Closure Of Abdominal Wall Defects Research Articles

Arterial hypertension in the newborn infant.

Blood pressure is low at birth. It increases with age by about 1 mm Hg per day within the period of 3-8 days. It rises by about 1 mm Hg per week between 5 and 6 weeks of age. Neonatal hypertension carries a risk of cardiorespiratory failure and cerebral distress. Causes of neonatal hypertension are either secondary to congenital malformations or to acquired disease states. Congenital etiologies include: renal artery stenosis, renal artery hypoplasia, abdominal aortic atresia, coarctation of the aorta, kidney cystic disease, reflux nephropathies. Acquired causes include: thrombo-embolic renal artery complications secondary to umbilical artery catheterization or to thrombosis of the ductus arteriosus, closure of abdominal wall defects, adrenal hematoma with renal artery compression, seizures in preterm infants, central nervous system disorders, drug-induced hypertension, infants of drug-dependent mothers. The morbidity and the mortality of neonatal hypertension are elevated. Death may be caused by severe uncontrollable hypertension or by concomitant problems. Morbidity may be related to drug-resistant hypertension, or to the side-effects of hypotensive drugs.

Hemodynamic effects of primary closure of omphalocele/gastroschisis in human newborns.

To determine whether they could establish reliable, objective criteria that would predict safe, primary closure of abdominal wall defects (omphalocele/gastroschisis) in newborn infants, the authors measured intraoperative changes in intra-gastric pressure (IGP), central venous pressure (CVP), cardiac index (CI), systolic arterial blood pressure (BP), and heart rate (HR). Eleven neonates, who averaged 2.7 kg (range 1.5-4.1 kg) and 36 weeks gestation (range 30-41 weeks) were anesthetized with fentanyl (7.5-12.5 micrograms/kg), metocurine (0.3 mg/kg), and oxygen. Three infants had defects that were too large to close primarily. Of the eight infants who underwent primary closure, four required re-operation within 24 h because of oliguria or poor peripheral perfusion. Infants who required re-operation had intra-gastric pressures of 20 mmHg or more, a decrease in CI of 0.78 1.min.m2 or more, and an increase in CVP of 4 mmHg or more. Heart rate, BP, and systemic vascular resistance did not differ in infants requiring and not requiring re-operation. The authors conclude that intraoperative measurement of changes in IGP, CVP, and/or CI can reliably predict success or failure of primary operative repair of abdominal wall defects in human neonates.

The relative merits of various methods of indirect measurement of intraabdominal pressure as a guide to closure of abdominal wall defects

Visceral ischemia secondary to increased intraabdominal pressure (IAP) following closure of abdominal wall defects presents a serious postoperative problem. Currently, the method of closure and postoperative management are determined by clinical impressions rather than measurement of IAP. In this study various methods of indirectly measuring IAP were compared in 17 rabbits in which IAP was sequentially increased with an intraabdominal balloon. Vesical and inferior vena caval (IVC) pressures were found to have good statistical correlation with IAP. Other methods tested were gastric, rectal, superior vena caval, femoral and brachial artery, and rectus compartment pressures. All were found to be poor indicators of actual IAP. In nine of the rabbits, radiolabeled microspheres were used to assess cardiac output and visceral blood flow. Renal blood flow was very sensitive to increased IAP with dramatic impairment at IAP above 10 to 15 mmHg. Small intestinal flow was less sensitive and did not become significantly diminished until IAP exceeded 25 to 30 mmHg. Our studies suggest that vesical and IVC pressure monitoring should be used to evaluate IAP in the clinical setting. If IAP is in excess of 10 to 15 mmHg surgical intervention is indicated to prevent the development of renal ischemia.

Hypertension in the neonate.

Blood pressure (BP) is low at birth. It increases with age, by about 1 mm Hg per day within the period of 3 to 8 days. It rises by about 1 mm Hg per week between ages 5 to 6 weeks. At a latter age, systolic BP is close to 95 +/- 10 mm Hg. Hypertension is a rare condition in the neonate, where it carries a high risk of cardiorespiratory failure and cerebral distress. Causes of neonatal hypertension are either secondary to congenital malformations or to acquired disease states: Congenital malformations: renal artery stenosis, renal artery hypoplasia, abdominal aortic atresia, coarctation of the aorta, kidney cystic disease, reflux nephropathies. Acquired diseases: thrombo-embolic renal artery complications secondary to umbilical artery catheterization or to thrombosis of ductus arteriosus, closure of abdominal wall defects, adrenal hematoma with renal artery compression, seizures in preterm infants, central nervous system disorders, drug-induced hypertension, infants of drug-dependent mothers. The morbidity and the mortality of neonatal hypertension are elevated. Death may be caused by severe uncontrollable hypertension or by concomitant problems. Morbidity may be related to drug-resistant hypertension, or to the side-effects of hypotensive drugs. Surgery in these severely ill infants also carries a significant risk.

Biologic material for closure of abdominal wall defects

A new preparation process was studied which should allow the implantation of collagen type I in its native structure in reconstructive surgery, in this special case for closure of incisional hernias. As experimental animals we used 30 female Lewis rats. A defect of the anterior abdominal wall - measuring 3 X 4 cm - was closed with our collagen substitute. Biopsies were taken after 4, 6 and 8 weeks and examined morphologically. As criteria for revitalization and revascularisation we used type of immigrated cells, depth and density of immigration and formation of new blood vessels. After 4 weeks the implants were immigrated by fibroblasts, density diminishing towards the centre. On the muscle-implant-interface good revascularisation could be seen. After 6 weeks density of immigrated cells has distinctly increased even in the centre of the collagen implant. Sporadically small vessels could be seen. Eight weeks after implantation density of immigrated cells was at the same high level, and capillary bundles could be seen within the whole implant. We think that the studied collagen implant is suitable for the closure of hernias as shown by its physical and morphological properties. Especially it seems to guarantee an earlier and tighter closure of hernias in comparison to other materials.

Hypertension in the Neonate

Blood pressure (BP) is low at birth. It increases with age, by about 1 mm Hg per day within the period of 3 to 8 days. It rises by about 1 mm Hg per week between ages 5 to 6 weeks. At a latter age, systolic BP is close to 95 +/- 10 mm Hg. Hypertension is a rare condition in the neonate, where it carries a high risk of cardiorespiratory failure and cerebral distress. Causes of neonatal hypertension are either secondary to congenital malformations or to acquired disease states: Congenital malformations: renal artery stenosis, renal artery hypoplasia, abdominal aortic atresia, coarctation of the aorta, kidney cystic disease, reflux nephropathies. Acquired diseases: thrombo-embolic renal artery complications secondary to umbilical artery catheterization or to thrombosis of ductus arteriosus, closure of abdominal wall defects, adrenal hematoma with renal artery compression, seizures in preterm infants, central nervous system disorders, drug-induced hypertension, infants of drug-dependent mothers. The morbidity and the mortality of neonatal hypertension are elevated. Death may be caused by severe uncontrollable hypertension or by concomitant problems. Morbidity may be related to drug-resistant hypertension, or to the side-effects of hypotensive drugs. Surgery in these severely ill infants also carries a significant risk.

Postoperative neonatal necrotizing enterocolitis

Neonatal necrotizing enterocolitis (NEC) classically occurs in stressed premature newborns within the first ten days of life. Although it has been sporadically described in other settings, it has not been frequently cited as a postoperative complication. This paper presents eleven surgical infants whose postoperative course was complicated by the development of NEC. During the last 5 yr, 11 newborns (mean 2.4 kg.) have been treated for postoperative NEC. Each of these had undergone a major operation within the first week of life. Diagnoses included gastroschisis (7), omphalocele (1), jejunal atresia (1), aganglionosis (1), and malrotation with duodenal web (1). The mean age at onset of symptoms was 36 days (range 5–136 days) and an average of 29 days postoperatively (range 5–120 days). NEC was documented in each case by the presence of pneumatosis intestinalis or surgical and/or autopsy specimen. Four infants responded to medical therapy. Seven required operation, three of whom had involvement of the entire midgut. Five of the eleven neonates (46%) died of overwhelming sepsis. Of the remaining six, two require T.P.N. for survival (15 and 16 months old) and two additional require frequent hospitalization for diarrhea (morbidity 67%). NEC resulted in substantial morbidity and mortality in these surgical neonates. It occurred late in the postoperative period and pursued a virulent course. In only three infants could etiologic factors be identified. Two occurred after attempts at closure of abdominal wall defects and the third suffered hypoxia prior to the onset of symptoms. In each of these, NEC became apparent early postoperatively (Avg. 7th postoperative day). In the remaining eight, however, contributing factors could not be identified and onset of symptoms occurred late (Avg. 39th postoperative day). The preponderance of abdominal wall defects suggests a possible increased susceptibility in these infants. NEC should be included in the differential diagnosis of gastrointestinal symptoms in postoperative neonates. Neonatal necrotizing enterocolitis (NEC) classically occurs in stressed premature newborns within the first ten days of life. Although it has been sporadically described in other settings, it has not been frequently cited as a postoperative complication. This paper presents eleven surgical infants whose postoperative course was complicated by the development of NEC. During the last 5 yr, 11 newborns (mean 2.4 kg.) have been treated for postoperative NEC. Each of these had undergone a major operation within the first week of life. Diagnoses included gastroschisis (7), omphalocele (1), jejunal atresia (1), aganglionosis (1), and malrotation with duodenal web (1). The mean age at onset of symptoms was 36 days (range 5–136 days) and an average of 29 days postoperatively (range 5–120 days). NEC was documented in each case by the presence of pneumatosis intestinalis or surgical and/or autopsy specimen. Four infants responded to medical therapy. Seven required operation, three of whom had involvement of the entire midgut. Five of the eleven neonates (46%) died of overwhelming sepsis. Of the remaining six, two require T.P.N. for survival (15 and 16 months old) and two additional require frequent hospitalization for diarrhea (morbidity 67%). NEC resulted in substantial morbidity and mortality in these surgical neonates. It occurred late in the postoperative period and pursued a virulent course. In only three infants could etiologic factors be identified. Two occurred after attempts at closure of abdominal wall defects and the third suffered hypoxia prior to the onset of symptoms. In each of these, NEC became apparent early postoperatively (Avg. 7th postoperative day). In the remaining eight, however, contributing factors could not be identified and onset of symptoms occurred late (Avg. 39th postoperative day). The preponderance of abdominal wall defects suggests a possible increased susceptibility in these infants. NEC should be included in the differential diagnosis of gastrointestinal symptoms in postoperative neonates.

Hypertension in the neonate following closure of abdominal wall defects

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