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Rapid progressive long esophageal stricture caused by gastroesophageal reflux disease after pylorus-preserving pancreatoduodenectomy.

Fukaya M, Abe T, Nagino M - BMC Surg (2016)

Bottom Line: In most cases, this morbidity is controllable by proton-pump inhibitor (PPI) and very rarely results in esophageal stricture.Even the administration of a proton pump inhibitor (PPI) for approximately five mouths did not improve esophageal stricture.Simultaneous 24-h pH and bilirubin monitoring confirmed that this patient was resistant to PPI.

View Article: PubMed Central - PubMed

Affiliation: Division of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho Showa-ku, Nagoya, 466-8550, Japan. mafukaya@med.nagoya-u.ac.jp.

ABSTRACT

Background: Delayed gastric emptying (DGE) is a major postoperative complication after pylorus-preserving pancreatoduodenectomy (PpPD) and sometimes causes reflux esophagitis. In most cases, this morbidity is controllable by proton-pump inhibitor (PPI) and very rarely results in esophageal stricture. Balloon dilation is usually performed for benign esophageal stricture, and esophagectomy was rarely elected. In the present case, there were two important problems of surgical procedure; how to perform esophageal reconstruction after PpPD and whether to preserve the stomach or not.

Case presentation: A 63-year-old man underwent PpPD and Child reconstruction with Braun anastomosis for lower bile duct carcinoma. Two weeks after surgery DGE occurred, and a 10 cm long stricture from middle esophagus to cardia developed one and a half month after surgery in spite of the administration of antacids. Balloon dilation was performed, but perforation occurred. It was recovered with conservative treatment. Even the administration of a proton pump inhibitor (PPI) for approximately five mouths did not improve esophageal stricture. Simultaneous 24-h pH and bilirubin monitoring confirmed that this patient was resistant to PPI. We performed middle-lower esophagectomy with total gastrectomy to prevent gastric acid from injuring reconstructed organ and remnant esophagus through a right thoracoabdominal incision, and we also performed reconstruction with transverse colon, adding Roux-Y anastomosis, to prevent bile reflux to the remnant esophagus. Minor leakage developed during the postoperative course but was soon cured by conservative treatment. The patient started oral intake on the 25th postoperative day (POD) and was discharged on the 34th POD in good condition.

Conclusion: Long esophageal stricture after PpPD was successfully treated by middle-lower esophagectomy and total gastrectomy with transverse colon reconstruction through a right thoracoabdominal incision. Conventional PD or SSPPD with Roux-en Y reconstruction rather than PpPD should be selected to reduce the risk of DGE and prevent bile reflux, in performing PD for patients with hiatal hernia or rapid metabolizer CYP2C19 genotype; otherwise, fundoplication such as Nissen and Toupet should be added.

No MeSH data available.


Related in: MedlinePlus

a. Endoscopic findings on the 150th POD after PpPD showed severe stricture of the middle thoracic esophagus and longitudinal esophageal ulcer scars on the oral side. b Endoscopic findings before PpPD showed sliding esophageal hiatal hernia and mild esophagitis, which was classified as Grade A according to the Los Angeles classification
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Fig2: a. Endoscopic findings on the 150th POD after PpPD showed severe stricture of the middle thoracic esophagus and longitudinal esophageal ulcer scars on the oral side. b Endoscopic findings before PpPD showed sliding esophageal hiatal hernia and mild esophagitis, which was classified as Grade A according to the Los Angeles classification

Mentions: The upper gastrointestinal series revealed a long stricture extending from the middle esophagus to just above the cardia portion, the length of which was approximately 10 cm, and the sliding esophageal hiatal hernia (Fig. 1). Gastrointestinal endoscopy showed circumferential stricture of the middle esophagus with longitudinal esophageal ulcer scars (Fig. 2a). The narrow lesion was biopsied, and the result showed no malignancy. Preoperative gastrointestinal endoscopy before PpPD revealed a sliding esophageal hiatal hernia and mild esophagitis (Fig. 2b). We speculated that postoperative DGE, hiatal hernia, and gastric hyperacidity exacerbated the patient’s reflex esophagitis. The patient was treated with an H2 blocker for 2 weeks just after the surgery and with PPI from the 14th POD until the 140th POD. PPI was replaced to the H2 blocker due to the decreased numbers of white blood cells to less than 2000/μl from the 141th POD. The number of white blood cells recovered to normal level soon. Severe extensive stricture remained observed. We suspected that this patient had resistance to PPI; thus, we performed simultaneous 24-h pH and bilirubin monitoring to estimate the extent to which gastric acid secretion was inhibited by omeprazole (20 mg/drip/twice a day). Proximal and distal pH sensors were positioned in the narrow lesion and in the stomach, respectively, and a bilirubin sensor was positioned just beyond the narrow lesion. In the stomach, a pH < 4 was observed 89.3 % of the time (Fig. 3). Usually, in patients with GERD or intermediate and poor metabolizer CYP2C19 genotype, the proportion of time for which the stomach is characterized by pH < 4 decreases to approximately 50 % with PPI [4, 5]. In this study, after treatment with omeprazole for 6 days, the white blood cell count decreased from 4000 to 1700/μl; this level increased to normal levels soon after the course of medication had been completed. We recognized that this patient was resistant to PPI. Neither an H2 blocker nor PPI could prevent the exacerbation of reflux esophagitis. We therefore concluded that medication therapy could not suppress gastric acid and considered performing total gastrectomy to prevent gastric acid from injuring reconstructed organs and the remnant esophagus.Fig. 1


Rapid progressive long esophageal stricture caused by gastroesophageal reflux disease after pylorus-preserving pancreatoduodenectomy.

Fukaya M, Abe T, Nagino M - BMC Surg (2016)

a. Endoscopic findings on the 150th POD after PpPD showed severe stricture of the middle thoracic esophagus and longitudinal esophageal ulcer scars on the oral side. b Endoscopic findings before PpPD showed sliding esophageal hiatal hernia and mild esophagitis, which was classified as Grade A according to the Los Angeles classification
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4836191&req=5

Fig2: a. Endoscopic findings on the 150th POD after PpPD showed severe stricture of the middle thoracic esophagus and longitudinal esophageal ulcer scars on the oral side. b Endoscopic findings before PpPD showed sliding esophageal hiatal hernia and mild esophagitis, which was classified as Grade A according to the Los Angeles classification
Mentions: The upper gastrointestinal series revealed a long stricture extending from the middle esophagus to just above the cardia portion, the length of which was approximately 10 cm, and the sliding esophageal hiatal hernia (Fig. 1). Gastrointestinal endoscopy showed circumferential stricture of the middle esophagus with longitudinal esophageal ulcer scars (Fig. 2a). The narrow lesion was biopsied, and the result showed no malignancy. Preoperative gastrointestinal endoscopy before PpPD revealed a sliding esophageal hiatal hernia and mild esophagitis (Fig. 2b). We speculated that postoperative DGE, hiatal hernia, and gastric hyperacidity exacerbated the patient’s reflex esophagitis. The patient was treated with an H2 blocker for 2 weeks just after the surgery and with PPI from the 14th POD until the 140th POD. PPI was replaced to the H2 blocker due to the decreased numbers of white blood cells to less than 2000/μl from the 141th POD. The number of white blood cells recovered to normal level soon. Severe extensive stricture remained observed. We suspected that this patient had resistance to PPI; thus, we performed simultaneous 24-h pH and bilirubin monitoring to estimate the extent to which gastric acid secretion was inhibited by omeprazole (20 mg/drip/twice a day). Proximal and distal pH sensors were positioned in the narrow lesion and in the stomach, respectively, and a bilirubin sensor was positioned just beyond the narrow lesion. In the stomach, a pH < 4 was observed 89.3 % of the time (Fig. 3). Usually, in patients with GERD or intermediate and poor metabolizer CYP2C19 genotype, the proportion of time for which the stomach is characterized by pH < 4 decreases to approximately 50 % with PPI [4, 5]. In this study, after treatment with omeprazole for 6 days, the white blood cell count decreased from 4000 to 1700/μl; this level increased to normal levels soon after the course of medication had been completed. We recognized that this patient was resistant to PPI. Neither an H2 blocker nor PPI could prevent the exacerbation of reflux esophagitis. We therefore concluded that medication therapy could not suppress gastric acid and considered performing total gastrectomy to prevent gastric acid from injuring reconstructed organs and the remnant esophagus.Fig. 1

Bottom Line: In most cases, this morbidity is controllable by proton-pump inhibitor (PPI) and very rarely results in esophageal stricture.Even the administration of a proton pump inhibitor (PPI) for approximately five mouths did not improve esophageal stricture.Simultaneous 24-h pH and bilirubin monitoring confirmed that this patient was resistant to PPI.

View Article: PubMed Central - PubMed

Affiliation: Division of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho Showa-ku, Nagoya, 466-8550, Japan. mafukaya@med.nagoya-u.ac.jp.

ABSTRACT

Background: Delayed gastric emptying (DGE) is a major postoperative complication after pylorus-preserving pancreatoduodenectomy (PpPD) and sometimes causes reflux esophagitis. In most cases, this morbidity is controllable by proton-pump inhibitor (PPI) and very rarely results in esophageal stricture. Balloon dilation is usually performed for benign esophageal stricture, and esophagectomy was rarely elected. In the present case, there were two important problems of surgical procedure; how to perform esophageal reconstruction after PpPD and whether to preserve the stomach or not.

Case presentation: A 63-year-old man underwent PpPD and Child reconstruction with Braun anastomosis for lower bile duct carcinoma. Two weeks after surgery DGE occurred, and a 10 cm long stricture from middle esophagus to cardia developed one and a half month after surgery in spite of the administration of antacids. Balloon dilation was performed, but perforation occurred. It was recovered with conservative treatment. Even the administration of a proton pump inhibitor (PPI) for approximately five mouths did not improve esophageal stricture. Simultaneous 24-h pH and bilirubin monitoring confirmed that this patient was resistant to PPI. We performed middle-lower esophagectomy with total gastrectomy to prevent gastric acid from injuring reconstructed organ and remnant esophagus through a right thoracoabdominal incision, and we also performed reconstruction with transverse colon, adding Roux-Y anastomosis, to prevent bile reflux to the remnant esophagus. Minor leakage developed during the postoperative course but was soon cured by conservative treatment. The patient started oral intake on the 25th postoperative day (POD) and was discharged on the 34th POD in good condition.

Conclusion: Long esophageal stricture after PpPD was successfully treated by middle-lower esophagectomy and total gastrectomy with transverse colon reconstruction through a right thoracoabdominal incision. Conventional PD or SSPPD with Roux-en Y reconstruction rather than PpPD should be selected to reduce the risk of DGE and prevent bile reflux, in performing PD for patients with hiatal hernia or rapid metabolizer CYP2C19 genotype; otherwise, fundoplication such as Nissen and Toupet should be added.

No MeSH data available.


Related in: MedlinePlus