A Khaleghnejad Tabari, Hr Noblett, D Frank,
Volume 9, Issue 1 (5-1995)
Abstract
From October 1977 to December 1988, 108 neonates born with esophageal
atresia (EA) and/or a tracheoesophageal fistula (TEF) were treated at
the Bristol Royal Hospital for Sick Children.
An incidence of I :4000-4500 live births was noted. 1I2.4% had the common-
type anomaly, 5.5% had pure esophageal atresia, and 6.5% had an H-type
anomaly. 2.8% had upper and lower fistulae and 2.8% had upper fistulae.
Forty-nine patients (45.3%) had associated anomalies of which the cardiovascular
system (16.6%) was the most commom. With consideration of
the urogenital system as a unique system, urogenital anomalies were the
most common associated anomalies (20.3%). Thirty (27.7%) of lOll neonates
had V ACTERL associated anomalies, which were more frequent in the common-
type anomaly. Seven of 9 deaths in the VACTERL associated group
were because of associated anomalies and cardiac anomalies were a common
cause of late death in this study. In full-term and well babies with common-type
anomalies, transanastomotic tubes significantly decreased hospital stay.
Every effort was made to maintain the neonate's own esophagus, and in
pure esophageal atresia 5 of 6 neonates were successfully treated by spontaneous
growth and anastomosis and only I neonate underwent gastric- tube
formation as an esophageal replacement. Anastomosis was done in one layer
by 5/0 silk , and 17.14% developed leak, 29.62% strictures, 1.90% recurrent
fistula, and the rate of anastomotic complications was markedly higher in
delayed and staged operations. Fifty-three neonates (50.47%) had respiratory
complications which were the most common complication. Thirty-three
(31.4%) had gastroesophageal reflux (GER), all but one of which were
treated medically. The routine policy now is that all babies are put on
Gaviscon until the child can adopt an upright position.
Low birth weight and pneumonia are not contraindications for surgery,
and with the improvement of surgical technique and postoperative care, do
not affect survival. There was 12.03% mortality and the main cause of death
was associated anomalies.
Husam Abazid, Nour Alabbas, Alaa Hammad, Osama I. Ramadan, Esraa Ebraheem Al Jomaa, Mumen Fathi Amer, Frank Scott Hall,
Volume 39, Issue 1 (1-2025)
Abstract
Background: Drug addiction is a serious public health concern. Tramadol addiction and dependence have been documented in recent years, most commonly in young adults, making tramadol use a significant health concern. The study investigated the long-term effects of tramadol intoxication on the γ-aminobutyric acid (GABA) system and tricarboxylic acid cycle enzymes in the brains of rats, focusing on regions with a high number of GABAergic neurons.
Methods: In this animal study, three treatment groups of adult male rats were considered. Rats were divided into three treatment groups: control no tramadol was given, Gp 25 mg/Kg tramadol was given 25 mg/kg for one month by oral gavage, and Gp 50 mg/Kg tramadol was given 50 mg/kg for one month by oral gavage for one month, and the enzyme activities for GABA transaminase (GABA-T), succinic semialdehyde dehydrogenase (SSA-DH), succinate dehydrogenase (SDH), and isocitrate dehydrogenase (IDH) were measured using ELISA kits, on brain tissue samples from the cerebellum, brain stem, cerebral cortex, thalamus, and hypothalamus. Histopathological analysis of the cerebral cortex was conducted using hematoxylin-eosin and Nauta silver staining. Statistical analysis for GABA shunt enzymes and tricarboxylic acid cycle enzymes was conducted using one-way ANOVA followed by Tukey’s multiple means comparisons.
Results: Tramadol significantly (P < 0.05) reduced the levels of GABA-T, SSA-DH, and IDH enzymes across various brain regions, with the most pronounced reductions observed in the brain stem and hypothalamus. In contrast, SDH enzyme levels remained largely unchanged in most regions. Additionally, structural changes in the brain were noted, including vascular congestion, neuronal degeneration, and disruption of cortical layers. These alterations were more severe in the high-dose group, suggesting that higher doses of Tramadol may lead to more extensive brain damage.
Conclusion: Tramadol exposure was found to cause biochemical and histopathological alterations in the nervous tissue through impairment of GABA metabolism.
