DOI: 10.1097/INF.0b013e31815b0004
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PMID: 18162955
Issn Print: 0891-3668
Publication Date: 2008/01/01
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Excerpt
Her past medical history was significant for prematurity and Noonan syndrome.1 She also had asthma, gastroesophageal regurgitation, and 1 episode of pneumonia. There was no recent history of travel, sick contacts, or exposure to pets. Her immunizations were up-to-date.
On admission her temperature was 39°C, heart rate 156 per minute, respiratory rate 30 per minute, and blood pressure 112/66 mm Hg. Her height was 76 cm and the weight 8.4 kg (<3rd percentiles). The left parotid measured 10 × 5 cm and was painful, erythematous, warm, and nonfluctuant. The Stensen duct was erythematous without pus. Left cervical lymph nodes were palpable near the parotid. The lips were dry, erythematous. No strawberry tongue or mouth ulcers were noticed. A III/VI harsh systolic murmur was audible over the precordium. On the 4th day of her illness, she developed bilateral nonexudative conjunctivitis and on the 7th day a transient blanching maculopapular rash over the torso.
A CT scan with contrast detected parotid enlargement, inflammation of the surrounding soft tissues, and left cervical lymphadenopathy. Blood culture was negative. She received 3 days ampicillin/sulbactam and vancomycin, for pressumed suppurative parotitis, considered to be secondary to decreased oral intake and sialostasis caused by prior illness. Therapy was switched to linezolid PO to finish a 10-day course. The parotitis improved but she continued to have daily fevers 38.5°C.
On the 11th day, she was afebrile and was discharged. On the 12th day, she returned febrile (38.5°C), irritable with painful swelling of the hands and feet, unable to bear weight. The conjunctivitis had almost resolved. The next day periungual desquamation of the fingers and toes occurred.
Laboratory findings on the second admission showed WBC 36.000/μL, with 67% neutrophils, 17% lymphocytes, and 15% monocytes. The hemoglobin was 10.7 g/dL, and the platelets were 637.000/μL. The ESR had increased to 68 mm/h from 30, and C-reactive protein was 4 mg/dL. The serum amylase had normalized from 101 U/L (upper normal 79). Urinalysis showed 6 WBC and 36 RBCs hpf. Liver function tests and electrolytes were normal. HIV antibodies were negative.
After these clinical and laboratory findings, Kawasaki disease was diagnosed. Twelve hours after the administration of IVIG 2gr/kg she became afebrile. She received aspirin 80 mg/kg/d for a few days and was discharged on a low dosage. Echocardiogram on admission and 6 weeks later showed no coronary artery dilations. She had no recurrent symptoms during the next 3 months.
Kawasaki is a multisystem disease.2 To our knowledge, this is the second case of acute parotitis associated with Kawasaki disease.3 Amano et al4 described the pathologic findings in a series of 37 autopsies in patients with KD in Japan. They describe intrasalivary gland arteritis in one-third of the patients and periductal and interacinar infiltration of lymphocytes and mononuclear cells in the salivary gland in 81%. Salivary gland fibrosis was identified in those who died long after the onset of the disease.4 Noonan syndrome is not associated with parotitis.1 Nonsuppurative parotitis should be added to the possible manifestations of Kawasaki disease.
