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Ann Thorac Surg 2003;76:341-342
© 2003 The Society of Thoracic Surgeons
a Pediatric Cardiothoracic Surgery, Children’s Hospital, 200 Henry Clay Ave, New Orleans, LA, USA 70118
To the Editor:
We appreciate the interest in our case report and the comments made by Dr Matsuo and colleagues. They described a patient with asplenia syndrome, status post repair of total anomalous pulmonary venous connection and pulmonary artery banding, who developed a chylothorax after undergoing total cavo-pulmonary shunt at 18 months of age. After 3 weeks of persistent drainage, somatostatin was given intravenously, causing a dramatic reduction in chest tube drainage, allowing chest tube removal 5 days after initiating somatostatin. The next day, 6 days after initiating somatostatin, the patient developed a midgut volvulus from malrotation necessitating emergent laparotomy. Dr Matsuo and colleagues assert that the somatostatin caused the volvulus.
Malrotation of the gut is quite common in patients with asplenia, polysplenia, or heterotaxy syndromes. In fact, one study demonstrated an 89% incidence of malrotation[1]. It is impossible, however, to predict which of these patients will go on to develop midgut volvulus, which can be a devastating and life-threatening complication. Volvulus of the malrotated gut is a mechanical process brought about by twisting of the malfixated mesentery. Intuitively, factors that increase the mechanical activity or peristalsis of the intestine (eg, gastroenteritis or toxic ingestion) would exasperate the process. One might also surmise that edematous or fluid-filled, dilated bowel might aggravate the situation as well. Based on the known pharmacologic effects of somatostatin, we expect that somatostatin would have an almost protective effect against volvulus, especially at the relatively low doses that we reported (1 to 2 µg/kg). Somatostatin reduces gastric, pancreatic, and intestinal secretion as it inhibits the release of serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide. Yes, it reduces splanchnic blood flow and, even if the splanchnic arteriolar resistance is increased, as the authors claim, we do not see how this would cause midgut volvulus. Based on the information provided, it is hard to know for sure what role, if any, the somatostatin played in this patient developing midgut volvulus. Questions that need to be answered are: Was the child being fed enterally and, if so, with what type of formula and for how long? Was there any ascites? Was there any cause for an ileus such as chronic narcotic administration or sepsis? Any of these factors may have played a role.
Dr Matsuo and colleagues are to be commended on successfully managing two very serious complications in an extremely high-risk patient. Their comments raise two very important issues. First, it appears that somatostatin can drastically reduce drainage in selected patients with persistent chylothoraces after congenital heart surgery however, as with any new therapy, patients need to be monitored closely for adverse effects. Second, patients with asplenia, polysplenia, or heterotaxy syndromes have a high incidence of intestinal malrotation and are at increased risk of midgut volvulus. This fact alone has led many centers to screen these patients with an upper gastroin-testinal barium study and perform prophylactic Ladd procedures before they leave the hospital.
References
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