CASE

A 6-year-old male was admitted to our hospital on the third day of illness presenting with a pruritic maculopapular eruption on his lower extremities, which subsequently spread to the trunk, upper extremities, and face, resulting in a confluent rash. The following day, he developed a high-grade fever (38.5-39°C), enlarged occipital lymph nodes, neck muscle pain, conjunctivitis, malaise, and periungual desquamation. His mother reported a history of multiple upper respiratory tract infections in the preceding months.

​

On admission, the patient appeared adynamic, unable to tolerate oral intake, with swollen eyelids, inflamed conjunctiva, and a purplish confluent, pruritic maculopapular rash with periungual desquamation, along with decreased skin elasticity. Physical examination revealed cervical, submandibular, and occipital non-tender lymphadenopathy, mucositis characterized by tongue and oral cavity mucosal redness, diminished heart sounds with a systolic murmur on both the apex and the base, decreased urine output, and enlarged liver and spleen (2-2.5cm and 2cm, respectively). The patient exhibited no bowel movement in the previous 24 hours, and while neck muscle pain was present, there were no signs of neck rigidity or other meningeal signs.

​

Laboratory investigations revealed significantly elevated inflammatory markers: CRP 171.0 mg/L, leukocytosis (14.2x10^9/L) with left shift to metamyelocytes (9%), bands (25%), lymphopenia (0.6x10^9/L), ESR 45mm/h, PCT 10 ng/ml, mild thrombocytopenia (151x10^9/L), elevated LDH (558 U/L), ferritin (311.7 mg/L), and hyponatremia (129.6 mmol/L). Coagulation parameters indicated coagulopathy: PT 20.3 sec, INR 1.26, and elevated D-dimer (4.59 mcg/ml). A rapid test for SARS-CoV-2, influenza A and B, and adenoviruses was negative. Ultrasound confirmed bilateral postauricular lymphadenopathy with decreased echogenicity, and cardiac ultrasound revealed pericardial effusion with 3-4mm separation.

​

Blood cultures were obtained, and the patient received intravenous broad-spectrum antibiotics and supportive treatment due to suspected bacterial infection. Despite treatment, the fever persisted, and pleural and peritoneal effusions developed. Renal function tests were normal, but hypoalbuminemia was noted (albumin 23.6 g/L). Given the clinical presentation and markedly elevated inflammatory markers, the SARS-CoV-2 antibody titer was measured (1:766 AU/ml), confirming the diagnosis of MIS-C. Treatment with IVIG 2g/kg, high-dose aspirin (50 mg/kg), and high-dose prednisolone (2mg/kg) was initiated. Blood cultures were negative. Following IVIG administration, the patient's condition improved, with resolution of fever and other symptoms, and normalization of inflammatory markers. Subsequently, the patient was transitioned to low-dose aspirin (5mg/kg) and prednisolone tapering. A comprehensive follow-up plan was established, and the patient was discharged from the clinic.

DISCUSSION