Cardiac perforation during minimally invasive repair of pectus excavatum: a rare complication.

Life-threatening complications (LTCs) and negative results of surgical treatments often go unreported. Minimally invasive repair of pectus excavatum (MIRPE) represents a procedure with a low incidence of adverse outcomes. However, 15 potentially fatal cases of MIRPE-related heart injury have been published. We report a case of cardiac perforation (CP) during MIRPE. A 12-year-old female was admitted for elective repair of a severe asymmetric pectus excavatum. Preoperative computed tomography showed a Haller index of 4.9. MIRPE was performed under bilateral video-assisted thoracoscopy. After the placement of the pectus bar, cardiac arrhythmias, hypotension and bilateral hemothorax occurred. Emergency thoracotomy without pectus bar removal showed CP. The wound sites were repaired and the pectus bar was eventually successfully implanted. The patient was discharged on postoperative day 11. After 10 months, she remains asymptomatic. Reporting rare complications is essential for accurate calculations of the true prevalence of LTCs, maintaining high alertness in pediatric surgeons.

Tumor necrosis factor α, protein gene product 9.5, matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 presence in congenital intra-abdominal adhesions in children under one year of age.

INTRODUCTION: The regulatory role of cytokines and extracellular matrix remodeling factors in congenital intra-abdominal adhesions has not yet been defined. The aim of this study was to assess the presence and relative distribution of tumor necrosis factor α (TNF-α), protein gene product 9.5 (PGP 9.5), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in adhesions. MATERIAL AND METHODS: TNF-α, PGP 9.5, MMP-2 and TIMP-2 were detected using immunohistochemical methods and their relative distribution was evaluated by means of the semiquantitative counting method. The results were analyzed using non-parametric statistical methods. RESULTS: A moderate number of TNF-α positive macrophages and fibroblasts was found. A positive correlation was observed between the immunoreactive structures for TNF-α and PGP 9.5. A positive reaction for PGP 9.5 was observed in nerve fibers and shape modified fibroblasts. In control group tissues, positive structures were seen in significantly higher counts for PGP 9.5. Few to moderate numbers of MMP-2 positive macrophages, epithelioid cells, fibroblasts and endotheliocytes were detected. There was no significant difference between the groups. A positive reaction for TIMP-2 was seen in fibroblasts, macrophages and endotheliocytes. In control group tissues, positive structures were found in significantly higher counts for TIMP-2. CONCLUSIONS: The positive correlation between the immunoreactive structures for TNF-α and PGP 9.5 suggests that nerve in-growth into intraabdominal adhesions might be induced by TNF-α and PGP 9.5 could have a role in maintaining inflammation. The down-regulation of PGP 9.5 suggests that pathogenesis of congenital intraabdominal adhesions may be related to hypoxia induced damage. The imbalance between MMP-2 and TIMP-2 may prove tissue fibrosis as a response to congenital peritoneal adhesions.

The Morphopathogenetic Aspects of Intraabdominal Adhesions in Children under One Year of Age.

Background and Objectives: The morphopathogenesis of adhesions is a complex process, characterized by the accumulation of an extracellular matrix, inflammation and hypoxia. The regulatory role between morphopathogenic factors in adhesions has not yet been defined. The aim was to investigate the appearance of transforming growth factor beta (TGFß), hepatocyte growth factor (HGF), basic fibroblast growth factor (FGF-2), fibroblast growth factor receptor 1 (FGFR1), vascular endothelial growth factor (VEGF), protein gene product 9.5 (PGP 9.5), chromogranin A (CgA), interleukin-1 alpha (IL-1α), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-7 (IL-7), interleukin-8 (IL-8), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFα), human beta defensine-2 (HBD-2), matrix metaloproteinase-2 (MMP-2) and matrix metaloproteinase-2 tissue inhibitor (TIMP-2) in intraabdominal adhesions. Materials and Methods: The study material was obtained from 49 patients under one year of age with total or partial bowel obstruction. All factors were detected using immunohistochemistry methods and their relative distribution was evaluated by means of the semiquantitative counting method. Results: Intraabdominal adhesions are characterized by increased TGFß, FGFR1, VEGF and decreased FGF-2, HGF, PGP 9.5, IL-1, IL-4, IL-8, TIMP-2 findings. The most significant changes observed were the remodulation of the extracellular matrix, promotion of neoangiogenesis and the maintenance of a prolonged inflammation. Conclusions: The increase in TGFß, relative to the decrease of HGF, as well as the disbalance between MMP-2 and TIMP-2 proves an increased fibrosis in intraabdominal adhesions. Less detected FGF-2 and more prominent FGR1 findings points out a compensatory receptor stimulation in response to the lacking same factor. The decrease in PGP 9.5 and the increase in VEGF-positive macrophages indicate hypoxic injury and proves the stimulation of neoangiogenesis. An unpronounced IL-1 and marked IL-10 finding indicate the local tissue protection reaction, the decrease in IL-4 could be the direct cause of giant cells, but the decrease of IL-8 could confirm a delayed chemotaxis of inflammatory cells.

The Distribution of Vascular Endothelial Growth Factor (VEGF), Human Beta-Defensin-2 (HBD-2), and Hepatocyte Growth Factor (HGF) in Intra-Abdominal Adhesions in Children under One Year of Age.

The regulatory role between ischemia related factors and antimicrobial peptides in congenital intra-abdominal adhesions has not yet been defined. The aim of this research was to investigate the appearance and relative distribution of VEGF, HBD-2, and HGF in congenital intra-abdominal adhesions compared with relatively healthy tissue controls. The study group material was obtained from 48 patients who underwent abdominal surgery due to partial or complete bowel obstruction. VEGF, HBD-2, and HGF were detected using immunohistochemistry methods and their relative distribution was evaluated by means of the semiquantitative counting method. The results were analyzed using nonparametric statistic methods. A moderate number of VEGF positive endotheliocytes were detected, but there was no statistically significant difference between the groups. In the experimental group, a moderate to high number of VEGF positive macrophages was observed. In control group tissues, such macrophages were seen in significantly lower number (U = 61.0, p = 0.001). The increase of VEGF positive cells indicates support of angiogenesis due to the hypoxic conditions in case of adhesion disease. The number of HBD-2 marked fibroblasts and macrophages was moderate to high, but only few positive endotheliocytes were observed. Persisting appearance of HBD-2 positive structures might be a result of the inflammatory process. Most specimens showed occasional HGF positive macrophages and fibroblasts and there was no statistically significant difference between the groups. The relatively weak appearance of HGF suggests that the lack of this factor promotes the formation of fibrotic changes in case of intra-abdominal adhesions.

Interleukin (IL)-1, 4, 6, 7, 8, 10 Appearance in Congenital Intra-Abdominal Adhesions in Children Under 1 Year of Age.

Several cytokines have been studied for their potential role in adhesion formation. Regulatory role between the cytokine pathways has not yet to be defined. This study was designed to investigate the relation between proinflammatory and anti-inflammatory cytokines in congenital intra-abdominal adhesions. Tissue samples used for research were obtained from abdominal surgery due to obstructive gut malrotation and several additional pathologies (rectal atresia without perforation, omphalocele). All tissue specimens were stained with hematoxylin and eosin and by immunohistochemistry for interleukin-1 (IL-1), IL-4, IL-6, IL-7, IL-8, and IL-10. The number of immunoreactive structures was graded semiquantitatively. Occasionally to moderate number of IL-1, IL-4, and IL-8 positive inflammatory cells and fibroblasts were observed in tissue. Few to moderate connective tissue cells contained IL-6, but moderate to numerous-IL-7 and IL-10. Statistically significant correlation was found between IL-7 and IL-1 (rs=0.471, P=0.001), IL-4 (rs=0.491, P<0.001), IL-8 (rs=0.440, P=0.001), IL-10 (rs=0.433, P=0.002). The relatively common finding of IL-6 in adhesions points out the relevance of lymphocyte balance regulation of an ongoing inflammation and regenerative processes. The coherence between the inflammation mediator IL-7 and other proinflammatory/anti-inflammatory cytokines suggests about activation of macrophages and chronic inflammatory aggregate formation. The essential IL-10 and less distinct IL-1 findings in the adhesion material points out strong local defense reactions.

Measurement of abdominal circumference in preterm infants.

BACKGROUND: Body weight, length and head and thoracic circumference are routinely measured in obstetric and neonatal departments. Reference values for these measurements have been established for the neonatal population. Neonatal abdominal circumference is not routinely measured, and no reference values for this measurement have been determined. To evaluate the increase in abdominal circumference in newborns with abdominal pathology such as necrotizing enterocolitis, information about normal abdominal circumference in healthy neonates shortly after birth is needed. The aim of this study was to determine the correlation between abdominal circumference and birth weight by measuring the abdominal circumference of premature neonates soon after birth. METHODS: Abdominal circumference was measured within 30 min of birth in 220 neonates born between 23 and 35 weeks' gestation. RESULTS: There was no statistically significant difference in abdominal circumference between boys and girls in the study population. A specific formula for estimating normal abdominal circumference was developed: y = 0.0053x + 14.83 (y = abdominal circumference in cm; x = body weight in g; 0.0053 = regression coefficient; 14.83 = regression constant). CONCLUSION: A positive linear correlation between abdominal circumference and birth weight was found in infants at birth. The correlation can be summarized as a linear regression equation. Further studies are needed to investigate possible factors associated with abdominal circumference in fed versus unfed preterm infants.

Growth factors, their receptors, neuropeptide-containing innervation, and matrix metalloproteinases in the proximal and distal ends of the esophagus in children with esophageal atresia.

OBJECTIVE: The pathogenesis of esophageal atresia (EA) remains unknown despite a relatively high incidence of this anomaly in population affecting 1 newborn per 3000 live births. The aim of this study was to examine the relative occurrence of growth factors, their receptors, neuropeptide-containing innervation, and tissue-degradating enzymes--matrix metalloproteinases--in the proximal and distal parts of the esophagus with EA. MATERIALS AND METHODS: A histopathological study was conducted on 15 patients with EA. Tissues were processed for NGFRp75, PGP 9.5, TGF-ß, FGFR, VEGF, EGFR and MMP-2 by means of biotin-streptavidin immunohistochemistry. RESULTS: In the control and EA-affected distal esophageal specimens, numerous and abundant NGFR-containing structures were detected, while in the proximal part of the esophagus, a decrease in their number was observed in patients. PGP 9.5 also marked neuronal structures similarly. TGF-ß was found only in occasional cells in the EA-affected esophageal specimens, while control material demonstrated moderate to numerous TGF-ß-containing structures. Abundance of FGFR and only occasional appearance of VEGF-positive cells were found in both the control and EA-affected material. A moderate number of connective tissue cells in controls contained EGFR. Compared with controls, the number of MMP-2 expressing cells in the EA-affected tissues was decreased in the proximal esophagus. CONCLUSIONS: A decrease in PGP 9.5-containing neuronal structures in the proximal esophagus supports insufficient innervation of this part of the organ in EA. A decrease in MMP-2 positive cells in the esophageal atresia-affected proximal esophagus indicates also a possible decrease of tissue adaptive and regenerative reactions. Low expression of TGF-ß and almost the absence of EGFR in the EA-affected specimens may result in disturbances of cell growth, proliferation, and differentiation, indicating a significant role of these substances in morphopathogenesis of EA. FGFR and VEGF seem not to characterize EA pathogenesis.