Cytomegalovirus, a member of the herpesvirus family, is among the most common viral infections encountered in the newborn period. International consensus distinguishes two forms by timing: virus detected within the first three weeks after birth indicates congenital infection acquired in the womb, while a negative result in those first weeks followed by a positive result later defines postnatal infection. In full-term infants, postnatal cytomegalovirus is usually silent. In very preterm or very low birth weight infants, however, the virus can cause sepsis-like illness, pneumonia, hepatitis, colitis, thrombocytopenia, neutropenia, and even death. Capillary leak syndrome, a condition in which plasma escapes the circulation into surrounding tissues, has only rarely been linked to this infection in neonates.

The infant in the report was one of twins born after premature rupture of membranes, weighing just 1,475 grams at birth. His mother carried antibodies to cytomegalovirus but showed no evidence of active infection during pregnancy. Testing at two weeks of age found no viral immunoglobulin M and no viral DNA in his urine, confirming that he had not been infected in utero. After an initial 42-day hospital stay, during which he received albumin infusions for low blood protein but no other blood products, he went home feeding well on fortified breast milk, reaching 2,260 grams.

The turning point came at 57 days of life, when he developed an intermittent cough and small petechial hemorrhages on his upper arms. By day 63 he was in respiratory distress and was readmitted to his birth hospital. Laboratory tests revealed a striking constellation: elevated white blood cells, falling platelets, and liver enzymes dramatically elevated, with alanine aminotransferase at 196 units per liter and aspartate aminotransferase at 467. Serum tested positive for cytomegalovirus immunoglobulin M, and viral DNA was detectable in both blood and urine. Cultures of blood and cerebrospinal fluid came back sterile, pointing away from bacterial meningitis or septicemia.

His respiratory failure escalated rapidly despite nasal cannula oxygen, continuous positive airway pressure, and noninvasive intermittent ventilation, forcing doctors to intubate him at 70 days of life. When he arrived at Hebei Children’s Hospital three days later, he was receiving 80 percent oxygen, his skin was mottled and swollen, and petechiae covered his body. Clinicians calculated his fluid overload at 32 percent of his admission body weight, a figure that would climb to 53.3 percent as edema worsened. Ultrasound and radiography revealed massive pleural effusions and ascites, while echocardiography documented a patent ductus arteriosus and severe pulmonary hypertension estimated at approximately 84 millimeters of mercury.

Viral load measurements told the story with unusual clarity. Real-time quantitative polymerase chain reaction detected more than 570,000 copies of cytomegalovirus DNA per milliliter of blood, with high levels also in urine, sputum, ascitic fluid, and pleural fluid. Crucially, the mother’s breast milk contained viral DNA at 1,934 copies per milliliter, and the infant had received no blood products other than albumin, making breastfeeding the most probable route of transmission. Every bacterial and fungal culture was negative, as were assays for beta-D-glucan, galactomannan, and Mycobacterium tuberculosis, effectively eliminating competing diagnoses. The team concluded the infant had postnatal cytomegalovirus infection complicated by sepsis, severe capillary leak syndrome, pulmonary hypertension, and shock.

The pathophysiology of capillary leak syndrome centers on endothelial injury. A hyperinflammatory insult damages the single-cell lining of capillaries, opening gaps that allow protein-rich plasma to flood into the interstitial space. Damaged endothelial cells themselves secrete proinflammatory cytokines, creating a self-reinforcing loop of vascular permeability. The classical triad is hemodynamic instability, intravascular hypovolemia, and generalized edema. Some researchers argue that microvascular leakage is not merely a complication of sepsis but a central driver of its mortality, a reframing that makes recognition of the syndrome in neonates critically important.

Treatment began along conventional lines: mechanical ventilation with inhaled nitric oxide for the pulmonary hypertension, dopamine to support blood pressure, plasma and platelet transfusions, and intravenous ganciclovir at 6 milligrams per kilogram every twelve hours. Despite these measures, urine output collapsed to 0.59 milliliters per kilogram per hour, body weight surged, and acute kidney injury set in. At 77 days of life the team initiated continuous renal replacement therapy in continuous veno-venous hemofiltration mode, using a catheter in the right internal jugular vein, heparin anticoagulation, a modest blood flow of 12 to 14 milliliters per minute, and ultrafiltration rates of 5 to 15 milliliters per hour. Over 51 hours the circuit removed 530 milliliters of fluid. Urine output rebounded to 3.5 milliliters per kilogram per hour, the edema receded, and the therapy was stopped.

Recovery was protracted but ultimately complete. The infant received three weeks of intravenous ganciclovir followed by two weeks of oral valganciclovir until blood viral DNA fell below the assay’s detection limit. A chest tube placed for the pleural effusion came out at 86 days, and mechanical ventilation ended the following day. He spent 52 days in the hospital before discharge at 125 days of life. Follow-up showed a brief viral rebound and months of abnormal liver enzymes and low platelets, but by nine months of age every laboratory parameter had normalized. Neurodevelopmental assessment at 18 months using the Gesell Developmental Schedules yielded scores between 87 and 93 across five domains, indicating normal development.

The case carries several lessons for neonatal practice. Breast milk transmission is the dominant source of postnatal cytomegalovirus in units that use leukoreduced, seronegative blood products, and a systematic review estimates that roughly 20 percent of very low birth weight infants acquire the virus this way, with 3.7 percent developing symptomatic disease. Some countries pasteurize milk for the smallest infants, though the practice remains debated because it destroys beneficial milk components. The authors argue that postnatal cytomegalovirus can precipitate life-threatening capillary leak syndrome and that clinicians should consider continuous renal replacement therapy early when antiviral drugs, fluid management, and circulatory support fail to control runaway fluid overload. They also call for larger prospective studies to define the optimal timing of antiviral treatment in this vulnerable population, noting that clinical vigilance for this rare but devastating complication remains insufficient.

Subject of Research: Severe capillary leak syndrome caused by postnatal cytomegalovirus infection in a very preterm infant, treated with continuous renal replacement therapy

Article Title: Severe capillary leak syndrome caused by postnatal cytomegalovirus infection in a very preterm infant: a case report

Article References: Fang, J., Chen, X., Li, T., Cao, L., & Ma, L. (2026). Severe capillary leak syndrome caused by postnatal cytomegalovirus infection in a very preterm infant: a case report. Frontiers in Pediatrics, 14, Article 1895522. https://doi.org/10.3389/fped.2026.1895522

Image Credits: AI Generated

DOI: 10.3389/fped.2026.1895522

Keywords: cytomegalovirus, capillary leak syndrome, preterm infant, breast milk transmission, neonatology, continuous renal replacement therapy, acute kidney injury, ganciclovir, very low birth weight, sepsis, pulmonary hypertension, neonatal intensive care