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Copy of Kawasaki Disease


Sondae Stevens

on 10 January 2013

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Transcript of Copy of Kawasaki Disease

Pharmacy/ UJ
3O.12.2010 Agenda: - History
- Definition
- Etiology
- Pathophysiology
- Clinical Signs
- Physical Symptoms
- Diagnosis.
- Treatment HISTORY 1961 -1967 1970 1974 1978 1984 DEFINITION - CDC defines of kawasaki disease; illness in a patient with fever of 5 or
more days duration. or fever until the date of administration of
intravenous immunoglobulin (IV IG) if it is given before the fifth day

- With the presence of at least 4 of the following 5 Clinical signs:
1. Rash.
2. Cervical Lymphedenopathy. - at least 1.5 cm in diameter-
3. Bilateral Conjuctival injection.
4. Oral mucosal changes.
5. Periphral extremity changes.

P.S. patients whose illness does not meet the above KS case definition
but who have fever and coronary artery abnormalities are classified as
having atypical or incomplete KS. ETIOLOGY Etiology of KD is still a dilemma for pediatricians; specially if
it's atypical or incomplete presentation.

But most epidemiologic and immunologic evidence indicate
that causative agent is probably INFECTIOUS.
Never the less, 2.4 % of KD patients in Japan involve siblings .
The overall presentation of patients with KD is similar to that
of patients with a viral or superantigenic disease.

Failing to isolate one pathogen highlights the likely hood that
the cause of this disease MULTI-FACTORIAL that is influenced
by GENETIC and IMMUNOLOGIC factors. Superantigens
and Cytotoxic T-cells
appeared to be involved Passive maternal immunity might account for
the faliure of most cases to develope before the
patient is aged 4 months. Various Infections KD has been linked to : 1. Parvovirus B19
2. Meningococcal septicemia
3. Coxiella burnetti
4.Bacterial toxins
5. HIV
6. Mycoplasma pneumonia
7. Adenovirus
8. Klebsiella pneumonia bacteremia
9. Parainfluenza type 3 virus
10. Rotavirus infection
11. Measles
12. Human lymphotropic virus
infection Kawasaki does not appear to be linked to: 1. Rickettisia conorii
2. Rickettisia typhi
3. Ehrlichia phagocyyopia
group allergens KD is not associated to: 1. Human herpes virus 8
2. Trasfusion transmitted virus
3. Hepatitis G virus ( GB-virus ) Pathophysiology - Most of the pathology of the disease is induced by medium vessel artirial vasculitis

- Initially, Nutrophils are present in great numbers, but the infiltrate rapidly switches to
monocellular cells, T-lymphocytes and immunoglubulin A (IgA) producing plasma cells.

- Inflamation involvels all 3 layers of the vessels.

- Esinophils are pereferentially accumulated in microvessels.

Recent immunohistochemical findings suggest that many vascular growth factors
then play a role in the formation of the coronary artery lesions.

- The activated cytotoxic T-cells increase.
- The suppressor T-cells decrease.
- Serum levels of interleukin (IL-1),
tumor necosis factor-alpha (TNF-alpha),
interferon-gamma (INF-gamma),
and IL-6
ARE ELEVATED! Clinical Signs - Acute Signs (1 -11 d ): 1. High fever T>104F.
2. Irritability.
3. Nonexudative bilateral conjubtivitis.
4. Anterior uvenitis.
5. Perianal erythmea.
6. Acral erythema and edema that impede embulation.
7. strawebarry toungue and lip fissures.
8. Hepatic, renal and GI dysfunction.
9. Myocarditis and peri carditis.
10. Lymphadenopathy, enlarged, nonsuppurative cervical node measuring
approximately 1.5 cm. Video - Subacute Stage ( 11-30 d) : 1. Presistent irritability, anorexia and conjuctival injection.
2. Decreased temperature.
3. Thrombocytosis.
4. Acral desquamation.
5. Aneurysm forms. Convalescent or Chronic phase
( >= 30 d): 1. Expantion aneurysm.
2. possible myocardial infarction.
3. A tendency for smaller aneurysms to resolve on
their own ( 6o% of cases) Pathophysiology: Physical Symptoms: 1. Fever, lasting more than 5 days and refractory to appropriate anibiotic therapy.

2. Polymorphous erythmatous rash.
3. Nonpurulent bilateral conjunctival injection
4. Oropharyngeal changes, including erythema, edema, induration, and descuamation.
5. nonpurulent cervical lymphadenopathy. Diagnosis of Kawasaki: - The commonest abnormalities were raised S-T segments.
- And prolonged corrected Q-T interval. Treatment High dose of Aspirin
to reduce inflamation and mildly
thin the blood to prevent
blood clot formation 1 2 IV Gamma globulin
administration. togather
with fluid.
decrease the chance of developing aneurysms in the coronory arteries. 3 Cortison medications are
sometimes given 4 Anti-inflamatory drugs are given
to presist joint pains
eg. Ibuprofen
Naproxen 5 Plasma Exchange 6 Medications that block
the effect of TNF
eg. Infliximab, Intranercept Further researches are still needed to design treatment programs for those
who are failing conventional treatment. The END..

Happy New Year! ( plasmapheresis )
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