The vanishing stent: Repeated fracture and dissolution of nitinol gastric stents in a long term cancer survivor
Christopher Randle Lunt, Pavan Najaran, Derek E. Edwards, Jon K Bell, Damian Mullan
Abstract
Nitinol self expandable metal stents are increasingly utilised for malignant obstruction in the proximal gastrointestinal tract. We describe a case in which repeated fracture of proximal duodenal stents with dissolution of the nitinol wire skeleton and covering membranes occurred in a long term cancer survivor. This necessitated placement of 4 stents for symptom control and to allow oral feeding until the patient’s death 20 months after the initial stent was inserted. Fracture of gastric and duodenal stents has rarely been described previously, some incidences of which were considered due to mechanical causes. Dissolution of stent metal skeletons has not previously been recognised in gastroduodenal stents but has been described in an oesophageal stent subject to reflux of gastric content and a biochemical mechanism has been proposed. With modern oncological treatment the prospect of patients outliving their stents is increasing and the need for repeat procedures should form part of the consent process.
Introduction
The use of nitinol self expandable metal stents (SEMSs) for the treatment of malignant obstruction within the gastrointestinal (GI) tract is well established. We describe a case in which repeated fracture of the stent and dissolution of the covering membranes occurred in a patient who survived for 20 months following initial stent placement and required multiple further stent insertions.
The possible mechanism of stent failure is discussed and we recommend considering the anticipated survival of the patient with modern oncological treatment when deciding on stent placement and as part of the consent process.
Case Report
A 75-year-old woman with metastatic breast cancer presented with persistent vomiting and was diagnosed with gastric outlet obstruction secondary to metastatic deposits at the pylorus and proximal duodenum identified with computed tomography (CT) scanning. Subsequent contrast examination confirmed the diagnosis and a 10 cm × 24 mm EGIS double covered SEMS (S&G Biotech, Yongin, Korea) was inserted fluoroscopically. The patient returned to tolerating diet and was commenced on further chemotherapy.
Symptoms recurred at 4 months and radiographs demonstrated reduced radio-opacity of the central portion of the stent (Fig. 1). A contrast study demonstrated recurrent occlusion (Fig. 2) and a further 10 cm × 24 mm double-covered EGIS stent was placed using fluoroscopic guidance with good clinical improvement. The patient was started on high dose proton pump inhibitor therapy. After a further 4 months symptoms recurred. CT and fluoroscopy again demonstrated central collapse of the stent and attenuation of the metal portion centrally (Fig. 3) requiring insertion of another stent (10 cm × 24 mm EGIS double covered).
Endoscopy was performed when the third stent occluded after a further 3 months (18 months after the original stent insertion). This demonstrated perishing of all three stents, with multiple fractures of the three double wire skeletons and perishing of the covering membranes (Fig. 4, 5).
It was not possible to negotiate the stricture endoscopically and a 25 × 82 mm EnterElla stent (ELLA-CS, Hradec Králové, Czech Republic) was inserted fluoroscopically. The patient was able to tolerate oral feeding up to her death 2 months later.
Discussion
Degradation of coving materials in upper GI,1 biliary,2 and pulmonary stents3,4 is well recognised, especially if the covering is manufactured from polyurethane 1.
Fracture of the nitinol skeleton has been reported much less commonly beyond the oesophagus. In three of these cases the fracture occurred shortly after insertion or following endoscopic manipulation of a pre-existing stent suggesting that these failures were due to either manufacturing defects or mechanical damage to the stent at the time of insertion or following manipulation.5–7
In the other 3 cases which involved both covered and uncovered stents fracture seemed un-precipitated, occurring spontaneously months after insertion.8–10
Our patient had repeated stent failure in the absence of an additional mechanical insult, suggesting a corroding effect of the gastric environment, which led to destruction of the covering membranes and dissolution of the metal skeleton and consequent loss of radiopacity, presumably due to changes at an atomic level as described by Racek et al11 allowing the stent skeleton to dissolve. Why the central portion of the stents was more prone to this is unclear, but potentially the constant pressure of the stricture may have an aggravating effect.
A similar event described in an oesophageal stent which was subject to reflux of gastric content, led to the hypothesis of an 8 step process of fatigue failure beginning with micro fracture of the titanium oxide surface leading to embrittlement and eventual nitinol fracture in stents which are exposed to electrolyte solutions such as gastric fluid.11,12
In an initial study analysing the metal skeleton of explanted oesophageal stents, loss of tensile strength and alteration of the nickel/titanium ratio could be demonstrated.13
With the ever extending life expectancy offered by modern oncological treatment regimens an increasing number of patients will outlive their stents. Nitinol is proving vulnerable to biochemical processes in the GI tract and episodes of failure will become increasingly common, causing dilemmas for both clinicians and stent manufacturers. It needs to be part of the consent process and be communicated to the patient that stents may fail, requiring re-intervention.
Conflicts of Interest
No potential conflict of interest relevant to this article was reported.
Article information
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