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Kawasaki disease: Difficult case scenario and guidelines

Published by Morgan Phillips Modified over 5 years ago

Presentation on theme: "Kawasaki disease: Difficult case scenario and guidelines"— Presentation transcript:

Hatem Eleishi, MD Rheumatologist STILL’S DISEASE.

Kawasaki disease is a rare condition. It is most common in children under five years old and most cases occur in children aged between nine months and.

CASE PRESENTATION Abhilash Sailendra GPST 1. AN 18 MONTH OLD WITH FEVER AND RASH AN 18 MONTH OLD WITH FEVER AND RASH High fever for 4 days. Four days.

Journal Club General Medicine C- 4/3/14

Viral Myocarditis.

Juvenile Rheumatoid Arthritis B. Paul Choate, M.D.

Kawasaki Disease Danielle Hann ST2 GPVTS Kawasaki Disease 80% cases aged 6/12 to 5 years Acute inflammatory vasculitis of medium sized arteries.

Acquired Heard Diseases MSN.Khitam moh ’ d Outline 1. Congestive Heart Disease 2. Rheumatic fever 3. Kawasaki Disease.

From Pediatric M&M Fort Carson MEDDAC

DR.IBTISAM JALI MEDICAL DEMONSTRATOR

KAWASAKI’S DISEASE By: Madeline Dixon and Megan Curry.

Kawasaki Disease Dr Paul A Brogan Senior Lecturer in vasculitis

What is Kawasaki Disease? Kawasaki Disease (KD) also known as Kawasaki Syndrome. An unusual and serious illness of young children. It is an autoimmune.

COURAGE: Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation Purpose To compare the efficacy of optimal medical therapy (OMT)

Kawasaki Disease: An Update

Update on Kawasaki Disease June 7 th, 2010 Aaron S. Miller, MD, MSPH Division of Hospitalist Medicine St. Louis Children’s Hospital.

Mucocutaneous lymph node syndrome Ma Lian

A 25 year old farmer with joint pain Laura Zakowski, MD* * No financial disclosures.

The Sick Infant: Five Deadly Misconceptions Todd Wylie, MD University of Florida Department of Emergency Medicine June , 2009.

Immunoglobulin plus prednisolone in severe Kawaski disease (RAISE study) Steph Borg 22 November 2012 SCH Journal Club.

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Kawasaki Disease: An Update of diagnosis and treatment - PowerPoint PPT Presentation

Kawasaki Disease: An Update of diagnosis and treatment

Kawasaki disease: an update of diagnosis and treatment this algorithm is a guide to evaluation of patients with suspected incomplete kawasaki disease (kd). – powerpoint ppt presentation.

Idiopathic multisystem disease characterized by vasculitis of small medium blood vessels, including coronary arteries
Fever for at least 5 days
At least 4 of the following 5 features
Changes in the extremities
Edema, erythema, desquamation
2. Polymorphous exanthem, usually truncal
3. Conjunctival injection
4. Erythema/or fissuring of lips and oral cavity
5. Cervical lymphadenopathy
Illness not explained by other known disease process
Present with lt 4 of 5 diagnostic criteria
Compatible laboratory findings
Still develop coronary artery aneurysms
No other explanation for the illness
More common in children lt 1 year of age
2004 AHA guidelines offer new evaluation and treatment algorithm
Acute (1-2 weeks from onset)
Febrile, irritable, toxic appearing
Oral changes, rash, edema/erythema of feet
Subacute (2-8 weeks from onset)
Desquamation, may have persistent arthritis or arthralgias
Gradual improvement even without treatment
Convalescent (Months to years later)
AHA classify coronary arteries aneurysms
Small (5 mm internal diameter),
medium (5 to 8 mm internal
or giant (8 mm internal diameter).
The Japanese Ministry of Health Classify coronary arteries asabnormal
the internal lumen diameter is 3 mm in children 5 years old or 4 mm in children 5 years old
the internal diameter of a segment measures 1.5 times that of an adjacent segment
AHA-2004 80-100 mg/kg.
Pediatrics-1995 meta-analysis.
Initial CORTICOID vs ASPIRIN.
Initial CORTICOID ASPIRIN IVIG vs ASPIRINIVIG.
Resistance IVIG.
Response with IVIG 90
No response with IVIG 10
IVIG ONLY 2 g/kg (evidence level C).
STEROID ONLY.
PULSE STEROID IVIG Hashino et al RCT.
17 patients who did not respond to an initial infusion of 2 g/kg IVIG plus aspirin followed by an additional IVIG infusion of 1 g/kg.
Randomized to receive either a single additional dose of IVIG (1 g/kg) or pulse steroid therapy.
Patients in the steroidgroup had a shorter duration of fever and lower medical costs.
No significant difference in the incidence of coronary arteryaneurysms was noted between the 2 groups, but power to detect a difference was limited.
AHA-2004 recommends
Steroid treatment berestricted to children in whom 2 infusions of IVIG have been ineffective in alleviating fever and acute inflammation (evidence level C).
The most commonly used steroid regimen is intravenous pulse methylprednisolone, 30 mg/kg for 2 to 3 hours, administered once daily for 1 to 3 days.
IVIG 2g/kg as one-time dose
Beneficial effect 1st reported by Japanese
Mechanism of action is unclear
Significant reduction in CAA in pts treated with IVIG plus aspirin vs. aspirin alone (15-25?3-5)
70-90 defervesce show symptom resolution within 2-3 days of treatment
Retreat those with failure of response to 1st dose or recurrent symptoms ? Up to 2/3 respond to a second course
High dose (80-100 mg/kg/day) until afebrile x 48 hrs /or decrease in acute phase reactants
Need high doses in acute phase due to malabsorption of ASA
Dosage of ASA in acute phase does not seem to affect subsequent incidence of CAA
Decrease to low dose (3-5 mg/kg/day) for 6-8 weeks or until platelet levels normalize ( evidence level C).
No evidence /effect on CAA when used alone
Due to potential risk of Reye syndrome instruct parents about symptoms of influenza or varicella
In case of persistent or recrudescent fever Repeat dose of IVIG 2 g/kg as single infusion consider IV methylprednisolone 30 mg/kg once a day may be repeated as necessary up to a total of three doses

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KAWASAKI DISEASE

Jul 23, 2014

310 likes | 616 Views

KAWASAKI DISEASE. Carreon G., Carreon J., Casaul J.R., Coronado M.C., Corpuz D., Credo C., Danguilan M.C., De Gracia C. AIM:. Review the clinical presentations of K awasaki disease, its progression, serious complications and management. Discuss the D/ Dx of Kawasaki disease. S>.

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KAWASAKI DISEASE Carreon G., Carreon J., Casaul J.R., Coronado M.C., Corpuz D., Credo C., Danguilan M.C., De Gracia C.

AIM: • Review the clinical presentations of Kawasaki disease, its progression, serious complications and management. • Discuss the D/Dx of Kawasaki disease.

S> • 14 m/o, M, from Antipolo City, Filipino, Catholic, born on May 21, 2010 • 1st admission at this institution (May 24, 2011)

CC: • Request for transfer of service, T/C Kawasaki Disease

Aspirin IVIG, zinc sulfate Paracetamol Cefuroxime chills rashes unilateral cervical lymph- adenopathy vomiting irritability swelling of hands and feet conjunctival injection diarrhea perineal desquamation dry, cracked lips strawberry tongue Day of Illness

1st DOI (5 days PTA) - 5/19/11 • (+) Fever (38.3-38.5 °C) • (+) Decreased appetite/activity • MEDs: • Paracetamol drops (12 mkdose, 120mg/5mL, 5mL, q4h) –slight relief

2nd DOI (4 days PTA) – 5/20/11 • (+) Fever (38.9) • LABs: • CBC • U/A: light yellow, clear, s.g 1.010, (-) protein, (-) sugar, 0 RBC, 0-1 WBC, rare epithelial cells • CXR: 1° Complex TB infection

2nd DOI (4 days PTA) – 5/20/11 • MEDs: • Paracetamol drops, 12 mkdose • Cefuroxime, 105 mkd, 350 mg IV, q8h • Budesoniode • Salbutamol

3rd DOI (3 days PTA) – 5/21/11 • (+) Fever (40°C) • (+) Diarrhea (greenish, soft, 3-5 episodes) • (+) Maculopapular, pruritic rash (hands>trunks>head>lower extremities) • LABs: • Fecalysis: brown, soft, 0-2 pus, 0-1 RBC, moderate bacteria • MEDs: • same

4th DOI (2 days PTA) – 5/22/11 • (+) Fever, rash, diarrhea (4-5 episodes) • (+) CLAD (R submandibular area, 2cm) • (+) bilateral, nonpurulentconjunctival injections with perilimbal sparing

4th DOI (2 days PTA) – 5/22/11 • LABs: • CBC • ESR: 65 • CRP: 48 • U/A: dark yellow, sl. Turbid, s.g. 1.020, trace albumin, (-) sugar, pH 6, 2-4 pus, 0-1 RBC, few epithelial cells, few bacteria, few amorphous materials • MEDs: same

Primary Impression • Kawasaki disease

5th DOI (1 day PTA) – 5/23/11 • Sx persisted • (+) stawberry tongue • MEDs: same

6th DOI (DOA) – 5/24/11 • Sx persisted • (+) fever and chills (40.1°) • (+) perineal desquamation • (+) swelling of hands and feet • 37.2-39.6°C>123-180>26-45 + 4BM

6th DOI (DOA) – 5/24/11 • LABs: • CBC • Re-reading of CXR (wet read) • Pneumonia LU and both LLF • Mild pulmonary hyperinflation

6th DOI (DOA) – 5/24/11 *seen by a pediatric infectious disease specialist>> KAWASAKI DISEASE • MEDs: • Paracetamol, 12 mkdose • ASA, 80 mkd (100mg/tab, 2 tabs, q6h) • Cefuroxime, 100 mkd (250 mg IV, q6h)

7th DOI (2nd HD) – 5/25/11 • (+) conjunctival injection • Improvement on the rash • Progression of perineal desquamation (upto lower back) • (+) dry, cracked lips • 90-100/60>131-156>35-49>36.2-38.8 + 1 BM • MEDs: same

8th DOI (3rd HD) – 5/26/11 • (-) conjunctival injection • Improvement on the rash • (+) perineal desquamation up to the lower back • Improvement on strawberry tongue • (+) dry cracked lips

8th DOI (3rd HD) – 5/26/11 • LABs: • 2D-echo: • R coronary artery dilated (0.21 cm proximally, 0.18 cm distally) • L coronary artery dialted (0.22 cm proximally) • Mild pulmonic and tricuspid regurgitation • Mild pulmonary HTN, pulmonary artery pressure at 51 mmHg • Slight L ventricular hypertrophy • Fair L ventricular systolic fxn, EF 56 mmHg • Minimal pericardial effusion noted posteriorly

8th DOI (3rd HD) – 5/26/11 • LABs: • Re-reading of CXR (official result) • Sub-optimal for evaluation d/t motion artifacts. Repeat study suggested. • MEDs: • Paracetamol, 12 mkd • Cefuroxime, 100 mkd • ASA, 100 mkd • IVIG • Zn sulfate drops, 5.5 mkd, 27.5mg/mL, 2mL, OD

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Kawasaki disease: a comprehensive review

Kamleshun ramphul.

1 Department of Pediatrics, Shanghai Xin Hua Hospital affiliated to the Shanghai Jiao Tong University, School of Medicine, Shanghai, China

Stephanie Gonzalez Mejias

2 Department of Pediatrics, Robert Reid Cabral Children’s Hospital affiliated to the University Iberoamericana UNIBE, School of Medicine, Santo Domingo, Dominican Republic

Kawasaki disease is an acute systemic vasculitis that was first reported in 1961. Over the last 5 decades multiple papers have been published to further understand this disease. The diagnosis of Kawasaki disease is made based on the clinical findings. Atypical Kawasaki disease includes patients who do not meet all the criteria for diagnosis. The main complication of Kawasaki disease is coronary aneurysm, and the treatment is intravenous immunoglobulin and aspirin. A second dose of immunoglobulin is given if the patient does not improve, and several other treatment options have been proposed over the last few years as second and third line options.

Introduction

Kawasaki disease (KD) is characterized as an acute systemic vascular disease that affects mostly medium sized and small vessels [ 1 ]. It is generally self-limited and the highest incidence occurs in children under five years of age. Multiple theories have been proposed for the pathophysiology of the condition but the etiology of KD remains poorly understood. Proper diagnosis based on clinical findings, proper investigations and follow-ups are important to treat and prevent associated complications of the disease.

History of Kawasaki disease

In January 1961, Dr. Tomisaku Kawasaki encountered his first case of Kawasaki disease [ 2 ]. A 4-year-old male patient presented with high fever for 2 weeks, bilateral conjunctival hyperemia, fissured, dried, reddish and bleeding lips, strawberry tongue, and diffuse erythema of the oral cavity and mucous membrane. The patient also had initial left then subsequent right cervical lymphadenopathy. Red palms and soles as well as polymorphous erythema were present all over his body. It was followed by membranous desquamation of the hands and feet over the next 2 weeks.

When the case was presented at the pediatric department meeting of the hospital, the differential diagnosis of atypical scarlet fever and milder forms of Steven-Johnson syndrome was suggested, but no proper diagnosis was confirmed on discharge. Dr. Kawasaki then encountered a second case a year later in 1962 in a 2-year-old male patient presenting with similar symptoms, and by October that year he had come across another 5 cases. He reported these 7 cases in a paper at the Chiba Prefecture Pediatric meeting; however there was no positive feedback at that time.

Over the next 5 years following the initial case, Dr. Kawasaki observed 50 cases with similar presentations, following which he published a paper entitled ‘Acute febrile musculocutaneous lymph node syndrome: clinical observation of 50 cases’ in the Japanese Journal of Allergy in 1967. His paper received proper recognition 35 years later from the western side of the world when Dr. Jane Burns from the University of California San Diego presented the paper in English in the Pediatric Infectious Diseases Journal. From 1970, Dr Kawasaki managed to obtain proper funding to study the disease and the initial diagnostic guidelines were established. The committee also came across cases resulting in death and the autopsy showed presence of coronary aneurysm. Coronary angiography was performed to confirm the presence of coronary aneurysm in some of the patients and the introduction of better 2D echocardiography in 1976 allowed better progress to be made in the field [ 3 ].

Epidemiology

Kawasaki disease has a universal distribution and has been found in children of different ethnicities worldwide. The prevalence of KD is higher in Asian countries such as Japan, where the annual incidence rate rose from 239.6 per 100 000 children in 2010 [ 4 ] to 264 per 100,000 children recently [ 5 ]. It has been reported that the incidence of KD had peaks in January and June/July and was lowest in October. The incidence of the disease was also at its peak in the US during winter as well as early spring [ 6 ]. There is also a higher risk among Korean and Taiwanese children, where 134 and 66, respectively, out of 100 000 children under 5 years of age have the disease [ 7 , 8 ]. The prevalence is significantly lower in non-Asian countries; 8.39 per 100 000 children in England [ 9 ], and 9.34 per 100 000 children under 5 years in Australia [ 10 ].

Etiology and pathophysiology

Multiple theories have been hypothesized for the etiology of KD. It is currently believed that there is a genetic predisposition to the development of KD and the interaction of an unknown infective cause can also predispose to KD [ 11 ].

Current evidence strongly suggests that genetic factors have a more important role in the occurrence of KD. Polymorphisms of the IgG receptor can increase the susceptibility of children to KD and increase the risk of developing coronary artery aneurysm. The higher prevalence of KD among Asian countries such as Japan, Korea and Taiwan compared to non-Asian countries also suggests a strong genetic susceptibility based on ethnicity. Japanese American children in Hawaii had a higher incidence rate of 210 per 100 000 compared to 13 per 100 000 in Caucasian American children living in the same area in Hawaii [ 12 ]. Various genome-wide association studies in KD have also been reported [ 13 – 17 ].

An infective cause was also suggested for the incidence of KD. The major epidemics of KD in Japan have shown origination in specific areas and peak incidence in specific months [ 18 ]. The acute onset of the disease mimics viral and bacterial infection patterns. In 2013 Jaggi et al. suggested that there could be a relationship between an infection with adenovirus and the onset of KD. Other studies have suggested that a virus could have been inhaled and later engulfed by tissue macrophages leading to activation of the innate immune response. Further activation of the adaptive immune responses can lead to antigen specific T lymphocytes and plasma cell activation. The presence of the infection in coronary tissue leads to secretion of multiple growth factors such as vascular endothelial growth factors, tumor necrosis factor-α (TNF-α), and metalloproteinase 9, leading to destruction of the intima, and fragmentation of the internal and external elastic lamina of the coronary artery. This results in the development of a coronary artery aneurysm [ 19 ] Furthermore, it has also been suggested that KD antibodies can identify intra-cytoplasmic inclusion bodies in tissues. Other studies have also reported several inclusion bodies corresponding to aggregates of viral RNA and proteins that are yet to be identified [ 20 ].

The diagnosis of KD relies mostly on clinical signs and symptoms. The criteria in the US require the presence of fever for at least 5 days along with four of five other clinical features listed in Table I .

Diagnostic criteria for Kawasaki disease. Four of these five plus a fever of more than 5 days confirms the diagnosis of Kawasaki disease

An algorithm was created by the American Heart Association (AHA) in 2004 to help identify patients at risk [ 21 ]. The statement suggests the use of supportive laboratory testing and echocardiography to help detect patients who are at risk and do not meet all the criteria for diagnosis. These were termed “incomplete” KD or “atypical” KD patients, but they are still at risk for developing KD. An Australian study suggested that this occurs in up to 9.6% of cases of KD [ 10 ]. Suggested laboratory testing included markers of inflammation, presence of anemia, leukocytosis, thrombocytosis, hypoalbuminemia, elevated liver enzymes and possible sterile pyuria. An echocardiogram can also help rule out the presence of any early coronary artery abnormalities or involvement.

The multiple differential diagnosis to rule out KD includes drug hypersensitivity, Stevens-Johnson syndrome, staphylococcal scalded skin syndrome, juvenile idiopathic arthritis, toxic shock syndrome, viral infection, and streptococcal scarlet fever [ 21 ].

Kawasaki disease is treated with intravenous immunoglobulin (IVIG) and high dose aspirin, although the use of aspirin in the management has been controversial in some studies [ 22 – 24 ]. A meta-analysis showed that the use of corticosteroids with IVIG as initial treatment has a better effect on reducing the risk of coronary artery abnormalities compared to the use of IVIG only [ 25 ]. It is highly recommended to start the treatment immediately if the patient meets the clinical criteria for KD.

The IVIG can prevent the development of coronary artery aneurysms. The use and dose of IVIG have been supported by multiple randomized controlled trials [ 26 – 28 ]. It has a dose-dependent effect; a single dose of 2 g/kg is administered within 10 days of illness or later if the patient has signs of inflammation, persistent fever or aneurysm on echocardiography. It can lower the risk of giant aneurysm to 1% and coronary artery aneurysms from 25% to less than 5% [ 21 , 22 ]. The IVIG can influence the T cell activity and reduce the synthesis of antibodies and cytokines causing the symptoms of KD [ 21 , 29 – 32 ].

Aspirin is believed to modify the inflammatory state present in KD and prevent the risk of thrombosis. Some studies have however questioned the impact of aspirin use in KD to prevent the development of coronary aneurysm [ 21 , 22 , 24 , 33 ]. The AHA recommends administration of a high dose of aspirin of 80 to 100 mg/day divided into 4 doses until the patient is afebrile for 48 to 72 h. The dose is then reduced to 3 to 5 mg/kg/day as a single dose for 6 to 8 weeks after the onset of the disease. It is also recommended to continue the use of aspirin if there are any persisting coronary abnormalities [ 21 , 24 ]. Children on long courses of aspirin are recommended to receive the influenza vaccine to prevent the risk of Reye syndrome.

If the patient does not respond to the initial therapy, a second infusion of IVIG at 2 g/kg is administered. Kobayashi et al. conducted a retrospective study in 2013 and found that the use of corticosteroids along with IVIG for patients with refractory KD showed better improvement and also lowered the risk of coronary aneurysms [ 34 ]. The AHA has also suggested the use of TNF-α antagonists in patients who do not respond to IVIG. The use of infliximab had faster resolution compared to IVIG retreatment in some studies, while other studies have shown that the use of infliximab helped decrease the duration of fever but did not provide an improvement in treatment over IVIG and aspirin when used alone [ 35 ]. Patients with refractory KD and mild to moderate aneurysm can be treated with aspirin alone or along with antiplatelet agents. Larger aneurysms can be treated with heparin and warfarin as required [ 21 ].

Other possible treatment options that have been proposed include the use of cyclosporine A and methotrexate. Cyclosporine A is a calcineurin inhibitor that targets the Ca 2+ /NFAT signaling pathway. It leads to a decrease in inflammatory response [ 13 , 36 ]. It has been used as a third line of treatment in some cases of KD in Japan [ 37 , 38 ]. Methotrexate can lead to the accumulation of polyglutamate metabolites in the cells [ 39 ]. Since the mechanism of action and its role in KD are not fully understood, the AHA does not have any recommendations for its use in KD [ 40 ].

Prognostic factors

Some prognostic factors for the development of coronary aneurysm in KD patients identified in some studies that involved Japanese children are male sex, C-reactive protein (CRP) > 200 mg/dl, age less than 12 months old or more than 8 years old, albumin < 35 g/l, platelet count < 35 × 10 4 /mm 3 , delay of initiation of IVIG, lower dose of IVIG and recurrent KD [ 41 , 42 ]. One study suggested a score system to identify patients at risk of IVIG resistance as shown in Table II . A combined score of 0 to 3 predicted a low risk while a score of more than 4 suggested a higher risk of having resistance to IVIG therapy [ 43 , 44 ].

Predicting the risk of intravenous immunoglobulin (IVIG) resistance in Kawasaki disease

Long-term follow-up

The AHA recommends a baseline echocardiography examination during the acute phase of the illness. Repeated echocardiography is also recommended at week 2 and weeks 6–8 after the illness [ 21 ]. If there is evidence of higher risk factors or poor recovery, more frequent imaging is recommended.

The AHA also advised that patients who are at low risk and with no detectable coronary abnormalities should be followed for at least 10 to 20 years after being diagnosed with KD, even in the absence of any abnormalities. For moderate-risk patients if there is regression of the aneurysm at weeks 6 to 8, they can be treated as low-risk patients. Regular cardiac assessments every 3 to 5 years are recommended. High-risk patients have a higher likelihood of having progression to coronary artery stenosis. The long-term use of anti-platelet therapy and warfarin or heparin is strongly recommended. β-Blockers can be added to decrease the myocardial oxygen demand. A thorough cardiac examination, electrocardiogram and echocardiogram should be performed at least twice a year. It is also advised to do a yearly stress test and perfusion study. Patients should be advised to limit physical activities based on their conditions and their risks of bleeding. More invasive tests such as angiography can be performed as needed per case [ 45 ].

Conclusions

While Kawasaki disease remains a poorly understood condition, it can be managed with proper treatment and follow-up. A rapid diagnosis and treatment can immensely help improve the prognosis and lower the associated complications of KD. Recent advances in the treatment and detection of KD such as the discovery of NT-proBNP as a biomarker for early detection of the disease show a promising future to combat KD. More expert consensus along with multiple published clinical experiences will continue to help in guiding the proper management of KD.

Conflict of interest

The authors declare no conflict of interest.

Patient Care & Health Information
Diseases & Conditions
Kawasaki disease

Kawasaki disease causes swelling, called inflammation, in the walls of small to medium-sized blood vessels that carry blood throughout the body. Kawasaki disease most often affects the heart arteries in children. Those arteries supply oxygen-rich blood to the heart.

Kawasaki disease is sometimes called mucocutaneous lymph node syndrome. That's because it also causes swelling in glands, called lymph nodes, and mucous membranes inside the mouth, nose, eyes and throat.

Children with Kawasaki disease might have high fever, swollen hands and feet with skin peeling, and red eyes and tongue. But Kawasaki disease is often treatable. With early treatment, most children get better and have no long-lasting problems.

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Symptoms of Kawasaki disease include a fever greater than 102.2 degrees Fahrenheit (39 degrees Celsius) for five or more days. And the child has at least four of the following symptoms.

A rash on the main part of the body or in the genital area.
An enlarged lymph node in the neck.
Very red eyes without a thick discharge.
Red, dry, cracked lips and a red, swollen tongue.
Swollen, red skin on the palms of the hands and the soles of the feet. Later the skin on fingers and toes peels.

The symptoms might not happen at the same time. Let your child's healthcare professional know about a symptom that has gone away.

Other symptoms might include:

Belly pain.
Joint pain.

Some children get a high fever for five or more days but have fewer than four of the symptoms needed for a diagnosis of Kawasaki disease. They might have what's called incomplete Kawasaki disease. Children with incomplete Kawasaki disease are still at risk of damage to the heart arteries. They still need treatment within 10 days of when symptoms appear.

Kawasaki disease can have symptoms like those of a condition called multisystem inflammatory syndrome in children. The syndrome happens in children with COVID-19.

When to see a doctor

If your child has a fever that lasts more than three days, contact your child's healthcare professional. Treating Kawasaki disease within 10 days of when it began may reduce the chances of lasting damage to the arteries that supply the heart.

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No one knows what causes Kawasaki disease. But experts don't believe the disease spreads from person to person. Some think that Kawasaki disease happens after a bacterial or viral infection, or that it's linked to factors in the environment. Certain genes might make children more likely to get Kawasaki disease.

Risk factors

Three things are known to increase a child's risk of developing Kawasaki disease.

Age. Children under 5 years old are at highest risk of Kawasaki disease.
Sex. Children who are assigned male at birth are slightly more likely to get Kawasaki disease.
Ethnicity. Children of Asian or Pacific Islander descent have higher rates of Kawasaki disease.

Kawasaki disease tends to occur seasonally. In North America and countries with like climates, it most often happens in the winter and early spring.

Complications

Kawasaki disease is a leading cause of heart disease in children who live in developed countries. But, with treatment, few children have lasting damage.

Heart complications include:

Swelling of blood vessels, most often the arteries that send blood to the heart.
Swelling of the heart muscle.
Heart valve problems.

Any of these complications can damage the heart. Swelling of the heart arteries can weaken them and cause a bulge in the artery wall, called an aneurysm. Aneurysms raise the risk of blood clots. These can lead to a heart attack or cause bleeding inside the body.

Rarely, for children who get heart artery problems, Kawasaki disease can cause death.

Kawasaki disease care at Mayo Clinic

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Ferri FF. Kawasaki disease. In: Ferri's Clinical Advisor 2022. Elsevier; 2022. https://www.clinicalkey.com. Accessed Sept. 3, 2021.
Elsevier Point of Care. Clinical overview: Kawasaki disease. https://www.clinicalkey.com. Accessed Aug. 10, 2023.
AskMayoExpert. Kawasaki disease (child). Mayo Clinic; 2023.
Sundel R. Kawasaki disease: Clinical features and diagnosis. https://www.uptodate.com/contents/search. Accessed Aug. 10, 2023.
Sundel R. Kawasaki disease: Initial treatment and prognosis. https://www.uptodate.com/contents/search. Accessed Aug. 10, 2023.
Rife E, et al. Kawasaki disease: An update. Current Rheumatology Reports. 2020; doi:10.1007/s11926-020-00941-4.

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A more recent article on Kawasaki disease is available.

Patient information : A handout on this topic is available at https://familydoctor.org/familydoctor/en/diseases-conditions/kawasaki-disease.html .

Author disclosure: No relevant financial affiliations.

Kawasaki disease is an acute, systemic vasculitis that predominantly affects patients younger than five years. It represents the most prominent cause of acquired coronary artery disease in childhood. In the United States, 19 per 100,000 children younger than five years are hospitalized with Kawasaki disease annually. According to U.S. and Japanese guidelines, Kawasaki disease is a clinical diagnosis. Classic (typical) Kawasaki disease is diagnosed based on the presence of a fever lasting five or more days, accompanied by four out of five findings: bilateral conjunctival injection, oral changes such as cracked and erythematous lips and strawberry tongue, cervical lymphadenopathy, extremity changes such as erythema or palm and sole desquamation, and polymorphous rash. Incomplete (atypical) Kawasaki disease occurs in persons with fever lasting five or more days and with two or three of these findings. Transthoracic echocardiography is the diagnostic imaging modality of choice to screen for coronary aneurysms, although other techniques are being evaluated for diagnosis and management. Treatment for acute disease is intravenous immunoglobulin and aspirin. If there is no response to treatment, patients are given a second dose of intravenous immunoglobulin with or without corticosteroids or other adjunctive treatments. The presence and severity of coronary aneurysms and obstruction at diagnosis determine treatment options and the need, periodicity, and intensity of long-term cardiovascular monitoring for potential atherosclerosis.

Kawasaki disease, also known as mucocutaneous lymph node syndrome, is an acute, systemic vasculitis of small- and medium-sized arteries that predominantly affects patients younger than five years. It represents the most prominent cause of acquired coronary artery disease in childhood. 1 , 2

Kawasaki disease was first described in 1967 1 ; the causative factors are unknown. Pathologic changes theoretically result from an exaggerated immune response to a pathogen in patients with genetic susceptibility. 3 Aberrant production of tumor necrosis factor α (TNF-α), interleukin-6, and other inflammatory cytokines purportedly promote leukocyte-endothelial cell interactions that cause endothelial damage. 3

The annual incidence of hospitalizations of U.S. patients with Kawasaki disease (19 per 100,000 children younger than five years) has not changed significantly over the previous 20 years. 4 Asian and black Americans are 2.5 and 1.5 times more likely to develop Kawasaki disease than whites, respectively, suggesting a genetic link. 4 , 5 Approximately 75% to 80% of cases in the United States occur in children younger than five years; the median age at diagnosis is 1.5 years, and the male-to-female ratio is approximately 1.5:1. 4 Peak incidence occurs between January and March, suggesting an environmental contribution. 4 , 6

In 2004, the American Heart Association (AHA) published diagnostic criteria for classic (typical) and incomplete (atypical) Kawasaki disease 7 ( Table 1 1 , 7 – 12 ) . These criteria are similar to those of the Japanese Circulation Society. 8 In both forms, Kawasaki disease is a clinical diagnosis. There is no specific diagnostic test, although laboratory and echocardiographic findings (e.g., elevated erythrocyte sedimentation rate and C-reactive protein level, hyponatremia, hypoalbuminemia, coronary aneurysms) may be helpful in evaluating suspected cases and differentiating Kawasaki disease from other conditions 7 ( Table 2 7 , 12 ) . Coronary abnormalities, such as aneurysms, may develop within the first week of disease, making early diagnosis and treatment essential.

CLASSIC (TYPICAL) CRITERIA

Classic Kawasaki disease is diagnosed when patients have fever for five or more days with at least four of five principal clinical features: bilateral conjunctival injection, changes in the lips and oral cavity, cervical lymphadenopathy, extremity changes, and polymorphous rash 7 ( Table 1 1 , 7 – 12 ) . Patients who do not meet these criteria may be diagnosed with Kawasaki disease if they have fewer clinical findings in the presence of coronary artery abnormalities on echocardiography.

These clinical features tend to appear sequentially, which helps to differentiate Kawasaki disease from other disorders ( Table 2 7 , 12 ) . In the acute phase, conjunctival injection ( Figure 1 ) occurs soon after the fever and is usually bilateral, nonpurulent, and painless, and spares the limbus. Oral changes include cracking and erythema of the lips ( Figure 2 ) and a strawberry tongue. Cervical lymphadenopathy is unilateral and includes at least one lymph node greater than 1.5 cm in diameter. The polymorphous rash usually occurs within five days after fever onset and may present as a generalized maculopapular exanthema ( Figure 3 ) , erythema multiforme–like eruption, or scarlatiniform rash ( Figure 4 ) . Extremity changes may include induration and erythema of the hands ( Figure 5 ) and feet ( Figure 6 ) ; in the subacute phase, two to three weeks after fever onset, the fingers and toes may desquamate. Although not diagnostic, a variety of less common features, including gastrointestinal (diarrhea, emesis, and abdominal pain), respiratory (cough and rhinorrhea), and rheumatologic (joint pain and swelling) symptoms, may occur in patients with Kawasaki disease. 7 , 8

INCOMPLETE (ATYPICAL) CRITERIA

In some cases, patients do not fulfill the classic criteria for Kawasaki disease and are classified as having incomplete (atypical) disease. A recent Australian study estimates that this occurs in 9.6% of cases. 11 More common in younger infants and older children, incomplete disease is suspected when patients have a fever for at least five days with only two or three of the principal clinical features ( eFigure A ) . 7 As a result, it is important to consider the diagnosis of Kawasaki disease and the possible need for echocardiography in all infants younger than six months who have an unexplained fever lasting at least seven days with laboratory evidence of systemic inflammation. 7

Transthoracic echocardiography is the imaging modality of choice to detect coronary aneurysms and other cardiac artery abnormalities in Kawasaki disease, and it should be obtained as soon as the patient's symptoms suggest the diagnosis. 7 If needed, other imaging modalities may provide additional information. Three-dimensional echocardiography has been used to localize coronary anomalies such as thrombi, although they are more difficult to perform in smaller children with higher heart rates. Radionuclide imaging is useful in evaluating the presence and severity of coronary artery disease, but it is reserved for the evaluation of cardiac perfusion in those with persistent coronary changes. 8 Magnetic resonance coronary angiography is helpful after treatment for acute disease to visualize coronary artery stenosis, thrombi, and intimal hyperplasia in difficult-to-image locations like the circumflex and more distal arteries. 8

Treatment of Acute Disease

Intravenous immunoglobulin (IVIG) and high-dose aspirin have traditionally been the cornerstones of Kawasaki disease management, although the role of aspirin has been called into question. 13 – 15 Corticosteroids have been evaluated for the treatment of acute and refractory Kawasaki disease. A meta-analysis (n = 1,011) found that using corticosteroids in addition to IVIG as initial treatment significantly reduced the risk of coronary abnormalities compared with IVIG alone (odds ratio [OR] = 0.3; 95% confidence interval [CI], 0.20 to 0.46). 16 Treatment should begin without delay for echocardiography if the patient meets clinical disease criteria.

IVIG prevents the development of coronary aneurysms in a dose-dependent fashion. A single dose of 2 g per kg is administered within 10 days of illness or later if a patient has persistent fever, aneurysms, or inflammation. This approach reduces development of coronary artery abnormalities from approximately 25% to less than 5%; development of giant aneurysms is reduced to 1%. 7 , 13 The mechanism of action of IVIG is unknown, but effects may be from its modulation of cytokine production, influence on T-cell activity, and suppression of antibody synthesis. 7 , 17

Acute disease is also marked by inflammation and platelet activation; aspirin is believed to modify the inflammatory state and prevent thrombosis, but it does not appear to impact the development of coronary aneurysms. 7 , 13 – 15 The AHA guideline recommends high-dose aspirin, 80 to 100 mg per kg per day in four divided doses, until the patient is afebrile for 48 to 72 hours (some recommend continuing until the 14th day of illness has also passed). 7 Afterward, low-dose aspirin at 3 to 5 mg per kg per day is given as a single dose until six to eight weeks after disease onset; if coronary abnormalities develop or persist, aspirin may be needed indefinitely. 7 , 13 – 15 Because of concern for Reye syndrome, patients on long-term aspirin should receive the influenza vaccine, and varicella vaccination status should be checked and cautions given against potential exposure. 7

Treatment of Refractory Disease

Approximately 10% of patients have refractory disease that does not respond to initial therapy (i.e., fever persists or recurs 36 hours after initial IVIG dose). These patients usually receive a second infusion of IVIG at 2 g per kg. The AHA guideline states that the relative roles of repeated use of IVIG and other adjunctive therapies (e.g., corticosteroids, TNF-α antagonists, plasma exchange, cyclophosphamide) are uncertain, 7 although additional evidence has emerged since the last update. A retrospective study (n = 359) found that adding corticosteroids to IVIG for refractory Kawasaki disease decreased the number of patients whose condition did not respond to therapy (adjusted OR = 0.16; 95% CI, 0.09 to 0.31) and lowered the risk of coronary artery abnormalities at one month (adjusted OR = 0.40; 95% CI, 0.27 to 0.90). 18

TNF-α antagonists have also been used for disease that does not respond to IVIG. An open-label trial demonstrated resolution of inflammatory markers and symptoms in 18 of 20 patients given infliximab (Remicade) after IVIG was ineffective. 19 A retrospective cohort study found that patients given infliximab (n = 20) had faster resolution of fever and similar coronary outcomes compared with IVIG retreatment (n = 86). 20 A phase 3 randomized controlled study of infliximab for the primary treatment of Kawasaki disease (n = 196) found that although it decreased fever duration and some inflammatory markers, it did not improve treatment response over IVIG and aspirin alone. 21

A case series of 125 patients with Kawasaki disease refractory to IVIG who were later treated with plasma exchange found that patients without coronary artery abnormalities at the start of therapy remained lesion free during follow-up, whereas 12 of 14 patients with coronary dilatation and two of six patients with aneurysms at the start of exchange experienced symptom resolution. 22

Patients with mild to moderate aneurysms are treated with aspirin alone or in combination with other anti-platelet agents, such as clopidogrel (Plavix) or dipyridamole (Persantine). Heparin and warfarin (Coumadin) are reserved for treating larger aneurysms, and coronary thrombosis is treated with thrombolytic agents in conjunction with aspirin and heparin. 7

Long-Term Management

The 2004 AHA guideline provides recommendations for the long-term management and surveillance of cardiovascular risk in individuals with Kawasaki disease; these are echoed in the 2010 Japanese Circulation Society Joint Working Group guidelines. 7 , 8 Long-term risk of coronary disease is a result of intimal thickening and stenosis in segments adjacent to giant aneurysms and in areas of resolved smaller aneurysms. 23 Patients without aneurysms or stenosis tend not to have late complications, although evidence of long-term atherosclerotic risk is mixed. 24 – 28 Guideline recommendations for periodic cardiovascular risk assessment and the long-term management of Kawasaki disease are detailed in Table 3 . 7 These guidelines can help physicians navigate therapeutic options. Support groups can help patients and families navigate acute and long-term treatment and recovery. Two helpful resources are the Kawasaki Disease Foundation (patient advocacy group; http://www.kdfoundation.org ) and the Kawasaki Disease Research Center (hospital research group with resources for parents and professionals; https://www.pediatrics.ucsd.edu/research/Research_Centers/Kawasaki-Disease/Pages/default.aspx ).

Data Sources : A PubMed search was completed using the keyword and medical subject heading (MeSH) Kawasaki disease. The search included randomized controlled trials, meta-analyses, clinical trials, systematic reviews, clinical practice guidelines, and review articles. Also searched were Essential Evidence Plus, the National Guideline Clearinghouse, and the Cochrane Database of Systematic Reviews. Search dates: November 2013 through September 2014.

Figures 2 and 4 courtesy of Brent Lee Lechner, DO, Walter Reed National Military Medical Center, Bethesda, Md.

The views expressed in this paper are the authors' own and do not necessarily represent the views of the U.S. Army or the Department of Defense.

Kawasaki T. Acute febrile mucocutaneous syndrome with lymphoid involvement with specific desquamation of the fingers and toes in children. Arerugi. 1967;16(3):178-222.

Huang SK, Lin MT, Chen HC, Huang SC, Wu MH. Epidemiology of Kawasaki disease: prevalence from national database and future trends projection by system dynamics modeling. J Pediatr. 2013;163(1):126-131.e1.

Takahashi K, Oharaseki T, Yokouchi Y. Update on etio and immunopathogenesis of Kawasaki disease. Curr Opin Rheumatol. 2014;26(1):31-36.

Uehara R, Belay ED. Epidemiology of Kawasaki disease in Asia, Europe, and the United States. J Epidemiol. 2012;22(2):79-85.

Onouchi Y. Genetics of Kawasaki disease: what we know and don't know. Circ J. 2012;76(7):1581-1586.

Burns JC, Herzog L, Fabri O, et al.; Kawasaki Disease Global Climate Consortium. Seasonality of Kawasaki disease: a global perspective. PLoS One. 2013;8(9):e74529.

Newburger JW, Takahashi M, Gerber MA, et al. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. 2004;110(17):2747-2771.

JCS Joint Working Group. Guidelines for diagnosis and management of cardiovascular sequelae in Kawasaki disease (JCS 2008)—digest version. Circ J. 2010;74(9):1989-2020.

Ruan Y, Ye B, Zhao X. Clinical characteristics of Kawasaki syndrome and the risk factors for coronary artery lesions in China. Pediatr Infect Dis J. 2013;32(10):e397-e402.

Callinan LS, Tabnak F, Holman RC, et al. Kawasaki syndrome and factors associated with coronary artery abnormalities in California. Pediatr Infect Dis J. 2012;31(9):894-898.

Saundankar J, Yim D, Itotoh B, et al. The epidemiology and clinical features of Kawasaki disease in Australia. Pediatrics. 2014;133(4):e1009-e1014.

Cox JR, Sallis RE. Recognition of Kawasaki disease. Perm J. 2009;13(1):57-61.

Terai M, Shulman ST. Prevalence of coronary artery abnormalities in Kawasaki disease is highly dependent on gamma globulin dose but independent of salicylate dose. J Pediatr. 1997;131(6):888-893.

Lee G, Lee SE, Hong YM, Sohn S. Is high-dose aspirin necessary in the acute phase of Kawasaki disease?. Korean Circ J. 2013;43(3):182-186.

Baumer JH, Love SJ, Gupta A, Haines LC, Maconochie I, Dua JS. Salicylate for the treatment of Kawasaki disease in children. Cochrane Database Syst Rev. 2006;4:CD004175.

Chen S, Dong Y, Yin Y, Krucoff MW. Intravenous immunoglobulin plus corticosteroid to prevent coronary artery abnormalities in Kawasaki disease: a meta-analysis. Heart. 2013;99(2):76-82.

Sato YZ, Molkara DP, Daniels LB, et al. Cardiovascular biomarkers in acute Kawasaki disease. Int J Cardiol. 2013;164(1):58-63.

Kobayashi T, Kobayashi T, Morikawa A, et al. Efficacy of intravenous immunoglobulin combined with prednisolone following resistance to initial intravenous immunoglobulin treatment of acute Kawasaki disease. J Pediatr. 2013;163(2):521-526.

Mori M, Imagawa T, Hara R, et al. Efficacy and limitation of infliximab treatment for children with Kawasaki disease intractable to intravenous immunoglobulin therapy: report of an open-label case series. J Rheumatol. 2012;39(4):864-867.

Son MB, Gauvreau K, Burns JC, et al. Infliximab for intravenous immunoglobulin resistance in Kawasaki disease: a retrospective study. J Pediatr. 2011;158(4):644-649.e1.

Tremoulet AH, Jain S, Jaggi P, et al. Infliximab for intensification of primary therapy for Kawasaki disease: a phase 3 randomised, double-blind, placebo-controlled trial. Lancet. 2014;383(9930):1731-1738.

Hokosaki T, Mori M, Nishizawa T, et al. Long-term efficacy of plasma exchange treatment for refractory Kawasaki disease. Pediatr Int. 2012;54(1):99-103.

Gersony WM. The adult after Kawasaki disease the risks for late coronary events. J Am Coll Cardiol. 2009;54(21):1921-1923.

Tobayama H, Takahashi K, Fukunaga H, et al. Analysis of arterial function in adults with a history of Kawasaki disease. J Cardiol. 2013;61(5):330-335.

Ishikawa T, Iwashima S. Endothelial dysfunction in children within 5 years after onset of Kawasaki disease. J Pediatr. 2013;163(4):1117-1121.

Gupta-Malhotra M, Gruber D, Abraham SS, et al. Atherosclerosis in survivors of Kawasaki disease. J Pediatr. 2009;155(4):572-577.

Holve TJ, Patel A, Chau Q, Marks AR, Meadows A, Zaroff JG. Long-term cardiovascular outcomes in survivors of Kawasaki disease. Pediatrics. 2014;133(2):e305-e311.

Selamet Tierney ES, Gal D, Gauvreau K, et al. Vascular health in Kawasaki disease. J Am Coll Cardiol. 2013;62(12):1114-1121.

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Kawasaki Disease

Kawasaki disease (KD), also known as mucocutaneous lymph node syndrome or infantile polyarteritis, is a medium-sized necrotizing vasculitis that predominantly affects children < 5 years of age. The e tiology is currently unknown, but it is postulated to involve a combination of environmental and genetic factors. Multiple systems are involved, but the disease displays a predilection for the coronary arteries, which may lead to serious complications. The diagnosis can be made based on clinical criteria. In cases where incomplete KD may be suspected, the diagnosis may be supported by laboratory studies and echocardiography. Management involves intravenous immunoglobulin and high-dose aspirin Aspirin The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. Nonsteroidal Antiinflammatory Drugs (NSAIDs) . Follow-up requires serial echocardiograms to monitor for coronary artery Coronary Artery Truncus Arteriosus aneurysm Aneurysm An aneurysm is a bulging, weakened area of a blood vessel that causes an abnormal widening of its diameter > 1.5 times the size of the native vessel. Aneurysms occur more often in arteries than in veins and are at risk of dissection and rupture, which can be life-threatening. Thoracic Aortic Aneurysms .

Last updated: May 16, 2024

Epidemiology and Etiology

Pathophysiology, clinical presentation, complications, differential diagnosis.

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Epidemiology

One of the most common vasculitides Vasculitides Vasculitides are a group of conditions characterized by vasculitis, ischemia, and damage to the organs supplied by the affected vessels. The affected arteries are of different sizes and locations and vary by the type of vasculitis. Vasculitides of childhood
Boys are more commonly affected than girls.
80%–90% of cases are in children younger than 5 years of age.
Highest incidence Incidence The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from prevalence, which refers to all cases in the population at a given time. Measures of Disease Frequency in children who live in East Asia ASIA Spinal Cord Injuries or are of Asian ancestry living in other parts of the world
Overall annual incidence Incidence The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from prevalence, which refers to all cases in the population at a given time. Measures of Disease Frequency of 20 per 100,000 children younger than 5 years in the United States
¼ of adult cases occur in patients Patients Individuals participating in the health care system for the purpose of receiving therapeutic, diagnostic, or preventive procedures. Clinician–Patient Relationship with HIV HIV Anti-HIV Drugs .

The etiology of Kawasaki disease (KD) is unknown. There are several theories:

Immunologic response theory:

Neutrophils Neutrophils Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes. Innate Immunity: Phagocytes and Antigen Presentation
CD8+ T cells T cells Lymphocytes responsible for cell-mediated immunity. Two types have been identified – cytotoxic (t-lymphocytes, cytotoxic) and helper T-lymphocytes (t-lymphocytes, helper-inducer). They are formed when lymphocytes circulate through the thymus gland and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen. T cells: Types and Functions
Eosinophils Eosinophils Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. Innate Immunity: Phagocytes and Antigen Presentation
IgA IgA Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory iga is the main immunoglobulin in secretions. Immunoglobulins: Types and Functions plasma Plasma The residual portion of blood that is left after removal of blood cells by centrifugation without prior blood coagulation. Transfusion Products cells
Macrophages Macrophages The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood monocytes. Main types are peritoneal macrophages; alveolar macrophages; histiocytes; kupffer cells of the liver; and osteoclasts. They may further differentiate within chronic inflammatory lesions to epithelioid cells or may fuse to form foreign body giant cells or langhans giant cells. Innate Immunity: Phagocytes and Antigen Presentation (unique among the vasculitides Vasculitides Vasculitides are a group of conditions characterized by vasculitis, ischemia, and damage to the organs supplied by the affected vessels. The affected arteries are of different sizes and locations and vary by the type of vasculitis. Vasculitides )
Adrenomedullin
Granulin
The stimulus for this gene Gene A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms. Basic Terms of Genetics expression and inflammatory infiltration is unknown.

Infection theory:

Febrile exanthem Exanthem Diseases in which skin eruptions or rashes are a prominent manifestation. Classically, six such diseases were described with similar rashes; they were numbered in the order in which they were reported. Only the fourth (Duke’s disease), fifth (erythema infectiosum), and sixth (exanthema subitum) numeric designations survive as occasional synonyms in current terminology. Varicella-Zoster Virus/Chickenpox with lymphadenitis Lymphadenitis Inflammation of the lymph nodes. Peritonsillar Abscess and mucositis Mucositis Stomatitis is a general term referring to inflammation of the mucous membranes of the mouth, which may include sores. Stomatitis can be caused by infections, autoimmune disorders, allergic reactions, or exposure to irritants. The typical presentation may be either solitary or a group of painful oral lesions. Stomatitis
↑ Incidence Incidence The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from prevalence, which refers to all cases in the population at a given time. Measures of Disease Frequency during winter Winter Pityriasis Rosea and summer
Occurs in epidemics Epidemics Sudden outbreaks of a disease in a country or region not previously recognized in that area, or a rapid increase in the number of new cases of a previous existing endemic disease. Epidemics can also refer to outbreaks of disease in animal or plant populations. Influenza Viruses/Influenza
Boys > girls
↑ Incidence Incidence The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from prevalence, which refers to all cases in the population at a given time. Measures of Disease Frequency in younger children
Adenovirus Adenovirus Adenovirus (member of the family Adenoviridae) is a nonenveloped, double-stranded DNA virus. Adenovirus is transmitted in a variety of ways, and it can have various presentations based on the site of entry. Presentation can include febrile pharyngitis, conjunctivitis, acute respiratory disease, atypical pneumonia, and gastroenteritis. Adenovirus
Cytomegalovirus Cytomegalovirus CMV is a ubiquitous double-stranded DNA virus belonging to the Herpesviridae family. CMV infections can be transmitted in bodily fluids, such as blood, saliva, urine, semen, and breast milk. The initial infection is usually asymptomatic in the immunocompetent host, or it can present with symptoms of mononucleosis. Cytomegalovirus
Rotavirus Rotavirus A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. Seven species (rotaviruses A through G) are recognized. Rotavirus
Bacterial: Mycoplasma Mycoplasma Mycoplasma is a species of pleomorphic bacteria that lack a cell wall, which makes them difficult to target with conventional antibiotics and causes them to not gram stain well. Mycoplasma bacteria commonly target the respiratory and urogenital epithelium. Mycoplasma pneumoniae (M. pneumoniae), the causative agent of atypical or “walking” pneumonia. Mycoplasma

Genetic predisposition theory:

Asian populations
Family members (siblings of those affected with KD have a higher likelihood of also developing KD than the general population)
Variations and polymorphisms of genes Genes A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms. DNA Types and Structure related to immune regulation and vascular homeostasis Homeostasis The processes whereby the internal environment of an organism tends to remain balanced and stable. Cell Injury and Death have been associated with KD.

Environmental factors theory:

Mercury Mercury A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200. 59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. Renal Tubular Acidosis
Dust mites Mites Any arthropod of the subclass acari except the ticks. They are minute animals related to the spiders, usually having transparent or semitransparent bodies. They may be parasitic on humans and domestic animals, producing various irritations of the skin (mite infestations). Many mite species are important to human and veterinary medicine as both parasite and vector. Mites also infest plants. Scabies
Rug shampoo
Pollen
Lacks supporting evidence

Commonly presenting symptoms

> 101.3°F (38.5°C)
Minimally responsive to antipyretics
Presents with great variability (polymorphous)
Usually NOT vesicular
Found on trunk, extremities, and perineal regions
Often described as “unconsolable”
Decreased activity and appetite are common.
Bilateral
Nonexudative
Limbic sparing
Begins within days of fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever
Sometimes seen with photophobia Photophobia Abnormal sensitivity to light. This may occur as a manifestation of eye diseases; migraine; subarachnoid hemorrhage; meningitis; and other disorders. Photophobia may also occur in association with depression and other mental disorders. Migraine Headache
Erythema Erythema Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of disease processes. Chalazion of the lips Lips The lips are the soft and movable most external parts of the oral cavity. The blood supply of the lips originates from the external carotid artery, and the innervation is through cranial nerves. Lips and Tongue: Anatomy and oral mucosa Oral mucosa Lining of the oral cavity, including mucosa on the gums; the palate; the lip; the cheek; floor of the mouth; and other structures. The mucosa is generally a nonkeratinized stratified squamous epithelium covering muscle, bone, or glands but can show varying degree of keratinization at specific locations. Stomatitis
“Strawberry tongue Tongue The tongue, on the other hand, is a complex muscular structure that permits tasting and facilitates the process of mastication and communication. The blood supply of the tongue originates from the external carotid artery, and the innervation is through cranial nerves. Lips and Tongue: Anatomy ”
Swelling Swelling Inflammation and/or erythema Erythema Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of disease processes. Chalazion on palms and soles
Periungual desquamation Desquamation Staphylococcal Scalded Skin Syndrome (SSSS)
Generally seen late in course of disease
Least consistent manifestation of KD
Tends to involve anterior cervical chain nodes
Nonspecific prodrome Prodrome Symptoms that appear 24–48 hours prior to migraine onset. Migraine Headache of respiratory or gastrointestinal (GI) symptoms

Edema and a polymorphous rash on the hands and feet in a 3-month-old patient with KD

Lip fissuring alongside a polymorphous rash in KD

Bilateral, non-exudative conjunctivitis observed in a patient with KD

Desquamation of fingers in kawasaki disease

Desquamation of the fingertips observed in KD at 10–14 days

Strawberry tongue and bright-red, swollen lips with vertical cracking and bleeding in a patient with KD

Less common manifestations

Diagnostic criteria.

Bilateral, non-exudative conjunctival injection
Fissured lips Lips The lips are the soft and movable most external parts of the oral cavity. The blood supply of the lips originates from the external carotid artery, and the innervation is through cranial nerves. Lips and Tongue: Anatomy
Strawberry tongue Tongue The tongue, on the other hand, is a complex muscular structure that permits tasting and facilitates the process of mastication and communication. The blood supply of the tongue originates from the external carotid artery, and the innervation is through cranial nerves. Lips and Tongue: Anatomy
Injected pharynx Pharynx The pharynx is a component of the digestive system that lies posterior to the nasal cavity, oral cavity, and larynx. The pharynx can be divided into the oropharynx, nasopharynx, and laryngopharynx. Pharyngeal muscles play an integral role in vital processes such as breathing, swallowing, and speaking. Pharynx: Anatomy
Erythema Erythema Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of disease processes. Chalazion of palms/soles
Edema Edema Edema is a condition in which excess serous fluid accumulates in the body cavity or interstitial space of connective tissues. Edema is a symptom observed in several medical conditions. It can be categorized into 2 types, namely, peripheral (in the extremities) and internal (in an organ or body cavity). Edema of hands/feet
Erythematous polymorphous rash Rash Rocky Mountain Spotted Fever
Cervical lymphadenopathy Lymphadenopathy Lymphadenopathy is lymph node enlargement (> 1 cm) and is benign and self-limited in most patients. Etiologies include malignancy, infection, and autoimmune disorders, as well as iatrogenic causes such as the use of certain medications. Generalized lymphadenopathy often indicates underlying systemic disease. Lymphadenopathy : at least 1 node > 1.5 cm in diameter
If < 4 criteria → incomplete Kawasaki, supplement with laboratories below

Diagnostic algorithm for children with fever/diagnosis of Kawasaki disease: Units: CRP in mg/dL; erythrocyte sedimentation rate (ESR) in mm/hr Positive labs (≥ 3 supplemental laboratory findings) include: Anemia (for age) ↑ Platelet count ↑ WBC ↓ Albumin ↑ ALT Pyuria

To recall the important clinical criteria for KD, remember CRASH and Burn :

C onjunctivitis R ash A denopathy S trawberry tongue Tongue The tongue, on the other hand, is a complex muscular structure that permits tasting and facilitates the process of mastication and communication. The blood supply of the tongue originates from the external carotid artery, and the innervation is through cranial nerves. Lips and Tongue: Anatomy H ands and feet Burn: fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever

Laboratory and imaging studies

↑ Platelet counts Platelet counts The number of platelets per unit volume in a sample of venous blood. Coagulation Studies
Anemia Anemia Anemia is a condition in which individuals have low Hb levels, which can arise from various causes. Anemia is accompanied by a reduced number of RBCs and may manifest with fatigue, shortness of breath, pallor, and weakness. Subtypes are classified by the size of RBCs, chronicity, and etiology. Anemia: Overview and Types
↑ Aspartate Aspartate One of the non-essential amino acids commonly occurring in the l-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. Synthesis of Nonessential Amino Acids aminotransferase ( AST AST Enzymes of the transferase class that catalyze the conversion of l-aspartate and 2-ketoglutarate to oxaloacetate and l-glutamate. Liver Function Tests ) and alanine Alanine A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. Synthesis of Nonessential Amino Acids aminotransferase ( ALT ALT An enzyme that catalyzes the conversion of l-alanine and 2-oxoglutarate to pyruvate and l-glutamate. Liver Function Tests )
↓ Albumin Albumin Serum albumin from humans. It is an essential carrier of both endogenous substances, such as fatty acids and bilirubin, and of xenobiotics in the blood. Liver Function Tests
↑ Erythrocyte sedimentation rate Erythrocyte Sedimentation Rate Soft Tissue Abscess ( ESR ESR Soft Tissue Abscess )
Urinalysis Urinalysis Examination of urine by chemical, physical, or microscopic means. Routine urinalysis usually includes performing chemical screening tests, determining specific gravity, observing any unusual color or odor, screening for bacteriuria, and examining the sediment microscopically. Urinary Tract Infections (UTIs) in Children : sterile Sterile Basic Procedures pyuria Pyuria The presence of white blood cells (leukocytes) in the urine. It is often associated with bacterial infections of the urinary tract. Pyuria without bacteriuria can be caused by tuberculosis, stones, or cancer. Urinary Tract Infections (UTIs)
May demonstrate changes related to myocarditis Myocarditis Myocarditis is an inflammatory disease of the myocardium, which may occur alone or in association with a systemic process. There are numerous etiologies of myocarditis, but all lead to inflammation and myocyte injury, most often leading to signs and symptoms of heart failure. Myocarditis , pericarditis Pericarditis Pericarditis is an inflammation of the pericardium, often with fluid accumulation. It can be caused by infection (often viral), myocardial infarction, drugs, malignancies, metabolic disorders, autoimmune disorders, or trauma. Acute, subacute, and chronic forms exist. Pericarditis , or myocardial ischemia Myocardial ischemia A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary artery disease), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Coronary Heart Disease /infarction
↑ PR interval PR interval Electrocardiogram (ECG)
Low voltage
↑ Size of left anterior descending artery or right coronary artery Right coronary artery Heart: Anatomy
Coronary artery Coronary Artery Truncus Arteriosus aneurysm Aneurysm An aneurysm is a bulging, weakened area of a blood vessel that causes an abnormal widening of its diameter > 1.5 times the size of the native vessel. Aneurysms occur more often in arteries than in veins and are at risk of dissection and rupture, which can be life-threatening. Thoracic Aortic Aneurysms observed
↓ Left ventricular function
Valvular dysfunction (e.g., regurgitation Regurgitation Gastroesophageal Reflux Disease (GERD) )
Pericardial effusion Pericardial effusion Fluid accumulation within the pericardium. Serous effusions are associated with pericardial diseases. Hemopericardium is associated with trauma. Lipid-containing effusion (chylopericardium) results from leakage of thoracic duct. Severe cases can lead to cardiac tamponade. Pericardial Effusion and Cardiac Tamponade
Should be performed in all patients Patients Individuals participating in the health care system for the purpose of receiving therapeutic, diagnostic, or preventive procedures. Clinician–Patient Relationship with KD
Establishes a reference point for longitudinal follow-up
Determines treatment efficacy
Used to observe aneurysms already detected via echocardiogram Echocardiogram Transposition of the Great Vessels
Not used for initial detection or diagnosis

Echocardiography view at the level of aortic valve demonstrating an increase in the size of a coronary artery aneurysm (arrowheads) secondary to KD

Angiography of a patient with KD showing ectatic left anterior descending coronary artery, with the largest aneurysm measuring 6.5 mm in diameter.

Kawasaki disease is self-limited!
Treatment is aimed at preventing complications and reducing symptoms.
2 g/kg administered as a single infusion over 8–12 hours
Started within 10 days of fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever onset, it reduces the risk of coronary artery Coronary Artery Truncus Arteriosus aneurysms.
Observe for 24 hours following completion of IVIG IVIG Dermatomyositis infusion to confirm fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever resolution.
Patients Patients Individuals participating in the health care system for the purpose of receiving therapeutic, diagnostic, or preventive procedures. Clinician–Patient Relationship at high risk for IVIG IVIG Dermatomyositis resistance Resistance Physiologically, the opposition to flow of air caused by the forces of friction. As a part of pulmonary function testing, it is the ratio of driving pressure to the rate of air flow. Ventilation: Mechanics of Breathing are additionally treated with systemic glucocorticoids Systemic Glucocorticoids Glucocorticoids .
30–50 mg/kg daily divided into 4 doses
Anti-inflammatory and antiplatelet effects
Prevents thrombus in coronary arteries Arteries Arteries are tubular collections of cells that transport oxygenated blood and nutrients from the heart to the tissues of the body. The blood passes through the arteries in order of decreasing luminal diameter, starting in the largest artery (the aorta) and ending in the small arterioles. Arteries are classified into 3 types: large elastic arteries, medium muscular arteries, and small arteries and arterioles. Arteries: Histology
Follow-up with serial echocardiograms at 2 and 6 weeks
KD shock Shock Shock is a life-threatening condition associated with impaired circulation that results in tissue hypoxia. The different types of shock are based on the underlying cause: distributive (↑ cardiac output (CO), ↓ systemic vascular resistance (SVR)), cardiogenic (↓ CO, ↑ SVR), hypovolemic (↓ CO, ↑ SVR), obstructive (↓ CO), and mixed. Types of Shock syndrome (KDSS) is sustained systolic hypotension Hypotension Hypotension is defined as low blood pressure, specifically Hypotension or clinical signs of poor perfusion.
Thrombocytosis
Younger age
Coronary artery Coronary Artery Truncus Arteriosus abnormalities
Coronary artery Coronary Artery Truncus Arteriosus dilation, aneurysm Aneurysm An aneurysm is a bulging, weakened area of a blood vessel that causes an abnormal widening of its diameter > 1.5 times the size of the native vessel. Aneurysms occur more often in arteries than in veins and are at risk of dissection and rupture, which can be life-threatening. Thoracic Aortic Aneurysms , and/or stenosis Stenosis Hypoplastic Left Heart Syndrome (HLHS)
Myocardial ischemia Myocardial ischemia A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary artery disease), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Coronary Heart Disease or infarction
Ventricular dysfunction
Valvular regurgitation Regurgitation Gastroesophageal Reflux Disease (GERD)
Pericardial effusions
Monitor with serial echocardiograms.
Activation and proliferation of macrophages Macrophages The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood monocytes. Main types are peritoneal macrophages; alveolar macrophages; histiocytes; kupffer cells of the liver; and osteoclasts. They may further differentiate within chronic inflammatory lesions to epithelioid cells or may fuse to form foreign body giant cells or langhans giant cells. Innate Immunity: Phagocytes and Antigen Presentation and T cells T cells Lymphocytes responsible for cell-mediated immunity. Two types have been identified – cytotoxic (t-lymphocytes, cytotoxic) and helper T-lymphocytes (t-lymphocytes, helper-inducer). They are formed when lymphocytes circulate through the thymus gland and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen. T cells: Types and Functions
Disseminated intravascular coagulopathy
Cytopenias Cytopenias IPEX Syndrome
Thrombosis Thrombosis Formation and development of a thrombus or blood clot in the blood vessel. Epidemic Typhus
Caused by peripheral arterial obstruction
Can involve the viscera or limbs
Sterile Sterile Basic Procedures pyuria Pyuria The presence of white blood cells (leukocytes) in the urine. It is often associated with bacterial infections of the urinary tract. Pyuria without bacteriuria can be caused by tuberculosis, stones, or cancer. Urinary Tract Infections (UTIs) (common)
Acute interstitial nephritis Acute interstitial nephritis Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of kidney tubules and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see glomerulonephritis. Infiltration of the inflammatory cells into the interstitial compartment results in edema, increased spaces between the tubules, and tubular renal dysfunction. Acute Kidney Injury
Mild proteinuria Proteinuria The presence of proteins in the urine, an indicator of kidney diseases. Nephrotic Syndrome in Children
Acute kidney injury Acute Kidney Injury Acute kidney injury refers to sudden and often reversible loss of renal function, which develops over days or weeks. Azotemia refers to elevated levels of nitrogen-containing substances in the blood that accompany AKI, which include BUN and creatinine. Acute Kidney Injury
Hydrops Hydrops Cholecystitis of the gallbladder Gallbladder The gallbladder is a pear-shaped sac, located directly beneath the liver, that sits on top of the superior part of the duodenum. The primary functions of the gallbladder include concentrating and storing up to 50 mL of bile. Gallbladder and Biliary Tract: Anatomy is a common finding during KD’s acute phase Acute phase Short Bowel Syndrome
Rapidly resolves upon IVIG IVIG Dermatomyositis administration
Irritability is a common feature of KD’s acute phase Acute phase Short Bowel Syndrome
Thought to be related to CSF pleocytosis Pleocytosis Tick-borne Encephalitis Virus
Sensorineural hearing loss Sensorineural hearing loss Hearing loss resulting from damage to the cochlea and the sensorineural elements which lie internally beyond the oval and round windows. These elements include the auditory nerve and its connections in the brainstem. Hearing Loss : can occur in KD’s acute phase Acute phase Short Bowel Syndrome , but rarely persists
Scarlet fever Scarlet fever Infection with group a Streptococci that is characterized by tonsillitis and pharyngitis. An erythematous rash is commonly present. Scarlet Fever : a disease that occurs as a result of a group A streptococcal infection, also known as Streptococcus Streptococcus Streptococcus is one of the two medically important genera of gram-positive cocci, the other being Staphylococcus. Streptococci are identified as different species on blood agar on the basis of their hemolytic pattern and sensitivity to optochin and bacitracin. There are many pathogenic species of streptococci, including S. pyogenes, S. agalactiae, S. pneumoniae, and the viridans streptococci. Streptococcus Pyogenes . Signs and symptoms include sore throat Sore throat Pharyngitis is an inflammation of the back of the throat (pharynx). Pharyngitis is usually caused by an upper respiratory tract infection, which is viral in most cases. It typically results in a sore throat and fever. Other symptoms may include a runny nose, cough, headache, and hoarseness. Pharyngitis , fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever , headaches, swollen lymph nodes Lymph Nodes They are oval or bean shaped bodies (1 – 30 mm in diameter) located along the lymphatic system. Lymphatic Drainage System: Anatomy , a characteristic rash Rash Rocky Mountain Spotted Fever (red and sandpaper-like), and red/bumpy tongue Tongue The tongue, on the other hand, is a complex muscular structure that permits tasting and facilitates the process of mastication and communication. The blood supply of the tongue originates from the external carotid artery, and the innervation is through cranial nerves. Lips and Tongue: Anatomy . The exudative pharyngitis Pharyngitis Pharyngitis is an inflammation of the back of the throat (pharynx). Pharyngitis is usually caused by an upper respiratory tract infection, which is viral in most cases. It typically results in a sore throat and fever. Other symptoms may include a runny nose, cough, headache, and hoarseness. Pharyngitis in KD can be confused with streptococcal pharyngitis Streptococcal Pharyngitis Rheumatic Fever . The diagnosis of scarlet fever Scarlet fever Infection with group a Streptococci that is characterized by tonsillitis and pharyngitis. An erythematous rash is commonly present. Scarlet Fever is usually confirmed with rapid antigen detection Antigen detection Respiratory Syncytial Virus or throat Throat The pharynx is a component of the digestive system that lies posterior to the nasal cavity, oral cavity, and larynx. The pharynx can be divided into the oropharynx, nasopharynx, and laryngopharynx. Pharyngeal muscles play an integral role in vital processes such as breathing, swallowing, and speaking. Pharynx: Anatomy culture. Management is with penicillin Penicillin Rheumatic Fever or amoxicillin Amoxicillin A broad-spectrum semisynthetic antibiotic similar to ampicillin except that its resistance to gastric acid permits higher serum levels with oral administration. Penicillins .
Measles Measles Measles (also known as rubeola) is caused by a single-stranded, linear, negative-sense RNA virus of the family Paramyxoviridae. It is highly contagious and spreads by respiratory droplets or direct-contact transmission from an infected person. Typically a disease of childhood, measles classically starts with cough, coryza, and conjunctivitis, followed by a maculopapular rash. Measles Virus : infection by the paramyxovirus Paramyxovirus Mumps Virus/Mumps that presents with fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever , conjunctivitis Conjunctivitis Conjunctivitis is a common inflammation of the bulbar and/or palpebral conjunctiva. It can be classified into infectious (mostly viral) and noninfectious conjunctivitis, which includes allergic causes. Patients commonly present with red eyes, increased tearing, burning, foreign body sensation, and photophobia. Conjunctivitis , and a polymorphous rash Rash Rocky Mountain Spotted Fever that is highly contagious. Discrete intraoral lesions of KD can be confused with Koplik spots of measles Measles Measles (also known as rubeola) is caused by a single-stranded, linear, negative-sense RNA virus of the family Paramyxoviridae. It is highly contagious and spreads by respiratory droplets or direct-contact transmission from an infected person. Typically a disease of childhood, measles classically starts with cough, coryza, and conjunctivitis, followed by a maculopapular rash. Measles Virus . Diagnosis is made by viral polymerase chain reaction Polymerase chain reaction Polymerase chain reaction (PCR) is a technique that amplifies DNA fragments exponentially for analysis. The process is highly specific, allowing for the targeting of specific genomic sequences, even with minuscule sample amounts. The PCR cycles multiple times through 3 phases: denaturation of the template DNA, annealing of a specific primer to the individual DNA strands, and synthesis/elongation of new DNA molecules. Polymerase Chain Reaction (PCR) ( PCR PCR Polymerase chain reaction (PCR) is a technique that amplifies DNA fragments exponentially for analysis. The process is highly specific, allowing for the targeting of specific genomic sequences, even with minuscule sample amounts. The PCR cycles multiple times through 3 phases: denaturation of the template DNA, annealing of a specific primer to the individual DNA strands, and synthesis/elongation of new DNA molecules. Polymerase Chain Reaction (PCR) ), and management involves isolation and supportive treatment.
Lyme disease Lyme disease Lyme disease is a tick-borne infection caused by the gram-negative spirochete Borrelia burgdorferi. Lyme disease is transmitted by the black-legged Ixodes tick (known as a deer tick), which is only found in specific geographic regions. Patient presentation can vary depending on the stage of the disease and may include a characteristic erythema migrans rash. Lyme Disease : an infectious disease caused by Borrelia burgdorferi Borrelia burgdorferi A specific species of bacteria, part of the borrelia burgdorferi group, whose common name is lyme disease spirochete. Borrelia , which spreads by ticks Ticks Blood-sucking acarid parasites of the order ixodida comprising two families: the softbacked ticks (argasidae) and hardbacked ticks (ixodidae). Ticks are larger than their relatives, the mites. They penetrate the skin of their host by means of highly specialized, hooked mouth parts and feed on its blood. Ticks attack all groups of terrestrial vertebrates. In humans they are responsible for many tick-borne diseases, including the transmission of rocky mountain spotted fever; tularemia; babesiosis; african swine fever; and relapsing fever. Coxiella/Q Fever . The most common sign is erythema Erythema Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of disease processes. Chalazion migrans that appear at the site of a tick bite about a week after it occurred. Other symptoms are joint pain Pain An unpleasant sensation induced by noxious stimuli which are detected by nerve endings of nociceptive neurons. Pain: Types and Pathways , severe headache Headache The symptom of pain in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of headache disorders. Brain Abscess , neck stiffness Neck Stiffness Meningitis or heart palpitations Palpitations Ebstein’s Anomaly . Diagnosis relies on clinical findings and tick exposure, and is supported by serologic testing. Antibiotics, such as doxycycline, are used for treatment.
Rocky Mountain spotted fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever : A bacterial infection that spreads by a bite from an infected tick. Symptoms include vomiting Vomiting The forcible expulsion of the contents of the stomach through the mouth. Hypokalemia , a sudden high fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever , headache Headache The symptom of pain in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of headache disorders. Brain Abscess , abdominal pain Abdominal Pain Acute Abdomen , rash Rash Rocky Mountain Spotted Fever , and muscle aches. Diagnosis is based on the clinical features, biopsy Biopsy Removal and pathologic examination of specimens from the living body. Ewing Sarcoma of the rash Rash Rocky Mountain Spotted Fever , and serologic testing. Treatment involves antibiotics, such as doxycycline.
Rotavirus Rotavirus A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. Seven species (rotaviruses A through G) are recognized. Rotavirus : Rotavirus Rotavirus A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. Seven species (rotaviruses A through G) are recognized. Rotavirus is a common cause of severe gastroenteritis Gastroenteritis Gastroenteritis is inflammation of the stomach and intestines, commonly caused by infections from bacteria, viruses, or parasites. Transmission may be foodborne, fecal-oral, or through animal contact. Common clinical features include abdominal pain, diarrhea, vomiting, fever, and dehydration. Gastroenteritis . The nonspecific prodrome Prodrome Symptoms that appear 24–48 hours prior to migraine onset. Migraine Headache of gastrointestinal (GI) symptoms such as diarrhea Diarrhea Diarrhea is defined as ≥ 3 watery or loose stools in a 24-hour period. There are a multitude of etiologies, which can be classified based on the underlying mechanism of disease. The duration of symptoms (acute or chronic) and characteristics of the stools (e.g., watery, bloody, steatorrheic, mucoid) can help guide further diagnostic evaluation. Diarrhea , abdominal pain Abdominal Pain Acute Abdomen , and vomiting Vomiting The forcible expulsion of the contents of the stomach through the mouth. Hypokalemia that can be seen in KD can be confused with an infection due to rotavirus Rotavirus A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. Seven species (rotaviruses A through G) are recognized. Rotavirus . Diagnostic testing for rotavirus Rotavirus A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. Seven species (rotaviruses A through G) are recognized. Rotavirus is generally not required. Oral rehydration Rehydration Dengue Virus therapy is the mainstay of treatment.
Pneumonia Pneumonia Pneumonia or pulmonary inflammation is an acute or chronic inflammation of lung tissue. Causes include infection with bacteria, viruses, or fungi. In more rare cases, pneumonia can also be caused through toxic triggers through inhalation of toxic substances, immunological processes, or in the course of radiotherapy. Pneumonia : an acute or chronic inflammation Chronic Inflammation Inflammation of lung tissue caused by infection with bacteria Bacteria Bacteria are prokaryotic single-celled microorganisms that are metabolically active and divide by binary fission. Some of these organisms play a significant role in the pathogenesis of diseases. Bacteriology , viruses Viruses Minute infectious agents whose genomes are composed of DNA or RNA, but not both. They are characterized by a lack of independent metabolism and the inability to replicate outside living host cells. Virology , or fungi Fungi A kingdom of eukaryotic, heterotrophic organisms that live parasitically as saprobes, including mushrooms; yeasts; smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi, commonly known as molds, refer to those that grow as multicellular colonies. Mycology that is considered a routine childhood illness. The nonspecific prodrome Prodrome Symptoms that appear 24–48 hours prior to migraine onset. Migraine Headache of respiratory and GI symptoms of KD can be mistaken for pneumonia Pneumonia Pneumonia or pulmonary inflammation is an acute or chronic inflammation of lung tissue. Causes include infection with bacteria, viruses, or fungi. In more rare cases, pneumonia can also be caused through toxic triggers through inhalation of toxic substances, immunological processes, or in the course of radiotherapy. Pneumonia . Diagnosis of pneumonia Pneumonia Pneumonia or pulmonary inflammation is an acute or chronic inflammation of lung tissue. Causes include infection with bacteria, viruses, or fungi. In more rare cases, pneumonia can also be caused through toxic triggers through inhalation of toxic substances, immunological processes, or in the course of radiotherapy. Pneumonia is based on the clinical history and examination, and supported by imaging (such as a chest X-ray X-ray Penetrating electromagnetic radiation emitted when the inner orbital electrons of an atom are excited and release radiant energy. X-ray wavelengths range from 1 pm to 10 nm. Hard x-rays are the higher energy, shorter wavelength x-rays. Soft x-rays or grenz rays are less energetic and longer in wavelength. The short wavelength end of the x-ray spectrum overlaps the gamma rays wavelength range. The distinction between gamma rays and x-rays is based on their radiation source. Pulmonary Function Tests ). Management involves supportive care and antimicrobial agents based on the etiology.
Adenovirus Adenovirus Adenovirus (member of the family Adenoviridae) is a nonenveloped, double-stranded DNA virus. Adenovirus is transmitted in a variety of ways, and it can have various presentations based on the site of entry. Presentation can include febrile pharyngitis, conjunctivitis, acute respiratory disease, atypical pneumonia, and gastroenteritis. Adenovirus : causes mild upper respiratory infections Infections Invasion of the host organism by microorganisms or their toxins or by parasites that can cause pathological conditions or diseases. Chronic Granulomatous Disease in young children. The prodrome Prodrome Symptoms that appear 24–48 hours prior to migraine onset. Migraine Headache of nonspecific respiratory symptoms and accompanying nonexudative conjunctivitis Conjunctivitis Conjunctivitis is a common inflammation of the bulbar and/or palpebral conjunctiva. It can be classified into infectious (mostly viral) and noninfectious conjunctivitis, which includes allergic causes. Patients commonly present with red eyes, increased tearing, burning, foreign body sensation, and photophobia. Conjunctivitis in KD can be mistaken for a common upper respiratory infection Upper respiratory infection Rhinitis caused by adenovirus Adenovirus Adenovirus (member of the family Adenoviridae) is a nonenveloped, double-stranded DNA virus. Adenovirus is transmitted in a variety of ways, and it can have various presentations based on the site of entry. Presentation can include febrile pharyngitis, conjunctivitis, acute respiratory disease, atypical pneumonia, and gastroenteritis. Adenovirus . Diagnosis of adenovirus Adenovirus Adenovirus (member of the family Adenoviridae) is a nonenveloped, double-stranded DNA virus. Adenovirus is transmitted in a variety of ways, and it can have various presentations based on the site of entry. Presentation can include febrile pharyngitis, conjunctivitis, acute respiratory disease, atypical pneumonia, and gastroenteritis. Adenovirus is confirmed with PCR PCR Polymerase chain reaction (PCR) is a technique that amplifies DNA fragments exponentially for analysis. The process is highly specific, allowing for the targeting of specific genomic sequences, even with minuscule sample amounts. The PCR cycles multiple times through 3 phases: denaturation of the template DNA, annealing of a specific primer to the individual DNA strands, and synthesis/elongation of new DNA molecules. Polymerase Chain Reaction (PCR) and antigen Antigen Substances that are recognized by the immune system and induce an immune reaction. Vaccination testing. Most infections Infections Invasion of the host organism by microorganisms or their toxins or by parasites that can cause pathological conditions or diseases. Chronic Granulomatous Disease are self-limited, so management is generally supportive.
Meningitis Meningitis Meningitis is inflammation of the meninges, the protective membranes of the brain, and spinal cord. The causes of meningitis are varied, with the most common being bacterial or viral infection. The classic presentation of meningitis is a triad of fever, altered mental status, and nuchal rigidity. Meningitis : inflammation Inflammation Inflammation is a complex set of responses to infection and injury involving leukocytes as the principal cellular mediators in the body’s defense against pathogenic organisms. Inflammation is also seen as a response to tissue injury in the process of wound healing. The 5 cardinal signs of inflammation are pain, heat, redness, swelling, and loss of function. Inflammation of the meninges Meninges The brain and the spinal cord are enveloped by 3 overlapping layers of connective tissue called the meninges. The layers are, from the most external layer to the most internal layer, the dura mater, arachnoid mater, and pia mater. Between these layers are 3 potential spaces called the epidural, subdural, and subarachnoid spaces. Meninges: Anatomy most commonly caused by bacteria Bacteria Bacteria are prokaryotic single-celled microorganisms that are metabolically active and divide by binary fission. Some of these organisms play a significant role in the pathogenesis of diseases. Bacteriology and viruses Viruses Minute infectious agents whose genomes are composed of DNA or RNA, but not both. They are characterized by a lack of independent metabolism and the inability to replicate outside living host cells. Virology . Irritability is a common manifestation of KD and meningitis Meningitis Meningitis is inflammation of the meninges, the protective membranes of the brain, and spinal cord. The causes of meningitis are varied, with the most common being bacterial or viral infection. The classic presentation of meningitis is a triad of fever, altered mental status, and nuchal rigidity. Meningitis . Other presenting signs and symptoms include fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever , altered mental status Altered Mental Status Sepsis in Children , and nuchal rigidity Nuchal Rigidity Meningitis . Diagnosis is confirmed with CSF analysis CSF analysis Meningitis . Management includes immediate broad-spectrum Broad-Spectrum Fluoroquinolones antimicrobial therapy, which can be tailored once the offending pathogen is identified.
Stevens-Johnson syndrome Stevens-Johnson syndrome Stevens-Johnson syndrome (SJS) is a cutaneous, immune-mediated hypersensitivity reaction that is commonly triggered by medications, including antiepileptics and antibiotics. The condition runs on a spectrum with toxic epidermal necrolysis (TEN) based on the amount of body surface area (BSA) involved. Stevens-Johnson Syndrome ( SJS SJS Stevens-Johnson syndrome (SJS) is a cutaneous, immune-mediated hypersensitivity reaction that is commonly triggered by medications, including antiepileptics and antibiotics. The condition runs on a spectrum with toxic epidermal necrolysis (TEN) based on the amount of body surface area (BSA) involved. Stevens-Johnson Syndrome ) : immune-complex mediated hypersensitivity reaction that can be triggered by infectious etiologies Infectious Etiologies High-Risk Headaches or the use of anticonvulsants, antibiotics, or other drugs. The syndrome is characterized by epidermal necrolysis, separation of the epidermis Epidermis The external, nonvascular layer of the skin. It is made up, from within outward, of five layers of epithelium: (1) basal layer (stratum basale epidermidis); (2) spinous layer (stratum spinosum epidermidis); (3) granular layer (stratum granulosum epidermidis); (4) clear layer (stratum lucidum epidermidis); and (5) horny layer (stratum corneum epidermidis). Skin: Structure and Functions from the dermis Dermis A layer of vascularized connective tissue underneath the epidermis. The surface of the dermis contains innervated papillae. Embedded in or beneath the dermis are sweat glands; hair follicles; and sebaceous glands. Skin: Structure and Functions , and the formation of skin Skin The skin, also referred to as the integumentary system, is the largest organ of the body. The skin is primarily composed of the epidermis (outer layer) and dermis (deep layer). The epidermis is primarily composed of keratinocytes that undergo rapid turnover, while the dermis contains dense layers of connective tissue. Skin: Structure and Functions blisters and bullae Bullae Erythema Multiforme on the face, lips Lips The lips are the soft and movable most external parts of the oral cavity. The blood supply of the lips originates from the external carotid artery, and the innervation is through cranial nerves. Lips and Tongue: Anatomy , throat Throat The pharynx is a component of the digestive system that lies posterior to the nasal cavity, oral cavity, and larynx. The pharynx can be divided into the oropharynx, nasopharynx, and laryngopharynx. Pharyngeal muscles play an integral role in vital processes such as breathing, swallowing, and speaking. Pharynx: Anatomy , and extremities. The bullous or vesicular rash Rash Rocky Mountain Spotted Fever in KD can be mistaken for SJS SJS Stevens-Johnson syndrome (SJS) is a cutaneous, immune-mediated hypersensitivity reaction that is commonly triggered by medications, including antiepileptics and antibiotics. The condition runs on a spectrum with toxic epidermal necrolysis (TEN) based on the amount of body surface area (BSA) involved. Stevens-Johnson Syndrome . The diagnosis of SJS SJS Stevens-Johnson syndrome (SJS) is a cutaneous, immune-mediated hypersensitivity reaction that is commonly triggered by medications, including antiepileptics and antibiotics. The condition runs on a spectrum with toxic epidermal necrolysis (TEN) based on the amount of body surface area (BSA) involved. Stevens-Johnson Syndrome is usually clinical, and management is largely supportive. Withdrawal of any causative agent is required.
Epstein-Barr virus Epstein-Barr Virus Epstein-Barr virus (EBV) is a linear, double-stranded DNA virus belonging to the Herpesviridae family. This highly prevalent virus is mostly transmitted through contact with oropharyngeal secretions from an infected individual. The virus can infect epithelial cells and B lymphocytes, where it can undergo lytic replication or latency. Epstein-Barr Virus : causes infectious mononucleosis Mononucleosis Infectious mononucleosis (IM), also known as “the kissing disease,” is a highly contagious viral infection caused by the Epstein-Barr virus. Its common name is derived from its main method of transmission: the spread of infected saliva via kissing. Clinical manifestations of IM include fever, tonsillar pharyngitis, and lymphadenopathy. Mononucleosis and is associated with Burkitt’s lymphoma Lymphoma A general term for various neoplastic diseases of the lymphoid tissue. Imaging of the Mediastinum , hemophagocytic lymphohistiocytosis Hemophagocytic lymphohistiocytosis A group of related disorders characterized by lymphocytosis; histiocytosis; and hemophagocytosis. The two major forms are familial and reactive. Epstein-Barr Virus , and Hodgkin’s lymphoma Lymphoma A general term for various neoplastic diseases of the lymphoid tissue. Imaging of the Mediastinum . The generalized lymphadenopathy Generalized Lymphadenopathy Lymphadenopathy observed in KD can be mistaken for the generalized lymphadenopathy Generalized Lymphadenopathy Lymphadenopathy of infectious mononucleosis Mononucleosis Infectious mononucleosis (IM), also known as “the kissing disease,” is a highly contagious viral infection caused by the Epstein-Barr virus. Its common name is derived from its main method of transmission: the spread of infected saliva via kissing. Clinical manifestations of IM include fever, tonsillar pharyngitis, and lymphadenopathy. Mononucleosis . The diagnosis is clinical and confirmed through heterophile antibody testing or serology Serology The study of serum, especially of antigen-antibody reactions in vitro. Yellow Fever Virus . Management is supportive.
Sundel, R. (2020). Kawasaki disease: Clinical features and diagnosis. In TePas, E. (Ed.), UpToDate. Retrieved February 15, 2022, from https://www.uptodate.com/contents/kawasaki-disease-clinical-features-and-diagnosis
Sundel, R. (2020). Kawasaki disease: Epidemiology and etiology. In TePas, E. (Ed.), UpToDate. Retrieved February 15, 2022, from https://www.uptodate.com/contents/kawasaki-disease-epidemiology-and-etiology
Sundel, R. (2020). Kawasaki disease: Initial treatment and prognosis Prognosis A prediction of the probable outcome of a disease based on a individual’s condition and the usual course of the disease as seen in similar situations. Non-Hodgkin Lymphomas . In TePas, E. (Ed.), UpToDate. Retrieved February 15, 2022, from https://www.uptodate.com/contents/kawasaki-disease-initial-treatment-and-prognosis
Raab, C.P. (2021). Kawasaki disease. [online] MSD Manual Professional Version. Retrieved February 15, 2022, from https://www.msdmanuals.com/professional/pediatrics/miscellaneous-disorders-in-infants-and-children/kawasaki-disease
Modesti, A.M., and Plewa, M.C. (2021). Kawasaki disease. [online] StatPearls. Retrieved February 15, 2022, from https://www.ncbi.nlm.nih.gov/books/NBK537163/
Sosa, T.K., and Shah, S.S. (2018). Kawasaki disease. In Steele, R.W. (Ed.), Medscape. Retrieved February 15, 2022, from https://emedicine.medscape.com/article/965367-overview

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Kawasaki disease
4. • Kawasaki disease (KD), formerly known as Mucocutaneous lymph node syndrome and Infantile polyarteritis nodosa , is an acute febrile illness characterized by inflammation of blood vessels throughout the body that primarily affects young children and infants. • It is now the most common cause of acquired heart disease in children.
Kawasaki disease
Kawasaki disease - Download as a PDF or view online for free. Submit Search. Upload. ... simple presentation Kawasaki disease. ... These are simplified slides discussing the regulation of cardiac output and venous return. Learning objectives: 1. Comprehend the determinants of cardiac output and factors affecting cardiac output 2.
Kawasaki disease
4. HISTORY 1967 - Tomisaku Kawasaki reports a series of 50 patients and establishes the clinical criteria for diagnosis (in Japanese) 1974 - first English language report of Kawasaki syndrome by Kawasaki 1976 - first series of American patients reported by Melish, Hawaii 1977 - landing and Larson establish that Kawasaki disease and infantile polyarteritis nodosa are pathologically ...
Kawasaki Disease: Slideshow
The clinical presentation of Kawasaki disease can be divided into 3 stages. The acute stage begins with the onset of fever and lasts 1 to 2 weeks. ... From here, the disease spreads to the perineal region (see next slide). A few days after the appearance of the eruption shown in the previous slide, the disease may affect the perineal region ...
PPT
Kawasaki Disease (KD ) also known as Kawasaki Syndrome . • An unusual and serious illness of young children. It is an autoimmune disease that can effect any type of blood vessel in the body, including arteries, veins, and capillaries. Download Presentation. specific virus.
Kawasaki disease: Difficult case scenario and guidelines
Kawasaki disease is the most common cause of multisystem vasculitis in childhood. ... Download ppt "Kawasaki disease: Difficult case scenario and guidelines" Similar presentations . Hatem Eleishi, MD Rheumatologist STILL'S DISEASE. Kawasaki disease is a rare condition. It is most common in children under five years old and most cases occur in ...
Kawasaki Disease Clinical Presentation
Phases of Kawasaki disease. The clinical presentation of KD varies over time, with the clinical course conventionally divided into 3 stages: acute, subacute, and convalescent (see the image below). Some authors add a fourth, chronic, phase. Clinical manifestations and time course of Kawasaki disease. Stage 1: acutefebrilestage.
PPT
Kawasaki Disease: An Update of diagnosis and treatment This algorithm is a guide to evaluation of patients with suspected incomplete Kawasaki disease (KD). - A free PowerPoint PPT presentation (displayed as an HTML5 slide show) on PowerShow.com - id: 3e3365-YWMwM
PPT
AIM: • Review the clinical presentations of Kawasaki disease, its progression, serious complications and management. • Discuss the D/Dx of Kawasaki disease. S> • 14 m/o, M, ... KAWASAKI. AMOUNT OF PRODUCTION. KAWASAKI. 710 views • 22 slides. Kawasaki Ninja 250R. Kawasaki Ninja 250R. Background on the Ninja 250R. An entry-level 250cc ...
Kawasaki Disease
Kawasaki disease' presentation also overlaps with other immunologic reactions such as multiple drug hypersensitivity reactions, juvenile idiopathic arthritis, infantile polyarteritis nodosa, and systemic lupus erythematosus. These can be differentiated from KD by the absence of classic clinical criteria and by chronicity and the number of ...
Kawasaki Disease: Practice Essentials, Background, Pathophysiology
Practice Essentials. Kawasaki disease (KD), also known as mucocutaneous lymph node syndrome and Kawasaki syndrome, is an acute febrile illness of early childhood characterized by vasculitis of the medium-sized arteries. Given its predilection for the coronary arteries, there is a potential for the development of coronary artery aneurysms (CAAs ...
Kawasaki disease
In the acute stage of Kawasaki disease, systemic inflammatory changes are evident in many organs. [10] Joint pain (arthralgia) and swelling, frequently symmetrical, and arthritis can also occur. [26] Myocarditis, [45] diarrhea, [13] pericarditis, valvulitis, aseptic meningitis, pneumonitis, lymphadenitis, and hepatitis may be present and are ...
Kawasaki disease: Clinical features and diagnosis
The clinical features of KD reflect widespread inflammation of primarily medium-sized muscular arteries. Diagnosis is based upon evidence of systemic inflammation (eg, fever) in association with signs of mucocutaneous inflammation. The characteristic bilateral nonexudative conjunctivitis, erythema of the lips and oral mucosa, rash, extremity ...
PDF What is Kawasaki Disease?
Kawasaki disease (KD), also known as. Kawasaki syndrome or mucocutaneous. lymph node syndrome, affects children. It causes inflammation of the blood vessels, particularly the coronary arteries. The average age of those affected is 2 years — about 77% are younger than 5, and boys are 1.5 times more likely than girls to get KD.
2021 Update on the Clinical Management and Diagnosis of Kawasaki Disease
Kawasaki shock syndrome, the presentation of KD disease with systolic hypotension or clinical signs of poor perfusion, has also been described as a rare presentation of KD . Multiorgan Involvement KD is a vasculitis that affects all medium-sized arteries in multiple organs/tissues, resulting in systemic inflammation and pathology can develop in ...
Kawasaki disease: a comprehensive review
Kawasaki disease is an acute systemic vasculitis that was first reported in 1961. Over the last 5 decades multiple papers have been published to further understand this disease. ... Dr. Kawasaki observed 50 cases with similar presentations, following which he published a paper entitled 'Acute febrile musculocutaneous lymph node syndrome ...
Kawasaki disease
Kawasaki disease is sometimes called mucocutaneous lymph node syndrome. That's because it also causes swelling in glands, called lymph nodes, and mucous membranes inside the mouth, nose, eyes and throat. Children with Kawasaki disease might have high fever, swollen hands and feet with skin peeling, and red eyes and tongue.
Kawasaki disease
Download now. Kawasaki disease. 1. Kawasaki Disease Diagnosis is the Key Presented by Chara Hall. 2. Also known as Kawasaki syndrome Mucocutaneous lymph node syndrome Involves the skin, mouth, and lymph nodes Inflammation of the blood vessels Main cause of acquired heart disease in kids No known cause Virus suspected - not contagious 2 What ...
Kawasaki Disease: Symptoms, Causes & Treatment
Kawasaki disease symptoms can include: Fever lasting for at least five days. Irritability. Red or pink eyes without discharge. Redness or cracking of your child's lips or tongue. Swelling and/or redness of your child's hands or feet. Peeling of your child's skin, usually beginning around their nails.
Diagnosis and Management of Kawasaki Disease
Patients with acute Kawasaki disease should be given high-dose aspirin, 80 to 100 mg per kg per day in four divided doses, until afebrile for 48 to 72 hours. C. 7. Kawasaki disease is accompanied ...
Kawasaki disease
43. 25-Feb-15 Diagnostic problems in Kawasaki disease Atypical or incomplete cases Most common in infants - greatest risk of CAA Children may have fever and < 4 clinical signs Reports of coronary AN with 3 diagnostic features Occasionally only prolonged fever is present, and diagnosis is only made after an ECHO.
Kawasaki Disease
Kawasaki Disease.ppt - Free download as Powerpoint Presentation (.ppt), PDF File (.pdf), Text File (.txt) or view presentation slides online. Scribd is the world's largest social reading and publishing site.
Kawasaki Disease
Kawasaki disease (KD), also known as mucocutaneous lymph node syndrome or infantile polyarteritis, is a medium-sized necrotizing vasculitis that predominantly affects children < 5 years of age. The etiology is currently unknown, but it is postulated to involve a combination of environmental and genetic factors.

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Kawasaki Disease: An Update of diagnosis and treatment

Kawasaki Disease

Kawasaki Disease: An Update

Kawasaki Ninja 250R

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Urine Proteomics in Kawasaki Disease

What is Kawasaki Disease?

Kawasaki Disease risk-associated snps

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