Pediatric Inflammatory Multisystem Syndrome (PIMS-TS) with Serous Effusions Due to Severe Hypoalbuminemia: A Case Report

A newly described pediatric syndrome related to COVID-19, termed Pediatric Inflammatory Multisystem Syndrome temporally associated with SARS-CoV-2 (PIMS-TS or MIS-C), presents with features overlapping Kawasaki disease, including rash, cheilitis, conjunctivitis, prolonged fever, lymphadenopathy, and potential gastrointestinal and cardiac involvement. The report highlights the importance of recognizing biological features, particularly hypoalbuminemia, as indicators of disease severity and risk of complications. It presents a case of a five-year-old male with PIMS-TS who developed serous effusions secondary to severe hypoalbuminemia and was successfully treated with intravenous immunoglobulins and oral prednisone.

Case report of a five-year-old Moroccan boy with 15 days of persistent fever unresponsive to paracetamol and antibiotics, accompanied by rash, vomiting, and general deterioration. There was known exposure to COVID-19 20 days prior. On examination: febrile (39.6°C), HR 110 bpm, RR 25/min, SpO2 98%, normal BP; bilateral nonsuppurative conjunctivitis, cheilitis, nonpitting lower limb edema, bilateral symmetric erythematous maculopapular lesions, hepatomegaly, and diffuse abdominal dullness. Laboratory findings: hypochromic microcytic anemia (Hb 9 g/dL), thrombocytopenia (67 G/mL), leukocytosis (15.5 G/L), elevated CRP (164 mg/L), elevated ESR (85 mm/h), severe hypoalbuminemia (19 g/L), positive SARS-CoV-2 IgG (ELISA), markedly elevated pro-BNP (9791 pg/mL); procalcitonin and fibrinogen not elevated; renal and hepatic functions normal. Cardiac imaging: transthoracic echocardiography showed dilated left ventricle, reduced LVEF 30%, myocarditis, pericarditis, mitral regurgitation, and right coronary artery dilation (3.5 mm). Additional imaging: ultrasound showed hydrocholecystis; chest radiography demonstrated moderate pleural effusion; peritoneal effusion present. Management initiated on hospital day 2 for suspected MIS-C: IV immunoglobulin 2 g/kg, high-dose oral acetylsalicylic acid 50 mg/kg/day during acute phase then reduced to 5 mg/kg/day after five days, and oral prednisone 2 mg/kg/day for seven days. Follow-up included clinical monitoring and serial biomarkers (CRP, albumin), with echocardiographic reassessment at three months.

- The child fulfilled MIS-C/PIMS-TS criteria (fever, mucocutaneous signs, gastrointestinal involvement, cardiac dysfunction, elevated inflammatory markers, SARS-CoV-2 serology positive, and exclusion of bacterial causes). - Severe hypoalbuminemia (19 g/L) was associated with significant serous effusions (pleural, pericardial, peritoneal) and hydrocholecystis. - Cardiac involvement included myocarditis, pericarditis, mitral regurgitation, right coronary artery dilation (3.5 mm), and reduced LVEF (30%); pro-BNP markedly elevated at 9791 pg/mL. - Inflammatory markers were markedly elevated (CRP 164 mg/L; ESR 85 mm/h) with cytopenias (Hb 9 g/dL; platelets 67 G/mL) and leukocytosis (15.5 G/L). - Treatment with IVIg 2 g/kg, prednisone 2 mg/kg/day for seven days, and aspirin (50 mg/kg/day then 5 mg/kg/day) led to rapid clinical and biochemical improvement: defervescence, resolution of rash and serous effusions, normalization of albumin and reduction of CRP. - At three-month follow-up, the patient was asymptomatic with normal echocardiography.

PIMS-TS is a hyperinflammatory syndrome temporally linked to SARS-CoV-2 and may mimic Kawasaki disease but typically affects older children, more frequently involves gastrointestinal and neurological symptoms, and demonstrates more severe myocardial involvement. This case emphasizes profound hypoalbuminemia as a key marker of severity, associated with serous effusions due to capillary leak and altered albumin kinetics during systemic inflammation. Recognizing hypoalbuminemia alongside cardiac and inflammatory biomarkers can help stratify risk and guide timely immunomodulatory therapy. The pathophysiological basis includes increased vascular permeability leading to extravascular albumin loss, potentially compounded by decreased hepatic synthesis and increased degradation during inflammation. The observed favorable response to IVIg, corticosteroids, and antiplatelet therapy aligns with current approaches for MIS-C, with resolution of inflammation, restoration of albumin levels, and recovery of cardiac function.

PIMS-TS can be life-threatening due to multisystem involvement. Clinicians should include hypoalbuminemia among severity biomarkers, in conjunction with cardiac and inflammatory parameters, to optimize early recognition and management. This case demonstrates that prompt treatment with IVIg, corticosteroids, and aspirin can reverse severe manifestations, including serous effusions and cardiac dysfunction.