[Perforated gastric ulcer: an increasing neonatal ICU disease? Report of 4 cases]. / Ulcera gástrica perfurada: doença em ascensão em UTI neonatais? Particularidades neste período e relato de quatro casos.

Between november 1994 and september 1995, there were 4 cases of premature infants in our Neonatal Intensive Care Unit (NICU) who developed gastrointestinal perforation and bleeding due to peptic ulcer and 3 died of this complication. In the first case, the neonate developed pneumoperitonium when weaning from the ventilator and was submitted to the operation with clinical diagnosis of Necrotizing Enterocolitis. Surprisingly, during the procedure, a perforated gastric ulcer was disclosed. Ever since, this NICU is aware of this diagnosis and try to better identify the possible risks factors. Asphyxia, prematurity, stress and situations where low gastrointestinal flow (asphyxia, exchange transfusion, pneumothorax, hemodynamic shock, cardiac arrest) were observed in almost every case. Treatment with dexamethasone or aminophilline was used in 3 of 4 cases and this potential serious side effect should be considered in all babies treated with steroids. The association of ranitidine (2 mg/kg 12/12 h) could not prevent the perforation in cases 1 and 3. Better understanding of physiopathology of the ulcer in this period of life and a effective preventable drug is still lacking.

Hyperekplexia, a cause of neonatal apnea: a case report.

We report a case of non-familial hyperekplexia which characteristically developed apnea and feeding difficulties in the neonatal period. The abnormal startle response was evident from the second week of life onwards. The infant showed a marked improvement of the startle response and muscle hypertonia with clonazepam. Clobazam was also tried with no apparent response. A prominent long latency C response was observed on EMG examination, suggesting a possible cortical neuronal hyperexcitability origin for the abnormal startle response observed in hyperekplexia.

Physiological red cell, 2,3-diphosphoglycerate increase by the sixth hour after birth.

As the available hemoglobin A1 at birth ranges from 20 to 30% a possible mechanism to favor oxygen release to the tissues could be a decrease of hemoglobin A1 affinity to oxygen. This may be accomplished by an increase in blood pH soon after birth and by an elevation in red cell 2,3-diphosphoglycerate (2,3-DPG). This hypothesis is supported by Valleri and Hirsch, who described a rapid 2,3-DPG recovery of transfused depleted 2,3-DPG red cells. That being so, we carried out this current study by assaying the 2,3-DPG of cord blood from 22 newborns and at 6, 24 and 72 hours after birth, as well as those enzymes assumed to be envolved in the 2,3-DPG levels regulation. 2,3-DPG (nmoles g-1 Hb) demonstrated the following values: cord blood: 9,770 +/- 1,026; 6h: 12,773 +/- 1,726; 72 h: 11,990 +/- 728, unveiling a distinct behavior of a sharp increase of 30% by the sixth hour. This confirmed our hypothesis. Regarding the metabolic mechanisms which can account for the 2,3-DPG increase, besides the rise of blood pH, we detected a significant decrease of the 2,3-DPG phosphatase activity, which might diminish the 2,3-DPG breakdown.