Coma due to hyperbilirubinemia is rare. It usually presents in the first days of life with jaundice, hypotonia, and poor suck. Fever and hypertonia with retrocollis and opisthotonos may follow. Double volume exchange transfusion should be tried if phototherapy fails to keep bilirubin below 18 mg/dL. Bilirubin-albumin displacing substances should be avoided and potential bilirubin-albumin displacing substancesshould be used at the lowest therapeutic concentrations. Premature neonates may require exchange transfusion at a lower level. Neonates with generalized glutathione synthetase deficiency are predisposed to hyperbilirubinemia. Glutathione synthetase deficiency is an autosomal disease. Low glutathione renders erythrocytes more vulnerable to oxidative damage. Neonates with glutathione synthetase deficiency may have partial albinism (Figure 67.1).

Bacterial meningitis is most often caused by group B streptococcus, Escherichia coli, Listeria monocytogenes, or Haemophilus influenzae. Early onset meningitis has a fulminant course. Signs of systemic failure, such as poor perfusion, hypothermia, and coma, occur simultaneously. Late onset meningitis has a more protracted course. Feeding problems and irritability precede coma by several hours. Seizures and a bulging fontanel are common. Neck rigidity is usually not present. Opsoclonus may also be the first sigh of meningitis. The typical cerebrospinal fluid findings are white blood cell count above 32 cells/mm, protein concentration above 90 mg/dL, and a cerebrospinal fluid to blood glucose ratio of less than 2:3. Nevertheless, a comatose neonate with cerebrospinal fluid white blood cell count of more than 10 cells/mm should be treated with antibiotics pending the results of the cerebrospinal fluid culture. Gram-stained smear and antigen detection, if positive, can be used to diagnose meningitis and to identify the organism. However, in most cases the diagnosis of bacterial meningitis depends on the identification of the organism in cerebrospinal fluid culture.