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Paediatrics > Infections and Immunity > Flashcards

Infections and Immunity Flashcards

1
Q
A

Chicken pox

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2
Q

What is chickenpox?

A

A highly infectious disease caused by primary infection with VZV

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3
Q

How does VZV spread?

A

Respiratory route

Chickenpox can be caught from someone with shingles

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4
Q

What is the incubation period of VZV?

A

10-21 days

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5
Q

What are the complications of chickenpox?

A
  • Secondary Bacterial Infection
  • Encephalitis
  • Purpura Fulminans
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6
Q

Describe secondary bacterial infection in chickenpox?

A

o Mainly with staphylococci and group A streptococci
o Can lead to toxic shock syndrome and necrotising fasciitis
o Should be considered when there is onset of a new fever or persistent high fever after the first few days

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7
Q

Describe encephalitis in chickenpox

A

o May be generalised
o Usually occurs early in the illness
o GOOD prognosis (as opposed to HSV encephalitis)
o Characteristically causes a VZV-associated cerebellitis

▪ The child becomes ataxic with cerebellar signs
o This usually occurs around 1 week after the onset of the rash

o Usually resolves within a month

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8
Q

Describe purpura fulminans in chicken pox.

A

o Consequence of vasculitis in the skin and subcutaneous tissues
o Best known in relation to meningococcal disease (purpuric rash)
o Can lead to the loss of large areas of skin by necrosis
o Rarely, after VZV infection, antiviral antibodies can cross-react and inactivate inhibitory coagulation factors (protein S and protein C), resulting in increased risk of clotting, which often manifests as a purpuric rash

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9
Q

How would VZV present in an immunocompromised patient?

A

• If patient is immunocompromised, primary VZV would result in severe progressive disseminated disease (up to 20% mortality)

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10
Q

What are the clinical features of chickenpox?

A

Fever initially

A characteristic skin rash

o VESICULAR rash that forms small, itchy blisters that eventually scab over o Usually starts on the chest, back and face
o Macular→papular→vesicular
o Systemic illness is mild

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11
Q

How do we think about the management of chickenpox?

A
  • ADVICE
  • Consider admission
  • Safety net
  • Mild/moderate/severe disease/ Immunocompromised / Neonatal
  • Prevention in immunocompromised
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12
Q

What advice do you need to give for chickenpox?

A
  • General advice:
    • Encourage adequate fluid intake
    • Dress appropriately to avoid overheating or shivering
    • Wear smooth, cotton fabrics
    • Keep nails short to minimize damage from scratching
    • Oral paracetamol and topical emollient (e.g.calamine lotion) to reduce itching
  • Advise that the most infectious period is 1–2 days before the rash appears, but infectivity continues until all the lesions are dry and have crusted over (usually around 5 days after onset of the rash). Avoid contact with:
    • School
    • Immunocompromised
    • Pregnant women
    • Infants < 4 weeks old
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13
Q

When should you admit a child with chicken pox?

A

Admit to hospital if there are serious complications:

o Pneumonia

o Encephalitis
o Dehydration(reduced urine output, lethargy, cool peripheries)
o Bacterial superinfection (sudden high-grade pyrexia with erythema and tendernessaround the original chickenpox lesions)

o Purpura fulminans

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14
Q

How do you treat mild-moderate, severe, neonatal, immunocompromised chicken pox?

A

Mild-moderate disease:
o General advice

Severe disease:
o Consider oral aciclovir 800 mg 5 times a day for 7 days if adolescent (aged 14 years or older) who presents within 24 hours of rash onset

Neonatal chickenpox:
o Seek immediate specialist advice

Immunocompromised children:
o IV aciclovir for 7 days if they present with 24 hours of the onset of the rash OR if the chickenpox is severe
o PO valaciclovir maybe substituted

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15
Q

What is the Prevention of chicken pox in Immunocompromised children?

A

o Human varicella zoster immunoglobulin should be used in high-risk immunocompromised individuals with deficient T cell function following contact with chickenpox

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16
Q
A

Roseola Infantum

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17
Q

What causes Roseola Infantum

A

Caused by HHV-6 and HHV-7.

This is also called Exanthema subitum

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18
Q

When do most children get affected by HHV-6 and -7?

A

By the age of 2 yrs

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19
Q

Which is more common out of HHV-6 and -7?

A

HHV-6

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20
Q

How is HHV-6/7 acquired in children?

A

MOST CHILDREN are infected by HHV6 or HHV7 by the age of 2 years, usually from the oral secretions of a family member

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21
Q

What is the presentation of roseola infantum?

A

o This is characterised by a high fever and malaise lasting a few days

o This is followed by a generalised macular rash, which appears at the fever wanes

o Many children will have the fever without the rash and many will have a subclinical infection

o Commonest cause of febrile seizures in children

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22
Q

What is roseola infantum often misdiagnosed as?

A

This is often misdiagnosed as measles or rubella - should have PCR or serology as rare

Infants seen in the febrile stage may be given antibiotics, and when the exanthema subitum rash appears, they can be misdiagnosed with an allergy to antibiotics

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23
Q

What is the management of roseola infantum?

A

The condition will resolve over a few days/week

Paracetamol (10-15mg/kg every 4-6hrs) or ibuprofen (5-10mg/kg every 4-6hrs) for symptomatic relief

Advise to maintain adequate hydration

Explain the risk of febrile seizures

School exclusion is NOT needed

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24
Q
A

HPV B19 / Erythema Infectiosum/ Fifth Disease / Slapped Cheek Syndrome

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25
Q

When are infections with HPV B19 more likely to occur?

A

Infections can occur at any time of the year but outbreaks are most common in spring

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26
Q

How is HPV B19 transmitted?

A

Transmission is via respiratory secretions from affected patients, by vertical

transmission from mother to fetus and by transfusion of infected blood products

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27
Q

What is the pathophysiology of HPV B19?

A

HPV-B19 infects the erythroblastoid red cell precursors in the bone marrow

It causes a range of clinical pictures

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28
Q

What are the clinical features of HPV B19 infection?

A

Raage of presentations:

o Asymptomatic infection

▪ Common

▪ 5-10% preschool children have antibodies

o Erythema infectiosum: most common

▪ Viraemic phase of fever, malaise, headache and myalgia

▪ This is followed by a characteristic rash on the face

▪ This rash progresses to a maculopapular, ‘lace’-like rash on the trunk and limbs

▪ In children, complications are rare. In adults, arthralgia and arthritis are relatively common

o Aplastic crisis: most common serious presentation

▪ In children with chronic haemolytic anaemias where there is increased RBC turnover e.g. SCD, thalassemia

▪ Also in immunocompromised children who are unable to produce an antibody response to neutralise the infectious agent

o Fetal disease
▪ Transmission of maternal HPV-B19 infection may lead to fetal hydrops and death due to severe anaemia, but majority of infected foetuses will recover

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29
Q

What are the investigations for HPV B19 infection?

A

• This is a clinical diagnosis via typical slapped-cheek rash with a lacy, reticular exanthem on extremities and torso seen on examination

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30
Q

What is the management of HPV B19 infection?

A

Paracetamol (10-15mg/kg every 4-6hrs) or ibuprofen (5-10mg/kg every 4-6hrs) for symptomatic relief

Encourage adequate fluid intake and rest

Secondary arthritis may be treated with ibuprofen (4-10mg/kg every 6-8hrs)

If infection persists >3wks:

o Give IVIG for 5d
o May need a RBC transfusion for anaemia

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31
Q
A

Measles

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32
Q

What is measles caused by?

A

A highly infectious disease caused by measles virus

RNA paramyxovirus

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33
Q

What is the incubation period of the measles virus? When are patients infectious?

A

Incubation period: 10- 14 days

Infective from prodrome until 4 days after rash starts

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34
Q

How has incidence of measles infection changed?

A

There has been a rise in cases due to anxiety about the MMR vaccine

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35
Q

Who tend to get worse measles infections?

A

Older children and adults tend to have more severe disease than the very young

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36
Q

What is the pathophysiology of measles?

A
  • Measles virus is transmitted via droplets and infects epithelial cells of the nose and conjunctivae. Virus multiplies in these epithelial cells and then extends to the regional lymph nodes
  • Note: in low income countries, where malnutrition and vitamin A deficiency leads to impaired cell-mediated immunity, measles often follows a protracted course with severe complications
  • Impaired cellular immune responses such as in HIV, may result in a modified/absence of rash with an increased risk of dissemination, including giant-cell pneumonia or encephalitis
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37
Q

What are the clinical features of measles infections?

A

Prodrome: irritable, conjunctivitis, fever, cough, coryzal symptoms

Koplik’s spots: occur before rash, red spots often with a bluish-white central dot on erythematous buccal mucosa

Rash: starts behind ears then to whole body; discrete maculopapular rash becoming blotchy and confluent; may desquamate in second week

38
Q

What are the complications of measles infections?

A

o Otitis media: most common complication

o Pneumonia: most common cause of death

o Encephalitis

▪ RARE (1 in 5000 cases)

▪ Typically 1-2 weeks after onset of illness

▪ Headache, lethargy and irritability→seizures and coma

▪ Up to 15% mortality

▪ Serious long-term sequelae include: seizures, deafness, hemiplegia, severe learning difficulties
o Subacute Sclerosing Panencephalitis (SSPE)

  • most of the children affected by this have had measles before the age of 2 yrs

▪ RARE but devastating
▪ Occurs 5-10 years after measles infection
▪ Caused by a variant of the measles virus that persists in the CNS

▪ Presents with loss of neurological function
▪ This progresses, over several years, to dementia and death

o Febrile convulsions
o Keratoconjunctivitis, corneal ulceration

o Diarrhoea
o Increased incidence of appendicitis
o Myocarditis

39
Q

What are the investigations for measles infection?

A

• Examine

  • Measles-specific IgM and IgG serology
    • IgM indicates acute infection
    • IgG indicates an infection in the past or prior vaccination
40
Q

How should you think about the management of measles infection?

A
  • Advice
  • Conservative management
  • Safety net
  • Notify the local Health Protection Team (HPT)
  • Management for complications
  • Think about vaccination status of patient and contacts - encourage
  • Think about immunocompromised patients
41
Q

What advice should we give for measles?

A

Advise that measles is a self-limiting disease, but it is likely to cause unpleasant symptoms e.g. rash, fever, cough and conjunctivitis

Rest and drink plenty

Stay away from school for at least or at least 4 days after the development of the rash

Encourage vaccinations once the acute episode has subsided

Find out the immunization status of close contacts

42
Q

What conservative management should be given in measles?

A

Paracetamol (10-15mg/kg every 4-6hrs) or ibuprofen (5-10mg/kg every 4-6hrs) for symptomatic relief

43
Q

What safety net advice should be given?

A

Seek urgent medical advice if they develop complications such as:

  • Shortness of breath
  • Uncontrolled fever
  • Convulsions or altered consciousness

Respiratory support can be given if pneumonia or neurological support in case of encephalitis

44
Q

What should be done for measles in hospital?

A

Respiratory support can be given if pneumonia or neurological support in case of encephalitis

Vitamin A is given orally for 2d, especially in those hospitalised or <2 years old

Children should be isolated in hospital

45
Q

What should be done for immunocompromised patients regarding measles?

A

In immunocompromised patients, ribavirin may be of use

46
Q
A

Mumps

47
Q

What causes mumps?

A

Mumps is an acute systemic infectious disease caused by an RNA paramyxovirus

48
Q

How has the incidence of mumps changed?

A

Occurs worldwide but incidence has declined since MMR vaccine

There has been a rise since decrease in MMR vaccine uptake

49
Q

When does mumps usually occur?

A

Mumps usually occurs in winter and spring months

50
Q

What is the incubation period of mumps?

A

Incubation period: 15-24 days

51
Q

What is the pathophysiology of mumps?

A

Spread by respiratory droplets, direct contact or contaminated fomites

It is spread by droplets to the respiratory tract where the virus replicates within epithelial cells.

The virus gains access to the parotid glands before further dissemination to other tissues

52
Q

What are the clinical features of mumps?

A

The disease begins with a fever, malaise and parotitis; classic feature = SWOLLEN

PAROTID GLANDS
o This may initially be unilateral, but it will eventually become bilateral after a few days
o Earache or pain when eating/drinking
o Examination of the parotid duct may show redness and swelling

In up to 30% of cases, the infection will be subclinical

The fever usually subsides after 3-4 days

Plasma amylase levels are usually elevated due to parotid inflammation

When associated with abdominal pain, consider pancreatic involvement

Infectivity lasts for up to 7 days after the onset of parotid swelling

The illness is usually mild and self-limiting

53
Q

What are the complications of a mumps infection?

A

o Orchitis: uncommon in pre-pubertal males but occurs in ~25% of post- pubertal males. Typically 4/5 days after start of parotitis

o Hearing loss: usually unilateral and transient

o Meningoencephalitis
o Pancreatitis

54
Q

What investigations can you do for mumps?

A
  • Examination
  • Salivary mumps IgM
55
Q

What is the management of mumps?

A
  • Advise that it is a self-limiting condition
  • Advise patient to rest and take in adequate fluids
  • Paracetamol (10-15mg/kg every 4-6hrs) or ibuprofen (5-10mg/kg every 4-6hrs) for symptomatic relief
  • Stay away from school for 5-7 days after the development of parotitis
  • Advise patient/ parents to seek help if they experience symptoms suggestive of meningitis or epididymo-orchitis
  • Find out the immunization status of close contacts and tell them to watch out for symptoms of mumps
  • Notify the local Health Protection Unit (HPU)
56
Q
A

Rubella

57
Q

What is rubella caused by?

A

A mild, self-limiting systemic infection caused by the rubella virus (togavirus)

58
Q

When does rubella typically occur?

A

Typically occurs in winter and sprin

59
Q

Why is rubella an important disease?

A

Important infection as it can cause severe disease in the fetus (see neonatal)

If infection occurs in a pregnant woman, it can cause congenital rubella syndrome →

triad of hearing loss + cataracts + heart defects

60
Q

What is the pathophysiology of rubella?

A

Spread by the respiratory route, frequently from a known contact

o Transmitted by direct or droplet contact with infected body fluids, usually nasopharyngeal secretions

o Patients may shed infectious virus from 7-30 days after infection

o But, infants with congenital rubella syndrome may be contagious for > 1 yr

• Incubation period is 15 – 20 days

o During this, virus replicates in nasopharynx and local lymph nodes and then spreads via blood stream throughout body, including in pregnant women to placenta and fetus

61
Q

What are the clinical features of rubella?

A

The prodrome is usually mild with a low-grade fever or none at all

The maculopapular rash is often first sign of infection, appearing initially on face and then spreading centrifugally to cover whole body.

Rash fades in 3-5 days

Lymphadenopathy, esp of suboccipital and postauricular nodes, is prominent

62
Q

What are the complications of rubella?

A

Complications - rare in childhood (MEAT)

o Arthritis
o Encephalitis
o Thrombocytopenia

o Meningitis

63
Q

What are the investigations of rubella?

A

• Serology

o Should confirm diagnosis serologically if there is any risk of exposure of a nonimmune pregnant woman

• FBC
o May show thrombocytopaenia

64
Q

What is the management of rubella?

A

Notify the local Health Protection Unit (HPU)

Rest and take in adequate fluids

Consider admitting if there is a serious complication such as haemorrhagic complications

(caused by thrombocytopaenia) or encephalitis

Should be kept at home until 4 days after onset of rash

65
Q

How should we treat rubella in a pregnant woman?

A

Pregnant women with known exposure to rubella who are susceptible to rubella or who have uncertain immunity (no or unknown immunisation history and no previous serological testing), whether or not they are symptomatic, should be referred to a high-risk perinatal specialist and a paediatric infectious disease specialist to evaluate the likelihood of fetal infection and risk of sequelae.

Pregnancy termination is an option for those at high risk of delivering a child with neonatal rubella.

66
Q

What causes malaria infection?

A
  • Most commonly caused by Plasmodium Falciparum
  • Transmitted by female Anopheles Mosquito - 40% of world’s population live here
67
Q

What is the morbidity associated with malaria?

A

Causes 250,000 child deaths in Africa/yr

68
Q

What are the clinical features of malaria?

A
  • Fever (often not cyclical)
  • Diarrhoea
  • Vomiting
  • Flu-like symptoms
  • Jaundice
  • Anaemia - children susceptible
  • Thrombocytopenia
  • Typical onset: 7-10 days after inoculation but symptoms can present months later (depending on Plasmodium species)

Children are particularly susceptible to cerebral malaria

69
Q

How do we investigate malaria?

A
  • Examination of thick blood films
  • The species (falciparum, vivax, ovale, malariae, or knowlesi) is confirmed by thin blood films
  • Repeated blood films may be necessary
  • Rapid diagnostic tests can also be used to establish diagnosis
70
Q

How do we prevent malaria infection?

A
  • When travelling to endemic areas, travellers should seek latest info on malaria prevention
  • Prophylaxis reduces but does not eliminate risk of infection
  • Prevention of mosquito bites with repellants and bed nets is important
  • Insecticide treated bed nets, indoor residual spraying of houses with insecticides, destruction of mosquito larvae and breeding areas, and prompt treatment with artemisinin-based combination therapy → significant effect
71
Q

What is the management of malaria infection?

A

• If uncomplicated P. falciparum disease:
o Artemisinin combination therapy (such as artemether with lumefantrine or artenimol with piperaquine phosphate)
o Quinine is second line(usually given with an antibiotic)

• If severe P. falciparum disease:
o Parenteral artesunate then after at least 24 hours treatment, switch to oral artemisinin combination therapy
o Supportive care +/- intensive care

If non-Falciparum malaria (Plasmodium vivax and less commonly by P. ovale, P. malariae, and P. knowlesi)

o Artemisinin combination therapy (such as artemether with lumefantrine) or chloroquine

Notify all cases to the local Health Protection Team (HPT)

72
Q

What is typhoid?

A

Typhoid fever is a bacterial infection caused by Salmonella type or paratyphi that can spread throughout the body, affecting many organs.

73
Q

How is typhoid transmitted?

A

Typhoid fever is highly contagious. An infected person can pass the bacteria out of their body in their poo or, less commonly, in their pee.

If someone else eats food or drinks water that’s been contaminated with a small amount of infected poo or pee, they can become infected with the bacteria and develop typhoid fever.

74
Q

Who is at highest risk of being affected by typhoid?

A

Worldwide, children are thought to be most at risk of developing typhoid fever. This may be because their immune system (the body’s natural defence against infection and illness) is still developing.

But children with typhoid fever tend to have milder symptoms than adults.

Typhoid fever is uncommon in the UK, with around 300 infections confirmed each year.

Most of these people became infected while visiting relatives in Bangladesh, India or Pakistan. But you’re also at risk if you visit Asia, Africa or South America.

75
Q

What is the clinical presentation of typhoid?

A
  • Child with worsening fever
  • Headaches
  • Cough
  • Abdo pain
  • Anorexia
  • Malaise
  • Myalgia
  • GI symptoms: Diarrhoea or constipation - may not appear until the second week

Signs:

  • Splenomegaly
  • Bradycardia
  • Rose-coloured spots on the trunk
76
Q

What are serious complications of typhoid infection?

A
  • GI perforation
  • Myocarditis
  • Hepatitis
  • Nephritis
77
Q

What are the investigations of typhoid?

A

A diagnosis of typhoid fever can usually be confirmed by analysing samples of blood, poo, or pee. These will be examined under a microscope for the Salmonella typhi bacteria that cause the condition. The bacteria aren’t always detected the first time, so you may need to have a series of tests.

78
Q

How do you manage typhoid fever?

A

Supportive care: IV fluids and antipyretics

Suspected: Ceftriaxone and azithromycin

Known:

o Ciprofloxacin 7d treatment
o If no response after 4/5d of treatment add azithromycin

o If encephalopathic, add high-dose dexamethasone

79
Q

What is dengue fever? How is it transmitted?

A

Dengue is a mosquito-borne viral haemorrhagic fever (VHF) transmitted by female mosquitoes mainly of the species Aedes aegypti and, to a lesser extent, Ae. albopictus.

80
Q

How is dengue classified?

A

The WHO classification encompasses two clinical entities, one of which is further divided:

  • Non-severe dengue - fever followed by recovery characterises non-severe dengue. It is subdivided into:
    • Dengue without warning signs - fever with two of the following: nausea/vomiting, rash, aches and pains, positive tourniquet test, leukopenia.
    • Dengue with warning signs - the above plus any of: abdominal pain, persistent vomiting, fluid accumulation, mucosal bleeding, lethargy, liver enlargement, increasing haematocrit with decreasing platelets. Those who deteriorate to develop severe dengue tend to have warning signs. They are likely to recover with intravenous rehydration.
  • Severe dengue - this is dengue with severe plasma leakage, severe bleeding, or organ failure. There may be shock, respiratory distress or organ damage. Further deterioration of dengue with warning signs is classified as severe dengue. A second subsequent infection with a different serotype of the dengue virus increases the risk of developing severe dengue.
81
Q

What is the pathophysiology of dengue?

A
  • Patients become infected once bitten by infected mosquitoes.
  • The virus passes to lymph nodes and replicates, mainly in monocytes and macrophages. It then spreads to the circulation and other tissues.
  • Incubation period is 2-7 days.
  • Initial immune activation leads to a flu-like illness of varying severity (dengue and severe dengue can be very similar at the start of the illness).
  • There is a tendency to haemorrhage associated with severe thrombocytopenia: this can also be seen in non-severe dengue.
  • Proliferation of T cells and the production of cytokines may lead to vascular endothelial cell dysfunction and to plasma leakage. When severe this capillary leak characterises severe dengue. It causes an increase in haematocrit, hypoalbuminaemia, pleural effusions and ascites.
  • In severe cases there may be multiple organ failure.
  • Multiple organ dysfunction can also result from direct viral damage to organs, particularly heart, brain and liver.
  • Recovery from infection by one dengue serotype provides full lifelong immunity only against that serotype. Cross-immunity to the other serotypes is partial and temporary.
  • Subsequent infections by other serotypes increase the risk of developing severe dengue.
  • Infants can develop severe dengue infection during their primary infection due to transplacental transfer of maternal antibodies to a different serotype from an immune mother. These amplify the infant’s immune response to the primary infection.
  • The pathogenesis of severe dengue is thought to be immune-mediated. Recent evidence suggests cross-reactive high pro-inflammatory cytokine producing T cells predominate in severe dengue. Studies also suggests that there may be a genetic susceptibility to severe disease[11].
82
Q

How do we investigate dengue?

A
  • FBC may show high PCV with low platelets. There may be paradoxical lymphocytosis (>15% circulating white cells) but overall leukopenia.
  • Clotting studies can reveal prolongation of APTT and PT. Fibrin degradation products may be elevated.
  • U&E may show electrolyte disturbance. LFTs can be elevated - especially AST.
  • Severe cases may show reduced bicarbonate due to acidosis.
  • Infection may be confirmed by isolation of virus in serum and detection of IgM and IgG antibodies by ELISA, monoclonal antibody or haemagglutination.
  • PCR-based techniques are increasingly being used.
83
Q

What is the management of dengue fever?

A

Notifiable disease

WHO group A (no warning signs)

o Tolerating adequate fluid volume, passing urine every 6hrs

o Sent home
o Rest and take oral fluids (rehydration products)
o Monitor for warning signs

o Paracetamol and tepid sponging can be used to reduce fever

WHO group B (developing warning signs)

o Hospital admission
o IV/oral fluids
o Monitor for progression of warning signs
o Discharge once patient is afebrile for >48hrs

WHO group C (established warning signs)
o Hospital admission to ICU
o Consider blood transfusion
o IV 0.9% NaCl: maintenance+ 5% fluid deficit

o100ml/kg for first 10kg 50ml/kg for second 10kg 20ml/kg for >20kg

o Monitoring for worsening signs
o Investigation for other causes
o Discharge once patient is afebrile for >48hrs

84
Q

Define Kawasaki Disease.

A

An acute, febrile, self-limiting, systemic vasculitis of unknown origin

o Vasculitis (inflammation of blood vessel) affecting large/medium sized vessels

85
Q

What is a major complication of Kawasaki Disease?

A

Uncommon but important to identify early, because coronary artery aneurysms are a potentially devastating complication→prompt treatment reduces incidence

86
Q

Who does Kawasaki affect?

A

Mainly affects children 6 months – 4 years of age, with a peak at the end of 1st yr of life

More common in Japanese, and to a lesser extent Black-Caribbean ethnicity than Caucasian

More common in boys

87
Q

Describe the epidemiology of Kawasaki disease.

A

Incidence increasing - 3000 affected annually

88
Q

Describe the pathophysiology of Kawasaki Disease.

A

Aetiology remains unknown

Observations suggest that the disease is triggered by an unknown infectious agent

Pathophysiology

o Endothelial cells in blood vessels become attacked→damaged→collagen and tissue factor found in tunica media become exposed→inc chance of coagulation→this can lead to thrombosis and ischaemia of heart muscles

o The artery walls also become weak→this can lead to coronary aneurysms

▪ Aneurysms occur as fibrin is deposited in the vessel walls to aid healing→fibrin causes vessels to become stiffer, less elastic and less pliable in response to blood

▪ Instead, the vessels form aneurysms

▪ Aneurysms 8mm or larger are at high risk of rupture→reducing blood flow to heart→ischaemia→MI

o In other cases, vessel walls are thickened causing reduced lumen diameter → also leads to ischaemia
• Self-limiting – so will resolve in 6-8 weeks but if untreated, there is a 20-25% risk of CVS complications

89
Q

What are the cardinal features of Kawasaki Disease?

A

Presence of fever for at least 5 * days with at least four of the five following clinical features:

  1. Bilateral bulbar conjunctival injection without exudate.
  2. Erythema and cracking of lips, strawberry tongue and/or erythema of oral and pharyngeal mucosa
  3. Cervical lymphadenopathy (≥1.5 cm diameter), usually unilateral
  4. Rash: maculopapular, diffuse erythroderma, or erythema multiforme-like
  5. Erythema and oedema of the hands and feet in acute phase and/or desquamation around the nails in subacute phase.

* The diagnosis can be made with 4 days of fever when at least four clinical features (particularly redness and swelling of the hands and feet) are present.

90
Q

What are the Ix for Kawasaki Disease?

A

• Initial

o FBC
▪ At beginning of disease

• Anaemia

Raised WCC with left-shift (i.e. inc immature WCC)

Platelet count typically rises in 2nd week of illness

o ESR – raised
o CRP – raised
o LFTs – raised liver enzymes
o Echocardiogram – to assess for aneurysms

• Others
o Microscopic urinalysis: will show mononuclear WBCs in urine without bacteria

Diagnosis is made based on clinical findings + lab tests – no specific diagnostic test

Note: patients that do not completely meet the criteria→incomplete Kawasaki→ sometimes, these patients are treated anyway to prevent potential CA aneurysm

91
Q

How do we manage Kawasaki Disease?

A

• First line: prompt treatment with IV immunoglobulin (IVIG) + high-dose aspirin

o IVIG if given within first 10 days, shown to lower risk of CA aneurysms
o Aspirin used to reduce risk of thrombosis – given as a high anti-inflammatory dose until fever subsides and inflammatory markers return to normal, and then continued at a low antiplatelet dose until echo of 6w shows presence or absence of aneurysms

▪ Acts by inhibiting cyclo-oxygenase to prevent platelet aggregation

▪ Note: aspirin is usually contra-indicated in children as it can lead to Reye syndrome (encephalopathy + liver injury) but in this case, risk is taken and child monitored carefully

  • Second line treatments include corticosteroids, infliximab and plasma exchange
  • 3rd line treatment options include cyclospirin or anakinra or plasma exchange
  • Child with giant coronary artery aneurysms may require long-term warfarin and close follow-up
  • If fever recurs despite treatment → second dose IVIG
  • If persistent inflammation and fever→may require corticosteroids, infliximab (monoclonal antibody against TNFa) or cyclosporin
92
Q

What would the risk assessment for Kawasaki’s dictate?

A

Risk assessment for myocardial ischaemia and coronary artery aneurysms is carried out:

o Low risk: no further medications after 8wks of aspirin
o Moderate risk: low dose aspirin until aneurysm regression is demonstrated, with ECG and echo follow up annually
o High risk: low dose aspirin long term, with ECG and echo follow up twice a year

Need long term warfarin (INR target: 2-3) May need clopidogrel

Paediatrics (15 decks)

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