Abstract
In September, 2013, a 57-year-old man presented with confusion and slurred speech. He had had a left upper lobectomy for adenocarcinoma of the lung 4 months earlier that had been complicated by aspiration requiring placement of a percutaneous endoscopic gastrostomy (PEG) tube (appendix). He had had a previous PEG a decade earlier, which was needed temporarily during the treatment of head and neck cancer. On examination he was hypothermic (34·4°C) and hypotensive (85/39 mm Hg) and he had an impressive anion gap metabolic acidosis (table, day 0). He had no obvious infection but an abdominal CT showed a fl uid-fi lled large bowel. We held his tube feeds and started antibiotics and intravenous fl uids. His encephalopathy and acidosis resolved. The next day we restarted tube feeds but by day 3 the patient’s confusion, slurred speech, hypotension, and gapped acidosis (table, days 3–4) returned. He was now incontinent of large volumes of liquid stool. Because this deterioration correlated with his tube feeds they were stopped and the patient improved. We theorised that he had D-lactic acidosis with a pathophysiology similar to that of short bowel syndrome, although he had no history of bowel resection. His urine D-lactate came back raised at 87·78 mmol/L (normal 0·0–0·25 mmol/L). Tests for toluene metabolites and organic acids, in particular pyroglutamic acid/5-oxoproline, were negative. We started a low carbohydrate tube feed and oral metronidazole. The patient’s encephalopathy, acidosis, and diarrhoea did not return and he was discharged to a rehabilitation facility. When reviewing this case for publication 9 months later we discovered that his abdominal CT had been misinterpreted—the internal bumper of his PEG tube was seated not within the gastric lumen but within the transverse colon (appendix), a buried bumper syndrome with transcolonic migration. The fl uid seen in his colon had been undigested tube feed. We frantically contacted the patient. Fortunately he was well, having decided shortly after discharge that he no longer wanted to use the feeding tube. A short time later the tube had fallen out. Buried bumper syndrome is a rare complication of PEG tubes, in which the internal bumper dislodges from the wall of the gastric lumen and migrates along the PEG tract toward the abdominal wall. The median interval from PEG placement to buried bumper syndrome is 18 months, although cases have been reported as early as 1–3 weeks. Transcolonic buried bumper syndrome, or transit of the internal bumper to within the lumen of the colon, is even less common. Our patient’s tube was placed via the Gauderer-Ponsky or pull method. We postulate that the introducer needle had accidentally perforated the colon, creating a transcolonic tract that was invisible until the internal bumper migrated outward along it. Adhesions from the previous PEG might have complicated placement of the second despite good transillumination and gastric insuffl ation. A similar case of D-lactic acidosis from accidental colonic tube feeding, involving exchange of a gastrostomy tube with a Foley catheter, prompted us to revisit our patient’s CT scan. The mechanism here is similar to a common cause of D-lactic acidosis—short bowel syndrome from small bowel resection or gastric bypass, in which a large undigested carbohydrate load enters the colon and is fermented into organic acids. Acidifi cation promotes overgrowth of acid-resistant bacteria, such as Lactobacillus spp, which produce D-lactate and further acidify the colon, creating a positive feedback loop. Systemic absorption of D-lactate can lead to encephalopathy and anion gap metabolic acidosis, hypothermia, and hypotension. Treatment consists of oral antibiotics targeting intestinal fl ora, a low carbohydrate diet, and occasionally bicarbonate and haemodialysis. As we eventually learnt transcolonic buried bumper syndrome can mimic short bowel syndrome as a cause of D-lactic acidosis in a patient with a PEG tube.
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