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Gastric volvulus (GV) is a rare surgical emergency, defined by the abnormal rotation of a part of the stomach around another part, leading to obstruction, and in some cases, tissue ischemia and necrosis. Anatomically, most cases are either organoaxial volvulus, occurring along the stomach’s longitudinal axis from the gastroesophageal junction to the pylorus, or mesenteroaxial volvulus, occurring perpendicular to the longitudinal axis, such that the pylorus and antrum come to lie above the gastroesophageal junction. Associated contributory diaphragmatic anomalies are common, especially in neonates, while splenic anomalies are also frequent.
GV may present as an acute or chronic condition. The mode of presentation varies depending on age. Neonates and infants may present with respiratory distress, non-bilious vomiting, excessive salivation, and regurgitation of feeds. Older children may present with Borchardt’s triad of non-productive retching, localized epigastric swelling, and failure to pass a nasogastric tube.
Diagnosis relies on index of suspicion, and is aided by plain radiography of the chest and abdomen, and upper gastrointestinal contrast series to clarify the anatomical orientation of the stomach. Suggestive plain radiography findings include spherically distended stomach with two air-fluid levels or a double retrocardiac air-fluid level, as is the case with intrathoracic GV.
In acute GV, surgery is the management of choice and involves correction of any contributory anatomical abnormalities such as diaphragmatic hernia as well as fixation of the stomach to the anterior abdominal wall with a gastrostomy and/or anterior gastropexy. Minimally invasive approaches are being more frequently employed to achieve these goals.
KeywordsVolvulus Organoaxial Mesenteroaxial Nasogastric Gastropexy Gastrostomy
Gastric volvulus is a rare, potentially life-threatening surgical emergency. It occurs when part of the stomach rotates abnormally with respect to another part of the stomach, leading to closed loop gastric obstruction and, in some cases, tissue ischemia and necrosis. It was first described in adults by Berti in 1866 and in children by Oltman in 1899 (Sivakumar 2008). Since then, over 640 cases of acute and chronic gas tric volvulus in children have been described in the literature. A comprehensive review of the world literature in 2008 found that 21% of cases presented in the neonatal period, 37% presented between 1 and 12 months of age, while just 14% present between the ages of 6 and 18 years (Cribbs et al. 2008). Associated contributory anomalies are common. Congenital or acquired defects in the diaphragm are the most commonly reported anomalies, while gastri c volvulus in older children is frequently associated with neurodevelopmental handicap and splenic abnormalities (McIntyre et al. 1994; Cribbs et al. 2008). Both operative and nonoperative management strategies have been described in the literature.
Gastric volvulus may be defined as an abnormal rotation of one part of the stomach around another; the degree of twist varies from 180° to 360° and is associated with closed loop obstruction and the risk of strangulation (Tanner 1968). Rotation of the stomach less than 1800 is termed gastric torsion, is probably common, and is frequently asymptomatic. Such cases may be associated with transient vomiting in infants, but spontaneous resolution is the rule (Eek and Hagelsteen 1958).
Gastric volvulus may be acute and complete – the variety most often seen in infancy – or chronic and partial, which is seen more commonly in older children. While no study has set out to formally define risk factors fo r gastric volvulus, certain congenital anomalies appear to have a contributory role to its pathogenesis. Eventration or herniation of the diaphragm is present in about two-thirds of all children presenting with gastric volvulus (Cribbs et al. 2008). However, this proportion is as high as 80% in some series of infants (Cole and Dickinson 1971). Diaphragmatic hernias are typically paraesophageal or posterolateral defects, but gast ric volvulus within a Morgagni hernia is also possible (Estevao-Costa et al. 2000). Abnormal upper gastrointestinal anatomy due to midgut malrotation, dextrogastria, or previous gastroesophageal surgery have been implicated in its etiology, as has aberrant splenic anatomy, such as wandering spleen and the asplenia syndrome (asplenism, congenital heart disease, with or without intestinal malrotation, and deficiency of the gastric ligaments) (Fung et al. 1990; Garcia et al. 1994; Cribbs et al. 2008; Aga et al. 2010; Joshi and Parelkar 2010; Mitsunaga et al. 2011; Mirza et al. 2012).
In patients with diaphragmatic eventration or herniation, the presumed mechanism of gastric volvulus is u pward displacement of the transverse colon, which pulls up the greater curve of the stomach into the expanded left upper quadrant. Dextrogastria may further facilitate this process (Aga et al. 2010; Menezes et al. 2010). Acute gastric volvulus may therefore present as an early complication of diaphragmatic defects.
Gastric distension may encourage the development of gastric volvulus. I nfantile hypertrophic pyloric stenosis may rarely be a predisposing factor, as has been reported in two cases. However, diaphragmatic defects were also present in both cases (Moreno Torres 1968; Anagnostara et al. 2003). Air swallowing can also cause gastric distension, and intermittent gastric volvulus has been reported in an aerophagic, neurologically impaired child (Komuro et al. 2005).
Other rare causes of gastric volvulus i n the neonate and infant include abnormal bands or adhesions producing an axis of rotation for the stomach (Cole and Dickinson 1971; Iko 1987; Gerstle et al. 2009), rectal atresia with consequent overdistension of the transverse colon (Mizrahi et al. 1988), congenital absence or resection of the left lobe of the liver which may promote abnormal gastric mobility (Chuang et al. 1993; Koh et al. 2008), and congenital deficiency of the gastrocolic omentum (Odaka et al. 1999). Nakada et al. reported gastric volvulus as a complication in 3 of 25 patients with asplenia, the youngest of whom was 1 month of age (Nakada et al. 1997). Anchoring gastric ligaments were deficient in all cases. Because of the potentially fatal outcome of acute gastri c volvulus in this situation, Okoye et al. have recommended prophylactic gastropexy in all patients with asplenia (Okoye et al. 1997). A review of gastric malformations in patients with the asplenic syndrome by Mitsunagaet al. in 2011, which included one case of gastric volvulus, described the hugely variable anatomy encountered in this condition (Mitsunaga et al. 2011). Defective fixation and ligamentous laxity also account for the association between gastric volvulus and a wandering spleen (Garcia et al. 1994). Intestinal malrotation is associated with gastric volvulus, even in the absence of asplenia (Iko 1987; Nakada et al. 1997; Gerstle et al. 2009).
Gastric volvulus in children may rarely arise as a postoperative complication. It has been described after Nissen fundoplication, presumably because the stomach has been extensively mobilized by division of gastrosplenic and gastrocolic attachments (Fung et al. 1990). It has also been described in two cases postoperatively for tracheoesophageal fistula/esophageal atresia repair with no associated deficiency of anchoring ligaments (Joshi and Parelkar 2010). There is one recorded case of g astric volvulus developing after repair of a diaphragmatic hernia and another as an iatrogenic complication of gastric transposition in infancy (Starshak and Sty 1983; Chan and Saing 1996). Diaphragmatic trauma from blunt injury due to falling and the Heimlich maneuver have also been reported to have predisposed to gastr ic volvulus in older children (Ragavan 2010; Matharoo et al. 2013).
The clinical features depend on the degree of rotation and obstruction. In adults, Borchardt’s triad of (1) unproductive retching, (2) acute localized epigastric distension, and (3) inability to pass a nasogastric tube is classically diagnostic of gastr ic volvulus. In neonates and infants, however, these features are not always present in combination, and symptoms and signs may be nonspecific, such as vomiting (usually, but not exclusively, non-bilious, depending on the degree of pyloric obstruction), respiratory distress (especially in those with an intrathoracic stomach), excessive salivation, and persistent regurgitation of feeds, similar to gastroesophageal reflux.
Hematemesis and anemia are well described, and occasionally the vomiting is described as projectile (Karabulut et al. 2009). Failure to thrive and chest infections are sometimes evident (Samuel et al. 1995). Upper abdominal pain and distension may be noted in older infants and children in whom the stomach is not intrathoracic (Campbell 1979; Starshak and Sty 1983).Difficulties in the normal placement of a nasogastric tube may provide evidence for the diagnosis; however, failure to pass a nasogastric tube may have several causes in the newborn, such as tracheoesophageal fistula/esophageal atresia or esophageal perforation (Soylu et al. 2013). Additionally, successful passage of a nasogastric tube does not exclude the diagnosis (Cole and Dickinson 1971; Cameron et al. 1995). Findings that should raise suspicion of gastric volvulus however include arrest of the nasogastric tube in the distal esophagus and radiographic abnormalities on routine films. Further investigation with contrast studies is indicated in this circumstance. Jaundice may be part of the presenting symptom complex if one lead point for the volvulus involves the second part of the duodenum (Menezes et al. 2010). In older children, especially those with neurological impairment, presenting symptoms may be intermittent, chronic, and nonspecific (Cameron et al. 1995).
Acute gastric volvulus, if untreated, can lead to ischemic necrosis, gastric perforation, and death. Infants and neonates can present with severe respiratory distress, especially in the presence of a diaphragmatic defect, and initial preoperative resuscitative measures should include supplementary oxygen therapy and, where exhaustion due to increased work of breathing is present, ventilation support. Gastric decompression wherever possible with a nasogastric tube should be attempted, although vigorous attempts to pass a tube must be avoided because of a risk of gastric perforation, especially in those suspected of ischemic necrosis (Cole and Dickinson 1971). Volume and electrolyte repletion are mandatory during initial resuscitation.
Definitive surgical management for acute gastric volvulus will depend on the contributory anatomical anomaly. Although the direct thoracic approach has been described (Zaki et al. 2010), an abdominal approach is recommended, even when the stomach lies in the chest, since this allows identification of any associated gastrointestinal anomalies and accurate diaphragmatic repair if required. Occasionally, preliminary needle aspiration of the stomach may be warranted before manipulating a tensely dilated stomach and reducing the volvulus (Asch and Sherman 1977). Any associated diaphragmatic defect should be repaired. Excision of hernia sacs where present should be attempted, and crural repair in those with paraesophageal hernia should be undertaken. Fixation of the stomach to the anterior abdominal wall may take several forms and should accompany any surgery for gastric volvulus .
Gastrostomy alone may be used for gastric fixation in neonates, since it provides adequate fixation, postoperative decompression, and a route for postoperative feeding. A Stamm gastrostomy using a 10 or 12 French gauge Malecot catheter secured by a double purse string absorbable suture is appropriate. In infants with no predisposing diaphragmatic defect, an anterior gastropexy should be added to the gastrostomy procedure. This involves suturing the greater curve of the stomach to the parietal peritoneum of the anterior abdominal wall and the under surface of the diaphragm by a series of nonabsorbable sutures. Low recurrence rates have been reported with this procedure in the majority of cases, even when the gastrostomy was removed after 2 weeks (Stephenson and Hopkins 1964; Colijn et al. 1993; Bawa et al. 2012). This approach has also been successfully employed for infants with associated diaphragmatic defects.
Fundoplication may be necessary if there is evidence of gross gastroesophageal reflux, but several authors have achieved good results in such cases with a crural repair alone, and a more conservative approach is warranted provided the tendency to volvulus is prevented (Samuel et al. 1995; Stiefel et al. 2000). Diaphragmatic crural repair must be performed meticulously, as there is often a common hiatus for the esophagus and aorta in these patients (Stiefel et al. 2000). There is no justification for gastroenterostomy or the colonic displacement operation described by Tanner in this age group, and gastric resection should be limited to those with grossly necrotic nonviable segments in all patients (Tanner 1968; Lal Meena et al. 2011). A Doppler probe can be used intraoperatively to evaluate for restoration of gastric perfusion in cases where viability is in doubt (Gerstle et al. 2009).
In 1993 Blair et al. gave one of the earliest descriptions of laparoscopic-guided gastropexy , suggesting its suitability was limited to children with intermittent ga stric volvulus with no underlying abnormality (Cameron and Blair 1993). This is now probably the operative treatment of choice for such patients (Odaka et al. 1999). The laparoscopic approach has been reportedly effective both in treating neonates and those with associated splenic and diaphragmatic anomalies (Shah and Shah 2003; Okazaki et al. 2010). Laparoscopic gastropexy , which involves securing the anterior wall of the reduced stomach to the peritoneum with nonabsorbable sutures, can be combined with splenopexy in those with wandering spleen by fashioning an extraperitoneal pouch, within which the spleen is secured by closure of the peritoneum, leaving space for the splenic vessels (Okazaki et al. 2010). Splenopexy alone may be sufficient in gas tric volvulus due to wandering spleen.
A number of well-described complications can result from gas tric volvulus including prolonged gastric ileus, gastric necrosis, and perforation (Gerstle et al. 2009). Following successful surgical treatment, ischemic sequelae can include lower esophageal stricture, gastric outlet obstruction, and microgastria. This may lead to long-term dependence on gastrostomy or jejunostomy feeding and ultimately a requirement for a stomach substitution procedure (Kulkarni et al. 2011). Examples of stomach substitution procedures include the Hunt-Lawrence J-pouch and the ileocecal pouch. The former procedure entails division of the proximal jejunum, formation of a J-pouch with the distal limb, followed by an esophageal-jejunal pouch anastomosis, and anastomosis of the afferent limb of jejunum distal to the pouch with an end-to-side anastomosis to reestablish continuity of the proximal jejunum with the small bowel. A feeding jejunostomy should also be formed as part of this operation. Alternatively, an ileocecal pouch can be utilized, with the vermiform appendix brought out as a feeding stoma. Patients with such complicated clinical courses are susceptible to malabsorption and, in particular, vitamin B deficiency, and their nutrition should be supplemented accordingly.
The mortality from gastr ic volvulus is difficult to assess with series reporting mortality rates of 7.1% in acute ga stric volvulus compared to 2.7% in chronic cases (Gerstle et al. 2009). One review of 581 cases found that 28% of all infants presented with acute gastric volvulus requiring life-saving resuscitation, with a mortality of 6.9% within this group (Cribbs et al. 2008). Untreated, ga stric volvulus has a mortality rate of up to 80%, highlighting the importance of prompt recognition and treatment. Deaths have been reported due to missed or delayed diagnosis, with subsequent gastric necrosis and perforation, or inadequate gastric fixation (Cole and Dickinson 1971; McIntyre et al. 1994; Gerstle et al. 2009; Kulkarni et al. 2011).
Most recent series report uncomplicated early outcomes after surgery. One long-term follow-up study of nine infants demonstrated no recurrences or late complications (McIntyre et al. 1994). A more recent series included ten cases, one of whom expired owing to multi-organ failure and polytrauma, while the remaining nine cases, of which three were primary gastr ic volvulus, had no recurrence at a median follow-up of 4 years (Mirza et al. 2012).
Conclusion and Future Directions
Gastric volvulus is a rare surgical condition which can present acutely or chronically. The acute form can be life-threatening and lead to significant morbidity, especially where diagnosis is delayed. There is a high incidence of associated contributory anatomical anomalies, in particular diaphragmatic hernia and eventration, paraesophageal hernia, splenic anomalies, and malpositioned viscera such as midgut malrotation. Abnormally lax or deficient gastric ligaments appear to be heavily implicated in the pathogenesis of gas tric volvulus.
The presenting features of gastric volvulus are relatively nonspecific, and a high index of clinical suspicion is key to successful and timely diagnosis. Given the diagnostic accuracy of fluoroscopic contrast series, it is likely that this will remain the imaging modality of choice to diagnose gastr ic volvulus. The limited additional benefit from cross-sectional imaging with CT and MRI is offset by drawbacks regarding radiation dosage and logistical difficulties, respectively, at this present time.
While it may be possible to manage a limited number of children with chronic gastric volvulus and no anatomical anomalies nonoperatively, the majority will continue to be managed surgically. The laparoscopic approach is gaining favor, especially in older children, as it provides excellent exposure of the structures in the epigastrium and left hypochondrium and yields a more favorable cosmetic outcome when compared to a laparotomy scar. As availability and expertise with laparoscopy increases, it is reasonable to expect the trend toward its increased use in the treatment of gastric volvulus to continue.
- Moreno Torres E. Estenosis per hipertrofia de piloro con volvulo gastrico. Bol Soc Valenciana Paediatr. 1968;10:231–2.Google Scholar