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Paediatrics STG > Paediatric Infections > Flashcards

Paediatric Infections Flashcards

1
Q

How is fever identified in children?

A

In a child <4 weeks a thermometer should be placed in the axilla, whereas in those >4 weeks an infrared tympanic thermometer can be used

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2
Q

Risk factors for infection

A

recent foreign travel, illness of other family members
Specific prevalence, Lack of immunisation, contact with animals (Brucellosis, Q fever, HUS), Immunodeficiency leading to susceptibility to encapsulated organisms

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3
Q

Red Flags in Febrile Child

A
  • Fever >39 (or >38 in a child under 3 months)
  • Pale, mottled, or blue skin
  • Features of meningism
  • Respiratory distress
  • Bile-stained vomiting
  • Shock
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4
Q

Green: Low risk child

A

Normal colour
Normal activity and behaviour, content, smiling
No signs of volume depletion

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5
Q

Amber: Intermediate risk

A

Pallor, not responding to social cues normally, decreased activity
Nasal flaring, Tachypnoea, Sats<95
Dry mucous membranes, poor feeding, raised CRT, tachycardia, fever, swelling of limb

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6
Q

Red-high risk

A 
Pale, mottled or blue 
No response to social cues 
Grunting, tachypnoea
Reduced skin turgor 
Temperature 
Non-blanching rash, bulging fontanelle, focal neurology
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7
Q

Ddx for fever

A
  • URTI, including otitis media and tonsillitis
  • LRTI
  • Meningitis or encephalitis
  • UTI
  • Gastroenteritis
  • Osteomyelitis or septic arthritis
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8
Q

Life threatening emergencies that should always be considered in the febrile child

A

meningitis, septicaemia, encephalitis, toxic shock syndrome, and necrotising fasciitis

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9
Q

Management

A

Any child with red features, or amber features with no diagnosis, should be referred to hospital for paediatric specialist assessment
If the child is <3 months, fever is most likely due to bacterial infection. Unless the cause is clear there should be a septic screen and IV antibiotics

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10
Q

What does a septic screen include

A

FBC, CRP, blood and urine cultures ± CXR, stool cultures, and LP

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11
Q

Causes of a maculopapular rash

A
  • Viral: parvovirus, HHV6/7, enterovirus
  • Bacterial: scarlet fever (group A strep), rheumatic fever, typhoid fever
  • Other: Kawasaki disease, JIA
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12
Q

Causes of a vesicular bullous or pustular rash

A
  • Viral: VZV, HSV

- Bacterial: impetigo, staphylococcal scalded skin

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13
Q

Causes of a petechial or purpuric rash

A
  • Bacterial: meningococcal or other sepsis

- Other: Henoch-Schonlein purpura, vasculitis

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14
Q

Kawasaki Disease: Clinical Features and Diagnosis

A

characterised by a prolonged fever, lasting >5 days. Diagnosis is clinical, requiring 3 essential criteria include (high fever, persistent and not responding to antipyretics) alongside 4/5 clinical criteria

  • Non purulent conjunctivitis
  • Oral mucositis
  • Cervical lymphadenopathy
  • Erythema of hands and feet. Extremities can become swollen and red, and start to peel
  • Rash, due to acute vasculitis. There can also be coronary artery aneurysms
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15
Q

Kawasaki Disease: Investigations and Management

A

There will be raised inflammatory markers, and thrombocytosis. Treatment is urgent, with IVIg and aspirin to reduce the risk of aneurysm and thrombosis
- It is important to do a baseline ECG

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16
Q

Immediate Management of Seriously Unwell Febrile Child

A

o Parenteral Abx immediately if seriously unwell; E.g. Third Gen Cephalosporin; If under 1/12 age, Ampicillin to cover Listeria infection; Aciclovir if HSV suspected
o Antipyretics e.g. NSAIDs, Paracetamol; No evidence for preventing febrile seizures

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17
Q

What is sepsis

A

• Bacteraemia leading to Host Immune Response (Cytokine Release, Endothelial Activation) leading to End-organ damage;

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18
Q

Causes of sepsis in the child

A

Most commonly Coagulase-negative Staphylococcus (CoNS), S aureus, Group B Streptococcus, S pneumo, Neisseria meningitidis, E coli

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19
Q

How should a septic child be managed?

A

• Requires Paediatric ICU care; Antibiotics started without delay; Correction of fluids due to maldistribution from inflammatory response and
loss of intravascular proteins due to Endothelial Dysfunction
• CVP and UO monitoring guide assessment of fluid balance
Management of Pulmonary Oedema and Respiratory Failure

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20
Q

How should myocardial dysfunction be managed?

A

Myocardial Dysfunction can occur due to Cytokines and Toxins depressing contractility; Inotropic support might be required

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21
Q

How can clotting derangements occur and how should they be managed

A

Disseminated Intravascular Coagulation (DIC); Abnormal clotting leads to widespread Microvascular Thrombosis and Consumption of Clotting Factors
o If bleeding occurs, clotting derangement corrected with FFP, CP and Platelets

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22
Q

Neonatal Infections: Early Onset

A

(<48hrs after birth) – Bacteria has ascended from birth canal and invaded amniotic fluid; Foetal lungs secondarily infected

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23
Q

Neonatal Infections: Early Onset-Risk Factors

A

o Risk increased if Prolonged Labour, Premature Rupture or Chorioamnionitis

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24
Q

Neonatal Infections: Early Onset-Presentation

A

Present with Respiratory Distress, Febrile/Cold, Distention, Jaundice, Shock etc

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25
Q

Neonatal Infections: Early Onset-Investigations

A

o CXR + Septic Screen (Normal CRP does not exclude infection, but 2 consecutively low values strong evidence against)

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26
Q

Neonatal Infections: Early Onset-Causes

A

Most commonly Group B Strep and E coli

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27
Q

Neonatal Infections: Early Onset-Management

A

Abx started immediately without waiting for culture; Should cover Group-B Strep, Listeria monocytogenes and other Gram-positive organisms; Typically, Benzylpenicillin or Amoxicillin used
o Abx safely stopped if Culture, CRP negative, no clinical indicators after 36-48hrs
o CSF must be examined if Culture-positive, or Neurological signs

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28
Q

Neonatal Infections: Late Onset

A

(>48hrs after birth) – Source typically environmental; Non-specific presentation; Nosocomial infections (Indwelling CVC, ET Tubes, Invasive procedures)
o Most commonly Coagulase-negative Staph (CoNS =Staphylococcus epidermidis); can involve wide range of pathogens

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29
Q

Neonatal Infections: Late Onset Management

A

o Initial Flucoxacillin and Gentamicin to cover Staph spp and Gram-negative organisms
▪ If no improvement, Vancomycin (for Staph or Enterococci) or Broad-Spectrum Abx (e.g. Meropenem) might be used

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30
Q

Neonatal Meningitis

A

Uncommon; 20-50% mortality; 1/3 have sequelae; Present non-specifically; classic meningitis picture are late signs
o Ampicillin, Penicillin or Cefotaxime if Meningitis suspected
o Complications include Cerebral Abscess, Ventriculitis, Hydrocephalus, SNHL and Neurodevelopmental Impairment

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31
Q

How is a diagnosis of meningitis confirmed

A

Confirmed by CSF WBC; Viral infections most common cause, and most are self-resolving

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32
Q

Assessment of Meningitis: History

A

Fever, Headache, Photophobia, Lethargy, Poor Feeding/Vomiting, Irritability, Hypotonia, Drowsiness, LOC, Seizures

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33
Q

Assessment of Meningitis: O/E

A

Fever, Purpuric Rash, Neck Stiffness, Bulging Fontanelle, Opisthotonos, Brudzinski (Flexion of neck causes flexion of Knees and Hips) and Kernig (Back Pain following Extension of Flexed Knee) sign positive, Shock, Focal Neurology, Altered Mental signs and Papilloedema

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34
Q

Assessment of Meningitis: Investigations

A

FBC, Glucose (for pairing), Blood gases (for Acidosis), Coagulation, CRP, U/E, LFT, Cultures, Rapid Antigen Testing, Viral PCR
o Consider CT/MR Head and EEG monitoring

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35
Q

What other investigations should be done if TB suspected

A

CXR, IGRA/Mantoux, Cultures

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36
Q

When is LP contraindicated

A

Cardiorespiratory Instability, Focal Neurology, Signs of raised BP, Coagulopathy, Thrombocytopaenia, Local infections of LP site

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37
Q

Meningitis Bacterial CSF

A

Turbid Appearance
Increased Polymorphs
Increased protein and decreased glucose

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38
Q

Meningitis Viral CSF

A

Clear Appearance
Increased lymphocytes
Normal (or raised but less than bacterial) protein
Normal (or reduced but less than bacterial) glucose

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39
Q

Bacterial Meningitis

A

Typically, sequelae of Bacteraemia; 80% occur below 16yrs; 5-10% Mortality; ~10% survivors left with long term neurological impairment

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40
Q

Bacterial Meningitis : Pathophysiology

A

Damage due to host immune response; Mediator release, WBC activation, Endothelial damage leading to Cerebral Oedema, Raised ICP and Decreased Cerebral Blood Flow
o Inflammation below Meninges causes Cerebral Cortical Infarction; Fibrin deposition blocks CSF resorption in Arachnoid Villi leading to Hydrocephalus

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41
Q

Common Bacteria based on age

A

o Up to 3/12 – Group B Strep, E coli, Listeria
o 1/12 to 6yrs – N meningitidis, S pneumoniae, HiB
o >6yrs – N meningitidis, S pneumoniae

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42
Q

Complications of bacterial meningitis: Hearing impairment

A

Inflammatory damage to Cochlear Hair cells; Auditory assessment required after Meningitis

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43
Q

Complications of bacterial meningitis: Local vasculitis

A

CN palsies, other Focal Neurological lesions

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44
Q

Complications of bacterial meningitis:Local cerebral infarction

A

Focal or Multifocal Seizures, which may result in Epilepsy

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45
Q

Complications of bacterial meningitis: Subdural Effusion

A

Particularly associated with HiB and Pneumococcal; Confirmed by CT/MRI; Most resolve spontaneously

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46
Q

Complications of bacterial meningitis: Hydrocephalus

A

Result from impaired CSF resorption (=Communicating) or Blockage of Cerebral Aqueduct or Ventricular outlets (=Non-Communicating)

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47
Q

Complications of bacterial meningitis: Cerebral Abscess

A

Drainage is required

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48
Q

Managing any febrile child with purpura

A

given IM Benzylpenicillin and admitted immediately

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49
Q

Management of bacterial meningitis

A

No delay in administering Abx and supportive therapy; Choice depends on likely pathogen
o 3rd generation Cephalosporin E.g. Ceftriaxone, Length of course depends on Causative Organism, and Clinical response

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50
Q

Management of bacterial meningitis : Dexamethasone

A

Beyond Neonatal period, some evidence for Dexamethasone to reduce long-term complications e.g. Deafness

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51
Q

Management of bacterial meningitis: Prophylaxis

A

Prophylaxis with Rifampicin or Ciprofloxacin to eradicate Nasopharyngeal Carriage to all household carriage; Patient does not require if given 3rd gen Cephalosporin
o Household contacts also should be vaccinated

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52
Q

Management of bacterial meningitis: When might rapid antigen screening and PCT be useful

A

If Bacterial Meningitis was partially treated with previous course of Abx for other illness, diagnostically hard to identify;

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53
Q

Common viral causes of viral meningitis

A

Enteroviruses, Epstein-Barr Virus, Adenovirus and Mumps (which is rare due to MMR vaccination)
o Much less severe, often make full recovery

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54
Q

How can viral meningitis be confirmed

A

Confirmed by Culture or PCR of stool, urine, NPA, throat swabs; or by Serology

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55
Q

What should be considered if clinical course is atypical or failure to respond to therapy

A

o Mycoplasma spp, Borrelial burgdorferi (=Lyme disease), TB, Fungal Infections
o More common in Immunocompromised patients, or if structural abnormalities of the skull and meninges that facilitate infection
o Asceptic Meningitis can also be seen in Malignancy or Autoimmune

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56
Q

Causes of encephalitis

A

Most commonly due to Enteroviruses, Influenza viruses, Herpesvirus (HSV, VZV, HHV-6); HSV is rare but can cause devastating consequences

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57
Q

HSV Presentation and Investigation in children

A

Most HSV children do not have outward signs e.g. Cold sores, skin lesions; PCR of CSF is most reliable indicator; Serology changes later in clinical course
o HSV encephalitis mortality 70%; Severe neurological sequelae
EEG and brain imaging reveal focal changes secondary to HSV Encephalitis

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58
Q

Management of Encephalitis

A

high-dose IV Aciclovir until ruled out

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59
Q

Meningococcal Infections: Prognosis

A

Of the three main causes of Bacterial Meningitis, has lowest risk of long-term complications
and highest rate of full recovery

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60
Q

Meningococcal Infections: presentations

A

Septicaemia usually accompanied by Purpuric rash;
not always present; Non-blanching on palpation,
irregular in size and outline, may have necrotic centre

61
Q

Meningococcal Infections: Management

A

IM Penicillin or IV 3rd Gen Cephalosporin if available

before urgent admission

62
Q

Meningococcal Infections: Vaccination

A

Men B more common than C following Men C vaccine
introduction; Men B vaccine recently introduced,
further reducing incidence

63
Q

Pneumococcal Infections: Streptococcal Pneumoniae

A

Often carried in Nasopharynx; Asymptomatic carriage prevalent
in young children, responsible for transmission by respiratory droplets
• Can cause Pharyngitis, Otitis Media, Conjunctivitis, Sinusitis

64
Q

Pneumococcal Infections: Invasive Disease

A

Invasive disease (Pneumonia, Bacterial Sepsis, Meningitis) – Mainly occurs in young infants,
due to poor immune response to encapsulated organisms
o PCV13 Vaccination has reduced incidence of invasive disease

65
Q

Pneumococcal Infections: Management of Children who are at Increased Risk

A

Children at increased risk (e.g. Hyposplenism or Asplenic, Nephrotic Syndrome) should be given daily prophylactic Penicillin to prevent infection by strains not covered by vaccine

66
Q

Haemophilus Infections

A

HiB can cause Otitis Media, Pneumonia, Acute Epiglottitis, Cellulitis, Osteomyelitis, Septic
Arthritis; used to be second most common cause of Meningitis
• Immunisation has rendered HiB systemic infections rare

67
Q

Staphylococcus and Group-A Streptococcal Infections: Pathophysiology

A

• Direct invasion of organisms; Causes disease by releasing toxins,
which act as Superantigens (Bind to common part of TCR leading
to massive T-cell Proliferation and Cytokine Release)
o Can lead to immune related sequelae – Post-Strep GN,
Rheumatic Fever

68
Q

Impetigo

A

Localised, Highly-contagious Staph/Strep infection of
Skin; More common in pre-existing skin disease (E.g. Eczema); Begin as Erythematous
Macules that may become Vesicular/Pustular, and into Crusted Eruptions
o Topical Abx (Mupirocin) for mild cases; Narrow-spectrum Systemic (Flucoxacillin) for
more severe infections; Broad-spectrum have easier regimens and ‘taste better’
o Affected children should not attend nursery or school until lesions dry

69
Q

Boils

A

Infections of Hair Follicles or Sweat Glands caused by S aureus; Treatment with
systemic antibiotics or incision; Nasal carriage acts as a reservoir of reinfection
o Rarely, manifestation of underlying immunodeficiency

70
Q

Periorbital Cellulitis

A

Fever, Erythema, Tenderness, Oedema; Unilateral; Might follow local trauma; May spread from Paranasal Sinus or Dental Abscess in older children
o IV Abx to prevent posterior spread into orbit; Which can lead to Proptosis, Painful Ocular Movement, Reduced Acuity; Complicated by Abscess Formation, Meningitis, Cavernous Sinus Thrombosis
o CT/MR Head to assess posterior spread of Infection

71
Q

Staphylococcal Scalded Skin Syndrome

A

Separation of Epidermal Skin through Granular cell layers; Nikolsky sign (Separation on gentle pressure); Rare
o IV Abx, Analgesia, Monitoring of Hydration and Fluid Balance

72
Q

Viral Infections in Children

A

• Most present with Fever and Rash; Incubation varies from 24-48hrs for Viral Gastroenteritis, to 2/52 for Chickenpox; Infectious period typically begins day or two before rash; Considered infectious until rash resolved, or lesions dried up

73
Q

HSV

A

Eight known HHV; After Primary infection, Latency established and long-term persistence occurs, usually in dormant state; Secondary Re-activation can occur after
• HSV infects mucosal membranes or skin; HSV1 typically lip and skin, HSV2 typically genital; but both viruses can cause both types

74
Q

HSV: Most common primary illness

A

Gingivo-stomatitis (Vesicular lesions of Lips, Gums, Tongue, Hard Palate; Progresses to extensive, painful Ulceration with bleeding

75
Q

HSV: Skin Manifestations

A

Cold sores (Recurrent HSV along Gingival-Lip margin), Eczema Herpeticum (Vesicular lesions on Eczematous skin, which can be superinfected with Bacterial Infections) and Herpetic Whitlows (White Pustules on sites of broken skin)

76
Q

HSV: Eye disease

A

Blepharitis or Conjunctivitis; May extend to affect Cornea, possibly leading to Scarring and Vision Loss; Requires urgent Ophthalmic opinion

77
Q

HSV: Treatment

A

Treatment with Aciclovir; used to treat severe symptomatic Skin, Ophthalmic, Cerebral and Systemic Infections

78
Q

VZV: Chickenpox

A

Typical, vesicular rash starting on Head/Trunk, progressing to Periphery; Crops of Papules, Vesicles and Pustules at different times; New lesions appearing beyond 10/7 suggests defective cellular immunity

79
Q

VZV: Chickenpox Complications

A

Few rare but serious complications – Secondary Staphylococcus Infection (Toxic Shock Syndrome, Necrotising Fasciitis), Encephalitis (Good prognosis compared to HSV), Purpura Fulminans (due to Cross-inactivation of Protein C/S of Antiviral Ig)
Can cause Severe, Progressive Disseminated disease with 20% mortality in Immunocompromised; Haemorrhagic lesions can occur

80
Q

VZV: Management

A

IV Aciclovir initially if immunocompromised; Oral Valaciclovir if no organ dissemination
o Human VZIg for High-risk Immunocompromised with deficient T cell function, following contact with VZV; Protection depends on early administration

81
Q

Shingles

A

Uncommon; Dermatomal distribution; Rarely Post-Herpetic Neuralgia (C/f adults

82
Q

EBV (Infectious Mononucleosis, Glandular Fever)

A

Tropism for B-cells and Oropharynx Epithelium; Infection by Oral contact, majority Subclinical course;

83
Q

EBV (Infectious Mononucleosis, Glandular Fever): Symptoms

A

May develop Fever, Often Severe Tonsillitis/Pharyngitis, LNA, Splenomegaly (50%), Hepatomegaly (10%), Maculopapular Rash (5%)

84
Q

EBV (Infectious Mononucleosis, Glandular Fever): Diagnosis

A

Atypical Lymphocytes on Blood film, Positive Monospot (Often negative in young children), Seroconversion (VCA, EBNA)

85
Q

EBV (Infectious Mononucleosis, Glandular Fever): Management

A

Symptomatic relief; Corticosteroids considered for Airway Compromise; If Co-infection with Group-A Strep, Penicillin should be used rather than Ampicillin or Amoxicillin, which can cause a florid maculopapular rash

86
Q

EBV (Infectious Mononucleosis, Glandular Fever): Associations

A

Also involved in Pathogenesis of Burkitt Lymphoma, Lymphoproliferative Disease in Immunocompromised hosts, and Nasopharyngeal Carcinoma

87
Q

CMV: Transmission

A

Transmission by Saliva, Genital Secretions or Breast Milk; Rarely Transplacental;

88
Q

CMV: Presentation

A

Mild or Subclinical Infection in normal hosts; Morbidity in Immunocompromised host or In-Utero
• Presents like EBV; Atypical Lymphocytes on film but Monospot negative

89
Q

CMV: Consequences

A

Can cause Retinitis, Pneumonitis, BM Failure, Encephalitis, Hepatitis, Oesophagitis and Enterocolitis in Immunocompromised hosts

90
Q

CMV: Treatment

A

Can be treated with IV Ganciclovir, Oral Valganciclovir or Foscarnet; Poor SE profile

91
Q

Parvovirus B19

A

Infects Erythroblastoid RBC Precursors in the Bone Marrow

92
Q

Parvovirus: Outbreaks and transmission

A

Outbreaks most common in Spring; Transmission by Respiratory secretions or Transplacental;

93
Q

Parvovirus: Presentation

A

Can present as Asymptomatic, Erythema Infectiosum (Slapped cheek appearance), Aplastic Crisis or as Foetal Disease

94
Q

Parvovirus: Aplastic Crisis

A

Occurs in patients with Chronic Haemolysis, increased rate of RBC turnover or Immunocompromised with impaired B-cell response

95
Q

Enteroviruses

A

Includes Coxsackie, Echoviruses, Polioviruses);

96
Q

Enteroviruses: Transmission

A

Faecal Oral Transmission or Respiratory Droplets

97
Q

Enteroviruses: Presentation

A

90% Asymptomatic or Non-specific Febrile Illness, some with GI symptoms
o Urgent Parenteral Abx and Rule out Sepsis by blood culture if rash is non-blanching

98
Q

Hand-Foot-Mouth Disease

A

Painful, vesicular Lesions; Generally mild, disease subsides within a few days

99
Q

Enteroviral Neonatal Sepsis Syndrome

A

Predominantly from Transplacental or Intrapartum; Mimics Bacterial Sepsis if severe; Hypotension, MOF requiring ITU care
o No antiviral drugs effective; Use of IVIg controversial

100
Q

TB: Infectability

A

related to proximity, Large Infectious Load and Sputum Smear positive, Underlying Immunodeficiency
Latent TB more likely to progress to Active TB in Infants and Young Children; Young children are generally non-infectious due to lower TB loads (Paucibacillary), usually acquired from
infected adult in same household

101
Q

TB: Spread

A

Nearly all cases spread by Respiratory route

102
Q

TB: Presentation

A

Typically, non-specific; Prolonged fever, Malaise, Anorexia, Weight Loss, LNA

103
Q

TB: Types

A

3/4 have Pulmonary TB; Extrapulmonary disease less common, includes Lymphadenitis, Osteoarticular TB, Genitourinary TB and TB Meningitis

104
Q

TB: Diagnostic Test

A

If TB suspected, Tuberculin test (Mantoux) performed; Can be falsely positive due to BCG; Alternatively, IGRA
(Assessing T cell stimulation in response to specific TB antigens); Negative IGRA cannot reliably rule out; Neither test can distinguish Active or Latent TB
o Both tests can be falsely negative in Immunosuppressed host; Especially HIV

105
Q

TB: Additional tests

A

All TB patients should be tested for HIV, and vice-versa due to overlapping epidemiology
• Sputum is difficult to obtain in children <8yrs; Gastric washings can be used
o AFB Staining techniques, Mycobacterial Cultures
o Urine, LN, CSF or Radiology as required
o Crucial to grow organism due to rise of MDR-TB; Need to assess sensitivity

106
Q

TB: Management

A

Triple or Quadruple Therapy (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) – Unless MDR-TB suspected (e.g. Household contact has MDR-TB)
o If MDR-TB: Rifampicin and Isoniazid for initial 2/12 until Abx sensitivities known

107
Q

TB Management: Uncomplicated Pulmonary TB

A

6/12 course; Longer for complicated

108
Q

TB Meningitis

A

Dexamethasone given initially to reduce risk of complications

109
Q

TB: Pyridoxine

A

Pyridoxine given weekly in Adolescents to prevent Peripheral Neuropathy associated with Isoniazid therapy; Not required in Young Children

110
Q

TB: Latent TB (asymptomatic with Mantoux or IGRA)

A

Rifampicin and Isoniazid 3/12, or Isoniazid 6/12 to reduce risk of reactivation later in life

111
Q

TB: Prevention

A 
BCR Vaccination (although incomplete protection); BCG is a live vaccine and should not be given to HIV positive or Immunocompromised patients
o Screen household; Children exposed need to be assessed for Latent TB; Prophylactic Isoniazid if <2yrs, if TST/IGRA negative at 6/52, can be discontinued and should be given BCG unless previously vaccinated
112
Q

Pertussis

A

=Whooping Cough, caused by Bordetella pertussis (Gram negative, Aerobic, Encapsulated Coccobacillus); High contagious; Endemic; Epidemics every 3-4yrs; Incubation about 10 days

113
Q

Pertussis: Catarrhal Phase

A

(Week of cold-like symptoms) preceding characteristic Paroxysmal/Spasmodic cough with inspiratory whoop, which can last up to 3/12
o Worse at night, culminate in vomiting; Can become breathless during Paroxysmal phase; Apnoea more common than Whoop in Infants
o Epistaxis and Subconjunctival haemorrhage can occur after vigorous coughing

114
Q

Pertussis: Convalescent Phase

A

Symptoms gradually decrease, although may persist for many months

115
Q

Pertussis: Complications

A

Pneumonia, Seizures, Bronchiectasis; Significant mortality especially in infants who have not completed Primary Vaccinations (5-in-1) at 4/12 age
o If Severe spasms of cough or Cyanotic attacks, for admission

116
Q

Pertussis: Investigations

A

Identified early from Nasal swab culture; PCR more sensitive; Marked Lymphocytosis (>15×109/L) on FBC

117
Q

Pertussis: Management

A

Macrolide Antibiotics (Erythro, Clarithro, Azithro); Effective to decrease symptoms only if given in Catarrhal phase; Prophylaxis of siblings, parents, school contacts

118
Q

Pertussis: Immunisation

A

• Immunisation does not guarantee protection; Reduce risk of infection and severity; Protection declines steadily during childhood
o Mothers should be re-immunised during pregnancy to reduce risk of transmission during first months of life; Currently recommended in UK due to re-emergence

119
Q

Gastroenteritis: Presentation

A

Sudden-onset Loose/Watery stool, Vomiting; May be in contact with affected, or recent travel abroad; Dehydration from shock is most serious complication

120
Q

Gastroenteritis: High Risk of Dehydration

A

High risk of Dehydration – Low Birthweight, <6/12 age, >6 stools/day, >3 vomiting/day, Unable to tolerate extra fluids, malnourished children
o Infants have greater surface area to weight ratio; greater insensate losses

121
Q

Gastroenteritis: Viral Causes

A

Most frequently Rotavirus (60% under <2yrs, particularly in Winter/Spring); Other viruses, such as Adenovir, Norovir, Calicivir, Coronavir and Astrovir

122
Q

Gastroenteritis: Bacterial Causes

A

Bacterial causes less common, but suggested if bloody stools; C jejuni (most common bacteria) associated with severe abdominal pain, Shigella and Salmonella Cause Dysenteric type of infection (Blood, Pus in stool, Pain, Tenesmus); Shigella accompanied by high fever, Cholera and ETEC with profuse diarrhoea

123
Q

Gastroenteritis: Protozoan Causes

A

Giardia, Cryptosporidium

124
Q

Gastroenteritis: Mimics

A

Sepsis, Meningitis, URTI, AOM, Hepatitis A, UTI, Pyloric Stenosis, Intussusception, Appendicitis, NEC, Hirschsprung, DKA, HUS, Coeliac, Allergies, Addisons

125
Q

Gastroenteritis: Assessment

A

Most accurate measure of water loss is weight; Not clinically detectable if <5%, Clinical dehydration if 5-10%, Shock if >10%; Must be identified quickly and managed
o Assess General Appearance, Consciousness, Urine
Output, Skin Colour and Turgor, Peripheral Temperature, Eyes, Mucous Membranes, HR, RR, Pulse Character, CRT, BP

126
Q

Gastroenteritis: Isonatraemic and Hyponatraemia Dehydration

A

Proportional loss, or high intake of water and other hypotonic solutions
o Hyponatraemia can lead to increased Intracellular water shifts; Can lead to Cerebral Oedema; More common type of dehydration in malnourished in developing countries

127
Q

Gastroenteritis: Hypernatremia Dehydration

A

Usually due to increased insensate losses (Febrile, Environment) or profuse, low-sodium diarrhoea
o Signs of ECF depletion less obvious; Difficult to recognise clinically, especially in obese infant; Can lead to Cerebral shrinkage and neurological signs
o Transient Hyperglycaemia can also occur; Self-correcting

128
Q

Gastroenteritis: Investigation

A

Typically, no investigation required; Stool culture if Septic, Blood or Mucous in stool, or Immunocompromised, or Foreign Travel (if not improved by 1/52 or uncertain dx)
• Plasma U/E, Glucose checked if IV fluids required, or Hypernatraemia suspected; If Abx given, blood cultures should be taken

129
Q

Gastroenteritis: Dehydration

A

If Clinical Dehydration, Oral Rehydration is mainstay; IV fluids only if Shock, or Deterioration, or Persistent Vomiting

130
Q

Gastroenteritis: Not dehydrated

A

Prevent by continuous breastfeeding, encourage fluid intake, discourage fruit juices and carbonated drinks; ORS if needed
o ORS + Hydrate 50ml/kg over 4hrs; Continue breastfeeding; Consider ORS by NGT if Inadequate Intake or Vomiting persistently

131
Q

Gastroenteritis: Shock

A

IV 0.9% Bolus and repeat if necessary; ICU if still shocked

132
Q

Gastroenteritis: IV rehydration

A

100ml/kg if shock present, 50ml/kg if not in shock; Consider Potassium supplementation

133
Q

Gastroenteritis: Anti diarrhoeal and antiemetics

A

Ineffective, prolongs bacterial excretion, Associated with SE, and focus attention away from rehydration

134
Q

Gastroenteritis: Antibiotics

A

Not routinely used even if bacterial cause; Only if suspected or confirmed Sepsis, Extra-intestinal spread, Malnourished or Immunocompromised, or Specific organisms (e.g. C diff, Cholera, Shigella, Giardiasis)

135
Q

HIV in children: Epidemiology

A

Globally, over 3 million children, mostly Sub-Saharan Africa (Notably, India as well); Over 2 million adolescents (10-19yrs); Marked declined in infection rate but still 150,000/yr

136
Q

HIV in Children: Transmission

A

Major route through Mother-to-Child – Intrauterine, Intrapartum or Breastfeeding; Also, though infected blood products, contaminated needles or sexual abuse

137
Q

HIV in children: Serology

A

• Children <18/12 will have transplacental Maternal anti-HIV IgG, if mother has HIV; If persists >18/12, diagnosis of HIV infection confirmed; If <18/12 HIV DNA PCR for diagnosis
o All infants born to HIV-infected mothers should be tested
o Two negative HIV DNA PCR within first 3/12, at least 2/52 after completing Post-Natal Anti-Retroviral-Therapy (ART) indicate infant is not infected

138
Q

HIV in Children: Likelihood of Vertical Transmission

A

Maternal Transmission more likely if High Viral Load and more advanced disease
o Mothers not taking ART can transmit to 25-40% of infants by breastfeeding

139
Q

HIV in Children: Prevention of Vertical Transmission-Antenatal

A

• Use of ART during Pregnancy and Intrapartum to achieve undetectable Maternal Viral Load at the time of delivery

140
Q

HIV in Children: Prevention of Vertical Transmission-Delivery

A

Active Management of Labour and Delivery to avoid prolonged Rupture of the Membranes; Avoiding unnecessary instrumentation (e.g. Forceps delivery)
o Prelabour Caesarean-section if maternal Detectable Viral Load close to EDD
• Post-exposure Prophylaxis given to infant at Birth

141
Q

HIV in Children: Prevention of Vertical Transmission: Postnatally

A

Avoidance of Breastfeeding
o NB: In less developed regions, not practical as formula milk increases risk of Gastroenteritis and Malnutrition; Instead; ART to breastfeeding mother and child

142
Q

HIV in Children: Progression

A

Proportion progress rapidly to symptomatic disease and AIDS in first yr; others remain asymptomatic for months/years before progressing
o Asymptomatic identified at routine screening following diagnosis in family

143
Q

HIV in Children: Clinical Features-Mild Immunocompromise

A

Lymphadenopathy and Parotid Enlargement, Hepatosplenomegaly, Recurrent PUOs, Thrombocytopaenia

144
Q

HIV in Children: Clinical Features-Moderate

A

Recurrent Bacterial Infections, Candidiasis, Chronic Diarrhoea, Lymphocytic Interstitial Pneumonitis (either due to HIV, or EBV superinfection)

145
Q

HIV in Children: Clinical Features-Severe/AIDS

A

Opportunistic infections (E.g. PCP), Growth faltering, Encephalopathy and rarely can lead to malignancies

146
Q

HIV in Children: Management-ART

A
  • In all infants, ART should start shortly after diagnosis due to higher risk of progression
  • Otherwise, decision to start ART based on Clinical Status, HIV viral load, CD4 count
147
Q

HIV in Children: Management-Prophylaxis

A

Prophylaxis against PCP (Co-Trimoxazole) for infants and older children with low CD4

148
Q

HIV in Children: Immunisation

A

Especially crucial to follow; Omit BCG (live vaccine); Consider Flu, Hep A/B and VZV vaccination

149
Q

HIV in Children: MDT Management

A

Concordance, Disclosure of diagnosis, Planning for the future
• Regular follow up – Weight, Developmental Progress, Symptoms

Paediatrics STG (17 decks)

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