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
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
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
4
Q
Green: Low risk child
A
Normal colour
Normal activity and behaviour, content, smiling
No signs of volume depletion
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
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
7
Q
Ddx for fever
A
- URTI, including otitis media and tonsillitis
- LRTI
- Meningitis or encephalitis
- UTI
- Gastroenteritis
- Osteomyelitis or septic arthritis
8
Q
Life threatening emergencies that should always be considered in the febrile child
A
meningitis, septicaemia, encephalitis, toxic shock syndrome, and necrotising fasciitis
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
10
Q
What does a septic screen include
A
FBC, CRP, blood and urine cultures ± CXR, stool cultures, and LP
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
12
Q
Causes of a vesicular bullous or pustular rash
A
- Viral: VZV, HSV
- Bacterial: impetigo, staphylococcal scalded skin
13
Q
Causes of a petechial or purpuric rash
A
- Bacterial: meningococcal or other sepsis
- Other: Henoch-Schonlein purpura, vasculitis
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
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
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
17
Q
What is sepsis
A
• Bacteraemia leading to Host Immune Response (Cytokine Release, Endothelial Activation) leading to End-organ damage;
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
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
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
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
22
Q
Neonatal Infections: Early Onset
A
(<48hrs after birth) – Bacteria has ascended from birth canal and invaded amniotic fluid; Foetal lungs secondarily infected
23
Q
Neonatal Infections: Early Onset-Risk Factors
A
o Risk increased if Prolonged Labour, Premature Rupture or Chorioamnionitis
24
Q
Neonatal Infections: Early Onset-Presentation
A
Present with Respiratory Distress, Febrile/Cold, Distention, Jaundice, Shock etc
25
Neonatal Infections: Early Onset-Investigations
o CXR + Septic Screen (Normal CRP does not exclude infection, but 2 consecutively low values strong evidence against)
26
Neonatal Infections: Early Onset-Causes
Most commonly Group B Strep and E coli
27
Neonatal Infections: Early Onset-Management
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
28
Neonatal Infections: Late Onset
(>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
29
Neonatal Infections: Late Onset Management
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
30
Neonatal Meningitis
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
31
How is a diagnosis of meningitis confirmed
Confirmed by CSF WBC; Viral infections most common cause, and most are self-resolving
32
Assessment of Meningitis: History
Fever, Headache, Photophobia, Lethargy, Poor Feeding/Vomiting, Irritability, Hypotonia, Drowsiness, LOC, Seizures
33
Assessment of Meningitis: O/E
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
34
Assessment of Meningitis: Investigations
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
35
What other investigations should be done if TB suspected
CXR, IGRA/Mantoux, Cultures
36
When is LP contraindicated
Cardiorespiratory Instability, Focal Neurology, Signs of raised BP, Coagulopathy, Thrombocytopaenia, Local infections of LP site
37
Meningitis Bacterial CSF
Turbid Appearance
Increased Polymorphs
Increased protein and decreased glucose
38
Meningitis Viral CSF
Clear Appearance
Increased lymphocytes
Normal (or raised but less than bacterial) protein
Normal (or reduced but less than bacterial) glucose
39
Bacterial Meningitis
Typically, sequelae of Bacteraemia; 80% occur below 16yrs; 5-10% Mortality; ~10% survivors left with long term neurological impairment
40
Bacterial Meningitis : Pathophysiology
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
41
Common Bacteria based on age
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
42
Complications of bacterial meningitis: Hearing impairment
Inflammatory damage to Cochlear Hair cells; Auditory assessment required after Meningitis
43
Complications of bacterial meningitis: Local vasculitis
CN palsies, other Focal Neurological lesions
44
Complications of bacterial meningitis:Local cerebral infarction
Focal or Multifocal Seizures, which may result in Epilepsy
45
Complications of bacterial meningitis: Subdural Effusion
Particularly associated with HiB and Pneumococcal; Confirmed by CT/MRI; Most resolve spontaneously
46
Complications of bacterial meningitis: Hydrocephalus
Result from impaired CSF resorption (=Communicating) or Blockage of Cerebral Aqueduct or Ventricular outlets (=Non-Communicating)
47
Complications of bacterial meningitis: Cerebral Abscess
Drainage is required
48
Managing any febrile child with purpura
given IM Benzylpenicillin and admitted immediately
49
Management of bacterial meningitis
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
50
Management of bacterial meningitis : Dexamethasone
Beyond Neonatal period, some evidence for Dexamethasone to reduce long-term complications e.g. Deafness
51
Management of bacterial meningitis: Prophylaxis
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
52
Management of bacterial meningitis: When might rapid antigen screening and PCT be useful
If Bacterial Meningitis was partially treated with previous course of Abx for other illness, diagnostically hard to identify;
53
Common viral causes of viral meningitis
Enteroviruses, Epstein-Barr Virus, Adenovirus and Mumps (which is rare due to MMR vaccination)
o Much less severe, often make full recovery
54
How can viral meningitis be confirmed
Confirmed by Culture or PCR of stool, urine, NPA, throat swabs; or by Serology
55
What should be considered if clinical course is atypical or failure to respond to therapy
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
56
Causes of encephalitis
Most commonly due to Enteroviruses, Influenza viruses, Herpesvirus (HSV, VZV, HHV-6); HSV is rare but can cause devastating consequences
57
HSV Presentation and Investigation in children
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
58
Management of Encephalitis
high-dose IV Aciclovir until ruled out
59
Meningococcal Infections: Prognosis
Of the three main causes of Bacterial Meningitis, has lowest risk of long-term complications
and highest rate of full recovery
60
Meningococcal Infections: presentations
Septicaemia usually accompanied by Purpuric rash;
not always present; Non-blanching on palpation,
irregular in size and outline, may have necrotic centre
61
Meningococcal Infections: Management
IM Penicillin or IV 3rd Gen Cephalosporin if available
| before urgent admission
62
Meningococcal Infections: Vaccination
Men B more common than C following Men C vaccine
introduction; Men B vaccine recently introduced,
further reducing incidence
63
Pneumococcal Infections: Streptococcal Pneumoniae
Often carried in Nasopharynx; Asymptomatic carriage prevalent
in young children, responsible for transmission by respiratory droplets
• Can cause Pharyngitis, Otitis Media, Conjunctivitis, Sinusitis
64
Pneumococcal Infections: Invasive Disease
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
Pneumococcal Infections: Management of Children who are at Increased Risk
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
Haemophilus Infections
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
Staphylococcus and Group-A Streptococcal Infections: Pathophysiology
• 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
Impetigo
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
Boils
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
Periorbital Cellulitis
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
Staphylococcal Scalded Skin Syndrome
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
Viral Infections in Children
• 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
HSV
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
HSV: Most common primary illness
Gingivo-stomatitis (Vesicular lesions of Lips, Gums, Tongue, Hard Palate; Progresses to extensive, painful Ulceration with bleeding
75
HSV: Skin Manifestations
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
HSV: Eye disease
Blepharitis or Conjunctivitis; May extend to affect Cornea, possibly leading to Scarring and Vision Loss; Requires urgent Ophthalmic opinion
77
HSV: Treatment
Treatment with Aciclovir; used to treat severe symptomatic Skin, Ophthalmic, Cerebral and Systemic Infections
78
VZV: Chickenpox
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
VZV: Chickenpox Complications
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
VZV: Management
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
Shingles
Uncommon; Dermatomal distribution; Rarely Post-Herpetic Neuralgia (C/f adults
82
EBV (Infectious Mononucleosis, Glandular Fever)
Tropism for B-cells and Oropharynx Epithelium; Infection by Oral contact, majority Subclinical course;
83
EBV (Infectious Mononucleosis, Glandular Fever): Symptoms
May develop Fever, Often Severe Tonsillitis/Pharyngitis, LNA, Splenomegaly (50%), Hepatomegaly (10%), Maculopapular Rash (5%)
84
EBV (Infectious Mononucleosis, Glandular Fever): Diagnosis
Atypical Lymphocytes on Blood film, Positive Monospot (Often negative in young children), Seroconversion (VCA, EBNA)
85
EBV (Infectious Mononucleosis, Glandular Fever): Management
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
EBV (Infectious Mononucleosis, Glandular Fever): Associations
Also involved in Pathogenesis of Burkitt Lymphoma, Lymphoproliferative Disease in Immunocompromised hosts, and Nasopharyngeal Carcinoma
87
CMV: Transmission
Transmission by Saliva, Genital Secretions or Breast Milk; Rarely Transplacental;
88
CMV: Presentation
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
CMV: Consequences
Can cause Retinitis, Pneumonitis, BM Failure, Encephalitis, Hepatitis, Oesophagitis and Enterocolitis in Immunocompromised hosts
90
CMV: Treatment
Can be treated with IV Ganciclovir, Oral Valganciclovir or Foscarnet; Poor SE profile
91
Parvovirus B19
Infects Erythroblastoid RBC Precursors in the Bone Marrow
92
Parvovirus: Outbreaks and transmission
Outbreaks most common in Spring; Transmission by Respiratory secretions or Transplacental;
93
Parvovirus: Presentation
Can present as Asymptomatic, Erythema Infectiosum (Slapped cheek appearance), Aplastic Crisis or as Foetal Disease
94
Parvovirus: Aplastic Crisis
Occurs in patients with Chronic Haemolysis, increased rate of RBC turnover or Immunocompromised with impaired B-cell response
95
Enteroviruses
Includes Coxsackie, Echoviruses, Polioviruses);
96
Enteroviruses: Transmission
Faecal Oral Transmission or Respiratory Droplets
97
Enteroviruses: Presentation
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
Hand-Foot-Mouth Disease
Painful, vesicular Lesions; Generally mild, disease subsides within a few days
99
Enteroviral Neonatal Sepsis Syndrome
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
TB: Infectability
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
TB: Spread
Nearly all cases spread by Respiratory route
102
TB: Presentation
Typically, non-specific; Prolonged fever, Malaise, Anorexia, Weight Loss, LNA
103
TB: Types
3/4 have Pulmonary TB; Extrapulmonary disease less common, includes Lymphadenitis, Osteoarticular TB, Genitourinary TB and TB Meningitis
104
TB: Diagnostic Test
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
TB: Additional tests
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
TB: Management
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
TB Management: Uncomplicated Pulmonary TB
6/12 course; Longer for complicated
108
TB Meningitis
Dexamethasone given initially to reduce risk of complications
109
TB: Pyridoxine
Pyridoxine given weekly in Adolescents to prevent Peripheral Neuropathy associated with Isoniazid therapy; Not required in Young Children
110
TB: Latent TB (asymptomatic with Mantoux or IGRA)
Rifampicin and Isoniazid 3/12, or Isoniazid 6/12 to reduce risk of reactivation later in life
111
TB: Prevention
```
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
Pertussis
=Whooping Cough, caused by Bordetella pertussis (Gram negative, Aerobic, Encapsulated Coccobacillus); High contagious; Endemic; Epidemics every 3-4yrs; Incubation about 10 days
113
Pertussis: Catarrhal Phase
(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
Pertussis: Convalescent Phase
Symptoms gradually decrease, although may persist for many months
115
Pertussis: Complications
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
Pertussis: Investigations
Identified early from Nasal swab culture; PCR more sensitive; Marked Lymphocytosis (>15×109/L) on FBC
117
Pertussis: Management
Macrolide Antibiotics (Erythro, Clarithro, Azithro); Effective to decrease symptoms only if given in Catarrhal phase; Prophylaxis of siblings, parents, school contacts
118
Pertussis: Immunisation
• 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
Gastroenteritis: Presentation
Sudden-onset Loose/Watery stool, Vomiting; May be in contact with affected, or recent travel abroad; Dehydration from shock is most serious complication
120
Gastroenteritis: High Risk of Dehydration
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
Gastroenteritis: Viral Causes
Most frequently Rotavirus (60% under <2yrs, particularly in Winter/Spring); Other viruses, such as Adenovir, Norovir, Calicivir, Coronavir and Astrovir
122
Gastroenteritis: Bacterial Causes
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
Gastroenteritis: Protozoan Causes
Giardia, Cryptosporidium
124
Gastroenteritis: Mimics
Sepsis, Meningitis, URTI, AOM, Hepatitis A, UTI, Pyloric Stenosis, Intussusception, Appendicitis, NEC, Hirschsprung, DKA, HUS, Coeliac, Allergies, Addisons
125
Gastroenteritis: Assessment
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
Gastroenteritis: Isonatraemic and Hyponatraemia Dehydration
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
Gastroenteritis: Hypernatremia Dehydration
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
Gastroenteritis: Investigation
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
Gastroenteritis: Dehydration
If Clinical Dehydration, Oral Rehydration is mainstay; IV fluids only if Shock, or Deterioration, or Persistent Vomiting
130
Gastroenteritis: Not dehydrated
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
Gastroenteritis: Shock
IV 0.9% Bolus and repeat if necessary; ICU if still shocked
132
Gastroenteritis: IV rehydration
100ml/kg if shock present, 50ml/kg if not in shock; Consider Potassium supplementation
133
Gastroenteritis: Anti diarrhoeal and antiemetics
Ineffective, prolongs bacterial excretion, Associated with SE, and focus attention away from rehydration
134
Gastroenteritis: Antibiotics
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
HIV in children: Epidemiology
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
HIV in Children: Transmission
Major route through Mother-to-Child – Intrauterine, Intrapartum or Breastfeeding; Also, though infected blood products, contaminated needles or sexual abuse
137
HIV in children: Serology
• 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
HIV in Children: Likelihood of Vertical Transmission
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
HIV in Children: Prevention of Vertical Transmission-Antenatal
• Use of ART during Pregnancy and Intrapartum to achieve undetectable Maternal Viral Load at the time of delivery
140
HIV in Children: Prevention of Vertical Transmission-Delivery
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
HIV in Children: Prevention of Vertical Transmission: Postnatally
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
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HIV in Children: Progression
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
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HIV in Children: Clinical Features-Mild Immunocompromise
Lymphadenopathy and Parotid Enlargement, Hepatosplenomegaly, Recurrent PUOs, Thrombocytopaenia
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HIV in Children: Clinical Features-Moderate
Recurrent Bacterial Infections, Candidiasis, Chronic Diarrhoea, Lymphocytic Interstitial Pneumonitis (either due to HIV, or EBV superinfection)
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HIV in Children: Clinical Features-Severe/AIDS
Opportunistic infections (E.g. PCP), Growth faltering, Encephalopathy and rarely can lead to malignancies
146
HIV in Children: Management-ART
* 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
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HIV in Children: Management-Prophylaxis
Prophylaxis against PCP (Co-Trimoxazole) for infants and older children with low CD4
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HIV in Children: Immunisation
Especially crucial to follow; Omit BCG (live vaccine); Consider Flu, Hep A/B and VZV vaccination
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HIV in Children: MDT Management
Concordance, Disclosure of diagnosis, Planning for the future
• Regular follow up – Weight, Developmental Progress, Symptoms
