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Editor,—We would like to bring to attention a complication of percutaneous endoscopic gastrostomy (PEG) that presented in two patients in one afternoon. Both patients were male, and they had both had a Fresenius PEG tube placed two years previously. One patient was 88 years old with a history of stroke who, although fully alert, was unable to swallow safely. The PEG had allowed him to be cared for in his own home. The second case was that of a young man who had developed subacute sclerosing panencephalitis in 1985 following measles infection at the age of 13. His general condition was gradually deteriorating, and he was being looked after in his own home by his family and carers.
In both cases, the Fresenius PEGs had been placed in the standard manner. The carers of the patients had followed the instructions that accompany the device without difficulty until a few weeks before presentation when they reported intermittent blockage of the tubes. On examination, the stoma site was healthy, but at endoscopy in both cases, we were unable to see the bumper (internal flange). Instead, there was a raised mound of oedematous gastric mucosa with a central small crevice, resembling a leiomyoma. Fluid could be injected under pressure through the PEG into the gastric lumen through this crevice. Radiological screening of the first case did not show any twist or disruption to the PEG tube, but the internal bumper had eroded into the anterior abdominal wall and there was a small cavity apparent between the bumper and the gastric mucosa. In both cases, a second PEG was placed in parallel to the first one without difficulty, and the first PEG was left in situ for a short period of time. Subsequently, in the first case the initial PEG was removed under local anaesthesia because it continued to discharge pus. In the second case, the patient died six weeks later from unrelated causes.
The literature records several cases of the buried bumper syndrome, and describes various methods of dealing with this complication.1–3 In our cases, it is likely that this complication occurred because of excessive pressure on the internal bumper as a result of over tightening of the external flange. However, to prevent this occurring we suggest that at regular intervals the external flange is loosened and the PEG is pushed in and out to ensure that the internal bumper moves freely. Then the external flange should be re-tightened sufficiently to hold the PEG in place, but not so tight as to encourage the bumper to become embedded. It is worth noting that these instructions are different from those that should be followed in the immediate period after PEG placement. In the first 48 hours, a reasonably firm pressure between the internal and external flanges should be maintained in order to prevent intraperitoneal leakage. This change in emphasis may be a source of confusion.
The instruction leaflet with the Fresenius tube does not indicate that the PEG should be able to move in and out when the external flange is loosened for skin care, and is therefore inadequate. As a result, we have surveyed the instruction leaflets provided by eight manufacturers of PEGs and found similar inadequate details in five. We have surveyed all our patients (n=20) with long term PEGs and no others have developed this complication.
We therefore recommend that the correct advice is given to those caring for patients with long term PEGs to prevent this complication from occurring and that manufacturers’ leaflets should mention this potential complication.
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