The importance of acid reflux patterns in neurologically damaged children detected by four-channel esophageal pH monitoring.

Multiple level esophageal pH studies were performed in 23 neurologically damaged infants and children for evaluation of gastroesophageal reflux (GER) and feeding difficulties. The patients were placed in one of three anatomic groups based on the extent of their neurologic injury. Seven children had an acute cerebral injury due to closed head trauma or infections. Six patients with perinatal asphyxia or progressive encephalopathy had a global CNS insult. Eight children with CNS malformations or intraventricular hemorrhage had subacute cerebral damage. Two patients with generalized seizure disorders could not be anatomically classified. In all groups, abnormalities detected at the distal esophagus were also noted at more proximal levels. The middle esophageal probe demonstrated a significant difference (P less than .02) for the longest reflux episode between patients with subacute cerebral injury and those with a global insult. The difference (P less than .02) for the longest reflux episode detected by the distal pH sensor in globally damaged children compared with those with acute cerebral injury also persisted at the middle and proximal esophageal levels. Comparing these same groups, a difference (P less than .02) in acid clearance time and percentage of time pH less than 4 was noted only at the proximal esophageal level. Only the middle and proximal pH probes detected differences (P less than .02) for acid clearance time between patients with both types of cerebral damage and those with a global injury. In infants and children with CNS damage and suspected GER, monitoring the proximal and middle esophageal pH provides important information not detected by the distal esophageal sensor.(ABSTRACT TRUNCATED AT 250 WORDS)

Cytomegalovirus and dual infection in infants.

In four unrelated infants without underlying immunodeficiency, dual infections with cytomegalovirus (CMV) and another microorganism developed. The patients included the following: (1) a 3-month-old girl with congenital CMV and perinatal cutaneous herpes simplex virus; (2) a 5-week-old girl with CMV and Pneumocystis carinii; (3) a 12-week-old girl with CMV and Haemophilus influenzae meningitis; and, (4) a 2 1/2-month-old girl with CMV and Escherichia coli meningitis. In all four cases, the patient's initial symptoms were referable not to CMV, but to the companion infecting organism. The diagnoses of CMV infection were made, respectively, by a high index of clinical suspicion in the first three cases and on the basis of a lucent parenchymal defect on computerized tomographic scan in the fourth patient. These cases provide additional evidence that CMV infection may predispose to secondary infection. We recommend that infants who have signs of infection and evidence of CNS abnormalities have cultures made for CMV. Both human CMV and experimental murine CMV infections have been associated with suppressed cellular and possibly humoral immunity.