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Early acute gastric dilatation following percutaneous endoscopic gastrostomy
rior mediastinum further helped to delineate the outline of the duct quite clearly. The thoracic duct lies in a space anteriorly limited by the posterior wall of the esophagus, laterally by the azygos vein and medially by the thoracic aorta. At the level of aortic arch the thoracic duct turns forward from the posterior aspects of the esophagus to the medial aspect of the left subclavian artery, and this was the most visible part of the duct cranially. Interestingly, the remaining part of the duct and its entry into the jugular-subclavian junction was not clearly visualized, probably because of a combination of poor distant resolution and motion artifacts caused by the discomfort experienced by the patients during imaging with the echoendoscope in the upper esophagus. Variations of the duct (double thoracic duct) described in the literature were not seen in our cases. 2 In conclusion, EUS can reliably identify the thoracic duct, and may offer a potentially useful method to evaluate a variety of disease processes which affect the anatomy and function of the thoracic duct.
Vinod K. Parasher, MD Emanuele Meroni, MD Pasquale Spinelli, MD National Cancer Institute Milan, Italy
REFERENCES 1. Rosenberg A, Abrahmns HL. Radiology of the thoracic duct. AJR Am J Roentgenol 1971;111:807-20. 2. Schnyder P, Hauser H, Moss A, et al. CT of the thoracic duct. Eur J Radio] 1983;3:18-23. 3. Jacobson KH, Thomsen HS, Nielsen SL, et al. Scintigraphic demonstration of the thoracic duct following oral ingestion of 123 I-hepatadecanoic acid. Gastrointest Radiol 1989;14:212-4.
Early acute gastric dilatation following percutaneous endoscopic gastrostomy
sion with no audible bowel sounds. Plain radiology not only confirmed pneumonia but also demonstrated a large dilated stomach, with no evidence of small bowel obstruction. Feeding was stopped; he received intravenous antibiotics and fluid replacement. A nasogastric tube was passed and the stomach decompressed. Once his respiratory status had improved a further endoscopy was performed to determine the status of the tube. This showed no abnormality--the PEG button was in a nolznal position with no evidence of its migration, nor any other structural cause for gastric outlet obstruction. We were able to recommence feeding through the same tube and, 1 year later, he has had no further feeding problems. To our knowledge there is only one previous description of this complication. 4 In that instance the PEG had been inserted 15 months previously and it appears that the dilatation was preceded by a wound infection. We believe that in this case the gastric dilatation was directly related to the PEG insertion. One might argue that it was the reinstatement of food to a relatively starved stomach that led to its dysmotility. Even so it would remain as a complication of PEG feeding. Delayed gastric emptying, 3 "late" vomiting, 1 and temporary ileus 5 have been described but never such an acute motility problem. Could it be related to multiple sclerosis? Certainly, large bowel motility disorders are well described. 6 Upper gastrointestinal symptoms may be more common in multiple sclerosis than usually appreciated, 7but there would appear to be only one previous report ofgastroparesis, s It is also far too coincidental that this man should have developed such a problem that resolved so rapidly at this particular time. We report this as another potential complication of an increasingly used feeding technique. PEG remains relatively safe, but we re-emphasize the need for vigilance in such patients.
G. Vautier, BM, BSc, MRCP B.B. Scott, MD, FRCP Department of Medicine County Hospital Lincoln, United Kingdom
To the Editor: Percutaneous endoscopic gastrostomy (PEG) feeding is now a well established means of giving long-term enteral nutrition to patients with chronic dysphagia.1 As experience grows with the technique, so does the list of possible complications.2, 3 We report the occurrence of acute early gastric dilatation, which we believe is directly related to the procedure. A 32-year-old man with a 10-year history of multiple sclerosis was referred to us with progressive dysphagia during the preceding 6 months. His nutritional status had begun to deteriorate and PEG feeding was believed appropriate. A 9-gauge PEG tube (Fresenius, Tannus, Germany) was inserted using the standard pull-through method with the patient under midazolam sedation. In accordance with the policy of this unit, an aseptic technique was used without antibiotic prophylaxis. For the first 12 hours small volumes of water were passed down the tube. Then, as tolerated, liquid formula was infused in gradually increasing rates up to 100 ml per hour -1. He was then discharged home. Three days after insertion he began to have profuse vomiting and developed abdominal distension. On readmission he was very ill, having aspirated his vomitus. He was in respiratory distress and clinical examination revealed tense abdominal distenVOLUME 42, NO. 2, 1995
REFERENCES 1. Hull MA, Rawlings J, Murray FE, et al. Audit of outcome of long-term enteral nutrition by percutaneous endoscopic gastrostomy. Lancet 1993;341:869-72. 2. Foutch PG. Complications ofpercutaneous endoscopicgastrostomy and jejunostomy. Gastrointestinal Endoscopy Clinics of North America 1992;2:231-48. 3. Park RHR, Allison MC, Lang J, et al. Randomised comparison of percutaneous endoscopicgastrostomy and nasogastric tube feeding in patients with persisting neurological dysphagia. BMJ 1992;304:1406-9. 4. Ghosh S, Eastwood MA, Palmer KR. Acute gastric dilatation--a delayed complication of percutaneous endoscopicgastrostomy. Gut 1993;34:859-60. 5. Larson DE, Burton DD, Schroeder KW, DiMagno EP. Percutaneous endoscopicgastrostomy; indications, success, complications, and mortality in 314 consecutive patients. Gastroenterology 1987;93:48-52. 6. Glick ME, Meshkinpour H, Haldeman S, Bhatia NN, Bradley WE. Colonic dysfunction in multiple sclerosis. Gastroenterology 1982;83:1002-7. 7. Sullivan SN, Ebers GG. Gastrointestinal dysfunction in multiple sclerosis. Gastroenterology 1983;84:1460. 8. Guta YK. Gastroparesis with multiple sclerosis. JAMA 1984; 252:42. GASTROINTESTINAL ENDOSCOPY
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Vinod K. Parasher, MD Emanuele Meroni, MD Pasquale Spinelli, MD National Cancer Institute Milan, Italy
REFERENCES 1. Rosenberg A, Abrahmns HL. Radiology of the thoracic duct. AJR Am J Roentgenol 1971;111:807-20. 2. Schnyder P, Hauser H, Moss A, et al. CT of the thoracic duct. Eur J Radio] 1983;3:18-23. 3. Jacobson KH, Thomsen HS, Nielsen SL, et al. Scintigraphic demonstration of the thoracic duct following oral ingestion of 123 I-hepatadecanoic acid. Gastrointest Radiol 1989;14:212-4.
Early acute gastric dilatation following percutaneous endoscopic gastrostomy
sion with no audible bowel sounds. Plain radiology not only confirmed pneumonia but also demonstrated a large dilated stomach, with no evidence of small bowel obstruction. Feeding was stopped; he received intravenous antibiotics and fluid replacement. A nasogastric tube was passed and the stomach decompressed. Once his respiratory status had improved a further endoscopy was performed to determine the status of the tube. This showed no abnormality--the PEG button was in a nolznal position with no evidence of its migration, nor any other structural cause for gastric outlet obstruction. We were able to recommence feeding through the same tube and, 1 year later, he has had no further feeding problems. To our knowledge there is only one previous description of this complication. 4 In that instance the PEG had been inserted 15 months previously and it appears that the dilatation was preceded by a wound infection. We believe that in this case the gastric dilatation was directly related to the PEG insertion. One might argue that it was the reinstatement of food to a relatively starved stomach that led to its dysmotility. Even so it would remain as a complication of PEG feeding. Delayed gastric emptying, 3 "late" vomiting, 1 and temporary ileus 5 have been described but never such an acute motility problem. Could it be related to multiple sclerosis? Certainly, large bowel motility disorders are well described. 6 Upper gastrointestinal symptoms may be more common in multiple sclerosis than usually appreciated, 7but there would appear to be only one previous report ofgastroparesis, s It is also far too coincidental that this man should have developed such a problem that resolved so rapidly at this particular time. We report this as another potential complication of an increasingly used feeding technique. PEG remains relatively safe, but we re-emphasize the need for vigilance in such patients.
G. Vautier, BM, BSc, MRCP B.B. Scott, MD, FRCP Department of Medicine County Hospital Lincoln, United Kingdom
To the Editor: Percutaneous endoscopic gastrostomy (PEG) feeding is now a well established means of giving long-term enteral nutrition to patients with chronic dysphagia.1 As experience grows with the technique, so does the list of possible complications.2, 3 We report the occurrence of acute early gastric dilatation, which we believe is directly related to the procedure. A 32-year-old man with a 10-year history of multiple sclerosis was referred to us with progressive dysphagia during the preceding 6 months. His nutritional status had begun to deteriorate and PEG feeding was believed appropriate. A 9-gauge PEG tube (Fresenius, Tannus, Germany) was inserted using the standard pull-through method with the patient under midazolam sedation. In accordance with the policy of this unit, an aseptic technique was used without antibiotic prophylaxis. For the first 12 hours small volumes of water were passed down the tube. Then, as tolerated, liquid formula was infused in gradually increasing rates up to 100 ml per hour -1. He was then discharged home. Three days after insertion he began to have profuse vomiting and developed abdominal distension. On readmission he was very ill, having aspirated his vomitus. He was in respiratory distress and clinical examination revealed tense abdominal distenVOLUME 42, NO. 2, 1995
REFERENCES 1. Hull MA, Rawlings J, Murray FE, et al. Audit of outcome of long-term enteral nutrition by percutaneous endoscopic gastrostomy. Lancet 1993;341:869-72. 2. Foutch PG. Complications ofpercutaneous endoscopicgastrostomy and jejunostomy. Gastrointestinal Endoscopy Clinics of North America 1992;2:231-48. 3. Park RHR, Allison MC, Lang J, et al. Randomised comparison of percutaneous endoscopicgastrostomy and nasogastric tube feeding in patients with persisting neurological dysphagia. BMJ 1992;304:1406-9. 4. Ghosh S, Eastwood MA, Palmer KR. Acute gastric dilatation--a delayed complication of percutaneous endoscopicgastrostomy. Gut 1993;34:859-60. 5. Larson DE, Burton DD, Schroeder KW, DiMagno EP. Percutaneous endoscopicgastrostomy; indications, success, complications, and mortality in 314 consecutive patients. Gastroenterology 1987;93:48-52. 6. Glick ME, Meshkinpour H, Haldeman S, Bhatia NN, Bradley WE. Colonic dysfunction in multiple sclerosis. Gastroenterology 1982;83:1002-7. 7. Sullivan SN, Ebers GG. Gastrointestinal dysfunction in multiple sclerosis. Gastroenterology 1983;84:1460. 8. Guta YK. Gastroparesis with multiple sclerosis. JAMA 1984; 252:42. GASTROINTESTINAL ENDOSCOPY
189