Herniation Of Abdominal Organs Research Articles

Thoracic manifestations of gastrointestinal diseases

Variety of gastrointestinal tract (GIT) changes that have their manifestation in thorax, disable their detailed review. Therefore, this article, represents short and overall over-view of these conditions. Standard chest x-ray can reveal esophageal disorders, herniation of abdominal organs into thorax, signs of GIT organs perforation, subphrenic abscess. Numerous diseases of intrabadominal organs of digestive tract can spread to the thorax, either per continuitatem or by lymphogenous or hemaotgenous dissemination. Therefore, chest x-ray is obliged by investigation of abdominal organs. If it is necessary additional diagnostic procedures are performed to confirm or exclude the association of lung or pleura features with GIT disorders. Above mentioned, just confirm that chest x-ray is first in algorithm of diagnostic procedures in these pathologic conditions. If there is any suspicion to conditions that require patients treatment, additional imaging methods like computerized tomography (CT), ultrasonography (US) and barium enema of digestive tract are necessary.

Management of traumatic rupture of the diaphragm.

Traumatic rupture of the diaphragm is a potentially serious injury which presents in different forms depending on the mechanism of the causative trauma. Over a 7 year period, 20 patients (17 male and 3 female) with traumatic rupture of the diaphragm were seen in our unit; their mean age was 25.6 years. Automobile accidents caused the diaphragmatic injuries in 65 per cent of cases while falls from trees were the cause of injury in 10 per cent. Ten patients (50 per cent) were seen within 7 days of the injury and 95 per cent within 3 months. The left hemidiaphragm was ruptured in 85 per cent and the right in 15 per cent of cases. Fifty ribs were fractured in fourteen patients (70 per cent) but there were no pelvic fractures. Fourteen patients (70 per cent) had gastrointestinal visceral herniation into the thorax, the stomach, omentum, colon and spleen being the commonest herniating organs. Successful surgical repair was achieved in 18 patients, 4 of whom also had splenectomy; 2 patients were treated conservatively. A high index of suspicion and early surgical treatment are the mainstay of successful management of traumatic rupture of the diaphragm with or without herniation of abdominal organs.

Management of traumatic diaphragmatic rupture.

Diaphragmatic rupture following trauma is often an associated and missed injury. This report documents our experience of treating traumatic diaphragmatic rupture (TDR). We retrospectively analyzed 18 patients who presented between 1993 and 2000 with TDR, caused by blunt injuries in 14 and by penetrating injuries in 4. The average age of the patients was 32 years and the female to male ratio was 4 : 14. The TDR was right-sided in 5 patients and left-sided in 13. The diagnosis was made by chest X-ray, thorax and upper abdominal computed tomography, and upper gastrointestinal contrast studies. The most common herniated organs were the omentum (n = 11), stomach (n = 10), spleen and colon (n = 9), and liver (n = 2). Sixteen diaphragmatic injuries were repaired primarily, and two were repaired using a prolene mesh graft. The mortality rate was 5.5% (n = 1). A high index of suspicion and early surgical treatment determine the successful management of TDR, with or without the herniation of abdominal organs. The surgical approach to TDR is individualized. Acute left-sided injuries are best approached through the abdomen, although we prefer the chest approach, adding laparotomy when necessary. Acute right-sided injuries and chronic injuries should be approached through the chest.

Missed Diaphragmatic Rupture and Progressive Hepatothorax, 26 Years after Blunt Injury

Cases of blunt diaphragmatic rupture are not as common as other thoracoabdominal injuries and may pose a diagnostic challenge. Depending upon the size of the right hemidiaphragmatic rupture, herniation of liver may be partial, as progressive hepatothorax. The diagnosis of progressive hepatothorax coincides with the onset of the first symptoms of herniation. In the patient presented here, the interval between the original injury and the onset of symptoms related to the herniation of the abdominal cavity organs in the thorax was 26 years. Herniation of abdominal organs into the thorax was apparently rather slow and asymptomatic. The first symptoms, 26 years after trauma, included epigastric pain, meteorism, nausea, and vomiting, and all of them were due to gastrothorax and elongated gaster. These symptoms were nonspecific and therefore interpreted as acute alcoholic gastritis. With deterioration of the patient’s condition, they were subsequently interpreted as subileus due to the strangulation of a portion of the elongated and dilated stomach. Laparoscopy proved to be the most reliable diagnostic method in this case.

The Impact of Positive Pressure Ventilation on the Diagnosis of Traumatic Diaphragmatic Injury

Initial chest radiography (CXR) has been noted to have limited diagnostic sensitivity to detect acute diaphragmatic injury (ADI). A further confounding variable may be intubation and positive pressure ventilation which may prevent herniation of abdominal organs until weaning is achieved. We sought to determine the impact of positive pressure ventilation on the sensitivity of the initial CXR to identify ADI as well as to document the incidence of late herniation occurring as positive pressure ventilation is weaned. A retrospective chart review of 166 patients over an 8-year period in whom diagnosis of ADI was made on the same admission was performed. Etiology was penetrating trauma in 91 (55%). Eighty-five (51%) patients were intubated and ventilated with positive pressure before the initial chest radiograph. Diagnosis was made within 24 hours in 144 (87%) cases. The ability to correctly identify ADI by CXR was affected by whether or not the patient was intubated (intubated 12% vs nonintubated 27%; P = 0.001), side (right 10% vs left 27%; p = 0.04), and injury size (> 5 cm 81% vs < or = 5 cm 3%, P = 0.02). Late diagnosis was made in 22 cases: eight during surgery, six because of persistent radiographic abnormalities, and six when high levels of ventilator support were decreased with subsequent herniation of stomach above the diaphragm. Two cases were described at autopsy. Diaphragmatic injuries cannot be excluded if patients are intubated. Late diagnosis can be facilitated if chest radiographs are reviewed in sequence as ventilator support is decreased.

Cell proliferation and apoptosis in experimental lung hypoplasia

Background/Purpose: Current treatment for lethal pulmonary hypoplasia in congenital diaphragmatic hernia (CDH) may be hampered by uncertainty over its origin. Herniation of abdominal organs into the chest was thought to produce lung hypoplasia by compression. Experimental CDH models suggest that disturbed lung growth precedes these events. Mammalian development comprises cell differentiation, proliferation and programmed cell death or apoptosis. Could lung hypoplasia in CDH result from alterations in these processes well before visceral herniation takes place? The aim of this study was to compare cell proliferation and apoptosis in normal and hypoplastic embryonic lungs before normal diaphragmatic closure using a CDH model. Methods: Sprague-Dawley rats were given 100 mg of nitrofen on day 9.5 of pregnancy to create lung hypoplasia and CDH in newborns (term, 22 days). Control rats received olive oil. Cell proliferation in embryonic lung specimens was measured by bromodeoxyuridine (BrdU) incorporation at 13.5 to 15.5 days' gestation, before normal diaphragmatic closure in this species (day 16.5). Apoptosis was measured by the in situ end-nick labelling (TUNEL) method in lung sections obtained from rat embryos of 13.5 to 16.5 days' gestation. Results: High levels of cell proliferation were seen in both normal control and nitrofen-exposed lungs. However, 24 hours before normal diaphragmatic closure, nitrofen-exposed lungs had significant reductions in cell proliferation on day 15.5 of gestation (P =.009 v controls). Apoptosis occurred at low levels throughout the developmental stages examined (<0.3%) without significant differences encountered between the study groups. Conclusions: These findings have shown high rates of cell division during normal lung development before diaphragmatic closure. Decreased levels over this critical period in gestation may contribute to early lung anomalies in the nitrofen CDH model. Strategies to promote cell proliferation in the fetal lung may therefore hold future promise in human CDH. Apoptosis appears not to play a major role in hypoplastic lung development. Therapies to inhibit apoptosis would seem unlikely to improve this early lung growth. J Pediatr Surg 35:129-133. Copyright © 2000 by W.B. Saunders Company.

Cell proliferation and apoptosis in experimental lung hypoplasia

Current treatment for lethal pulmonary hypoplasia in congenital diaphragmatic hernia (CDH) may be hampered by uncertainty over its origin. Herniation of abdominal organs into the chest was thought to produce lung hypoplasia by compression. Experimental CDH models suggest that disturbed lung growth precedes these events. Mammalian development comprises cell differentiation, proliferation and programmed cell death or apoptosis. Could lung hypoplasia in CDH result from alterations in these processes well before visceral herniation takes place? The aim of this study was to compare cell proliferation and apoptosis in normal and hypoplastic embryonic lungs before normal diaphragmatic closure using a CDH model. Sprague-Dawley rats were given 100 mg of nitrofen on day 9.5 of pregnancy to create lung hypoplasia and CDH in newborns (term, 22 days). Control rats received olive oil. Cell proliferation in embryonic lung specimens was measured by bromodeoxyuridine (BrdU) incorporation at 13.5 to 15.5 days' gestation, before normal diaphragmatic closure in this species (day 16.5). Apoptosis was measured by the in situ end-nick labelling (TUNEL) method in lung sections obtained from rat embryos of 13.5 to 16.5 days' gestation. High levels of cell proliferation were seen in both normal control and nitrofen-exposed lungs. However, 24 hours before normal diaphragmatic closure, nitrofen-exposed lungs had significant reductions in cell proliferation on day 15.5 of gestation (P = .009 v controls). Apoptosis occurred at low levels throughout the developmental stages examined (< 0.3%) without significant differences encountered between the study groups. These findings have shown high rates of cell division during normal lung development before diaphragmatic closure. Decreased levels over this critical period in gestation may contribute to early lung anomalies in the nitrofen CDH model. Strategies to promote cell proliferation in the fetal lung may therefore hold future promise in human CDH. Apoptosis appears not to play a major role in hypoplastic lung development. Therapies to inhibit apoptosis would seem unlikely to improve this early lung growth.

Diaphragmatic injuries

A 6-year series of 26 patients with diaphragmatic injury is presented, 15 with rupture from blunt injuries and 11 after penetrating injuries. All had associated injuries and seven died because of these. The diagnosis may be difficult and was consequently delayed in two patients. Eleven ruptured diaphragms were diagnosed before operation, 14 on the operating table and one at autopsy (dead on arrival). Herniation of abdominal organs was seen in nine of 15 patients after blunt injuries. In most patients repair was via laparotomy using absorbable sutures. It is still essential that the surgeon should be aware of the possibility of the diagnosis and the assoicated severe injuries.

No evidence of WT1 gene mutations in children with congenital diaphragmatic hernia

Children with congenital diaphragmatic hernia are born with a defect of the diaphragm that usually leads to a herniation of abdominal organs up into the thoracic cavity on the same side. The condition is often fatal, usually because of concomitant lung hypoplasia. The cause of this condition is unknown. The majority of cases are sporadic, but familial aggregation has been observed, indicating a genetic back-ground. The tumor suppressor gene WT1 is involved in normal early urogenital development, and it is expressed in the mesothelium in the early human fetus. Recently, knockout mice homozygous for WT1 gene mutations were con-structed. The embryos died between days 13 and 15 of gestation. Besides serious urogenital and thoracic malformations, the mice had defects in the diaphragm that caused herniation of lung tissue into the abdomen. These findings prompted the authors to screen for WT1 gene mutations in 27 children who had congenital diaphragmatic hernia. Using exon-per-exon polymerase chain reaction (PCR) amplifications and denaturing gradient gel electrophoresis, no WT1 mutations were detected. Southern blot analysis did not show any large rearrangements in the WT1 gene. These results exclude WT1 gene mutations as a major etiological factor for the isolated diaphragmatic defect. However, it is possible that other genes in the WT1 pathway are involved in this defect.

Vaginal rupture associated with herniation of abdominal viscera in pregnant ewes.

Seventeen cases of vaginal rupture with herniation of abdominal organs were examined. The injury consisted of a dorsal tear in the vagina and, most frequently, evisceration of the bowel. The tear was accompanied by extensive vaginal bleeding. Serum calcium concentrations were low in the affected cases and the concentrations of beta-hydroxybutyric acid and urea were high. The average age of the affected ewes was four years (range 3 to 6). They were generally in poor condition and carrying more than one fetus (2.7 lambs per ewe) although younger ewes and ewes in good condition were also affected. No primiparous ewes were affected. Ten of the 17 ewes were found dead and six were humanely destroyed; in one, the injury was repaired surgically but the ewe died 48 hours later.