Kawasaki disease presenting as Pleural effusion: an unusual case

Dr Elif Arslanoglu Aydin at the Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Turkey and colleagues have reported an unusual case of Kawasaki disease presenting as Pleural effusion. The case has appeared in the Journal of Medical Case Reports.

Kawasaki disease is an acute, febrile vasculitis of childhood that affects medium-sized arteries, predominantly the coronary arteries. It is a multisystem disease; therefore, it may present with non-cardiac findings of the disease. But it is quite unusual for it to present as Pleural effusion. This case highlights the importance of attending doctors considering the diagnosis of Kawasaki disease in the presence of pneumonia and pleural effusion that is nonresponsive to antibiotic therapy.

A 7-year-old Turkish girl presented to a local hospital with fever, chest pain, and vomiting. At hospital admission, she was febrile with a respiratory rate of 50 per minute. On physical examination, auscultation of her lungs revealed diminished breath sounds of the lower lobe of her left lung. An anteroposterior (AP) chest X-ray and chest ultrasonography showed a left lower lobar consolidation with minimal pleural effusion. She was hospitalized and sulbactam ampicillin (SAM), ceftriaxone, and clarithromycin were initiated. On the third day, her condition worsened with increasing pleural effusion. Thoracentesis was performed. SAM and ceftriaxone treatments were discontinued and meropenem and vancomycin were started. A chest tube was inserted and 130 mL of pus was drained. Light's criteria were positive for an exudative pleural effusion; a pleural fluid culture was sterile. After 4 days, the chest tube was removed. High fever persisted for 15 days despite broad-spectrum antibiotics, and acute-phase reactants remained high; therefore, she was referred to our hospital for further evaluation.

She had a fever with a temperature of 38.1 °C, her respiratory rate was 48/minute, heart rate was 125/minute, blood pressure was 90/65 mm Hg, and oxygen saturation was 95%. A physical examination revealed non-purulent conjunctivitis in both eyes, perianal peeling, and periungual desquamation on her hand, fingers, and toes. All other findings in the physical examination were unremarkable. She had unilateral cervical lymphadenopathy and a rash on her extremities while in the other hospital. Her past medical history was unremarkable, as was her family history. Immunizations were up-to-date for her age.

On admission to our hospital, the laboratory findings were as follows: hemoglobin 10.2 g/dL, white blood cells 14,000/μL, and platelets 736,000/μL. C-reactive protein (CRP) was 4.26 mg/dL (normal, 0–0.8 mg/dL), the erythrocyte sedimentation rate (ESR) was 42 mm/hour (normal, 0–20 mm/hour), and the albumin, creatinine, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase, blood urea nitrogen, calcium, sodium, chloride, and potassium levels were normal. Urine analysis was normal.

A chest X-ray was normal. Perivascular brightness and echogenicity of her right coronary artery was noted on transthoracic echocardiography (TTE). She was diagnosed as having KD based on the presence of fever, bilateral non-purulent conjunctivitis, cervical adenopathy, perianal peeling, periungual desquamation, elevated acute-phase reactants (ESR, CRP), thrombocytosis, and coronary artery involvement (CAI). Intravenous immunoglobulin (IVIG) (2 g/kg, infusion in 12 hours) and acetylsalicylic acid (60 mg/kg per day) were initiated. The fever resolved after IVIG infusion. At a 3-month follow-up visit, the acute-phase reactants and a TTE were normal. One year after the diagnosis, a TTE was normal and she was perfectly healthy.