of bronchopulmonary dysplasia?

A

Prematurity
Low birth weight
Neonatal respiratory infection

192
Q

What conditions is a patient with bronchopulmonary dysplasia at higher risk of?

A

Poor growth
Recurrent respiratory infections - Bronchiolitis
GORD
CP

193
Q

What are the most common causes of sepsis?

A

Staph A
Strep Pneumonia
Neisseria Meningitidis
E. Coli

194
Q

What is the presentation of sepsis?

A

Fever
Malaise, irritable, lethargy
Poor feeding

Tachycardia 
Tachypnoea 
Low blood pressure 
Purpuric rash (meningococcal) 
Shock- sweating, confused, LoC
Multiorgan failure
195
Q

What investigations should be done in sepsis?

A 
Blood cultures 
Urine output monitoring
Urinalysis 
Lactate 
Oximetry
196
Q

What is the management for sepsis?

A

Broad spectrum antibiotics

Fluid rescus- bolus + maintenance + 10% dehyd. for shock (i.e. extra 100ml/kg)

197
Q

What fluid boluses are given?

A

20ml/kg

Unless: 
Trauma 
Neonate 
DKA 
in which case 10 ml/kg
198
Q

What is the difference between neonatal and infant/child resus?

A

Neonate:
5 rescue breaths
then 3:1 compression: breaths

Infant/child:
5 rescue breaths
then 15:2 compression: breaths

199
Q

What is necrotising enterocolitis?

A

Inflammation and ischaemia of bowel leading to necrosis

200
Q

What is the presentation of necrotising enterocolitis?

A

Few days/ weeks after birth

Poor feeding
Vomiting (sometimes bile stained)
Abdominal distention

Fresh blood in stool

201
Q

What are the abdominal Xray findings in necrotising enterocolitis?

A

distended bowel loops
thickening bowel wall (intramural gas)
Gas in portal tract and under diaphragm

202
Q

What are the risk factors/ causes for necrotising enterocolitis?

A

Prematurity
SGA
Cow’s milk feeders

"Causes":
- largely unknown 
TORCH infections 
GBS 
E coli
203
Q

What are the risk factors for intraventricular haemorrhage in neonates?

A

Prematurity
SGA
Perinatal asphyxia
RDS

204
Q

When does intraventricular haemorrhage normally occur?

A

First 72 hours of life

205
Q

What is retinopathy of prematurity?

+ management

A

Dysregulated vascular proliferation leads to potential retinal detachment, fibrosis and blindness

Laser therapy and intravitreal anti-VEGF

206
Q

What is periventricular leukomalacia?

+ causes

+ prognosis

A

Degeneration and the formation of cysts in the periventricular white matter

As a result of hypoxia, prematurity

Causes cerebral palsy, epilepsy

207
Q

What is HUS?

A

Haemolytic Uraemic Syndrome;

Triad of:

  1. Renal railure
  2. Microangiopathic Haemolytic anaemia
  3. Thrombocytopaenia
208
Q

What is the pathophysiology of HUS?

A

Secondary to GI infection.
Toxins cause thrombotic reaction in renal endothelium.
This leads to thrombocytopaenia and microangiopathic haemolytic anaemia.

209
Q

What is the presentation of HUS?

A

Abdo pain
vomiting
haematuria
bloody diarrhoea

apyrexial

210
Q

What is the management of HUS?

A

Supportive + dialysis

211
Q

What is a BRUE?

Presentation

Investigations

Management

A

Briefly Resolved Unexplained Event

Presentation:

  • sudden +brief
  • LOC/ unresponsive
  • Cyanosis/ pallor
  • Absent/ decreased breathing
  • Change in tone (hyper/hypo)
  • *+++ ASYMPTOMATIC ON PRESENTATION **

Investigations:
ABCDE/ bedside investigations; obs, glucose, plot height/ weight, ECG, full systems examination
Bloods: FBC, U+E
Imaging: as required

Management: Safety net and reassurance

  • diagnosis of exclusion -
212
Q

Neonatal Sepsis

Presentation

Causative Organisms

Risk Factors

Management

A

Presentation:

  • Respiratory distress: grunting, increased effort, nasal flaring, use of accessory muscles, tachypnoea
  • lethargy
  • febrile
  • lots of nonspecific symptoms: abdo distention, jaundice, poor feeding, apnoea, vomiting etc.

Causative organisms: GBS, E. Coli

Risk Factors:

  • Maternal GBS
  • Maternal fever of any source
  • Prolonged rupture of membranes
  • Prematurity
  • Low birth weight

Management:

  • IV BenPen + Gentamicin
  • Supportive: oxygen, fluids, thermal regulation

Phase 3a (9 decks)

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