Colonic interposition for benign oesophageal disease.

1. Colonic interposition for benign oesophageal disease.

2. Case PC: KM, 53 year old male, referred from peripheral hospital with 4 year history of ongoing dysphagia secondary to achalasia. Associated 2 month history of recent weight loss: weight 50kg on admission. Associated post-prandial regurgitation of undigested food.

3. PMHx: Epilepsy since childhood, grand mal seizures. PSHX: OGD + pneumatic dilatation 2006, with oesophageal perforation, requiring thoracotomy and repair. Subsequent numerous OGD and dilatations. May 2007: Laparoscopic Nissen fundoplication and mesh repair of large para-oesophageal hernia. September 08: subsequent re-do and pyloroplasty. No symptomatic relief, complete dysphagia.

4. Investigations: Niopam swallow: marked distension of distal oesophagus, narrow OG junction. OGD: narrowed OG junction, dilated distal oesophagus. Bloods: anaemic (Hb 10.0), and malnourished (Alb 25).

5. Pre-op Management i) Admitted, central line inserted for TPN x 10 days. ii) CT thorax/abdomen: no aid in identifying gastric anatomy. iii) Bowel prep

6. Surgery Transhiatal oesophagectomy. Diseased stomach and oesophagus excised and colonic interposition. Stomach unusable due to scarring, fibrous adhesions, and interruption of the right gastro-epiploic arcade.

7. Post-op • No anastomotic leak identified on day 5 post-op niopam swallow. • Intra-abdominal collection lead to ongoing pyrexia

8. Surgical intervention in end-stage benign oesophageal motility disorders. Primary oesophageal motility disorders are characterised by distinct clinical, manometric, radiological and pathological features 1, 2. Spectrum of disorders: achalasia diffuse oesophageal spasm nutcracker oesophagus hypertensive lower oesophageal sphincter Non-specific oesophageal motility disorder

9. Achalasia Due to loss or relative absence of inhibitory cells in the myenteric (Auerbach's) plexus in oesophagus, with selective decrease in nitronergic inhibitory neurons. Unknown aetiology, potentially secondary to immune response to an infective agent such as a virus1. Usually a primary disease, may be secondaryto Chagas' disease.

10. Achalasia Presentation may be at any age, but is usually between 20-40 years. No association with gender or race4. Presentation usually due to progressive dysphagia, odynophagia, regurgitation of food, weight loss, dyspepsia1. Secondary symptoms include aspiration, RTIs, chronic cough1.

11. Investigations OGD to exclude obstruction from tumour or stricture (pseudoachalasia). Barium studies: 'bird's beak' appearance. Manometry testing Hypertensive LOS pressure Non-relaxing LOS Aperistalsis of oesophageal body Elevated baseline pressures in lower esophagus.

12. Treatment Achalasia treatment focussed on lowering LOS hypertension. Pharmacological agents Nitrates Calcium channel blockers May reduce LOS pressures by 30-60%, but only temporary effect 2 Endoscopic therapies: Endoscopic botox injection Endoscopic pneumatic dilatation

13. Surgical treatment The aim of surgical treatment is to relieve dysphagia while preventing iatrogenic GORD. Majority of surgeons now use laparoscopic distal oesophageal myotomy with partial fundoplication4. Alternate approaches include thorascopic, transthoracic and transabdominal approaches4.

14. Surgical treatment Indicators of end-stage disease are recurrent/complete dysphagia, with dyspepsia, aspiration/sepsis, perforation. Definitive operation is oesophagectomy.

15. Oesophagectomy with colonic interposition • i) Abdominal incision. • Isoperistaltic segment of colon is mobilised. Usually left colon is used. Colonic blood supply is examined to ensure good perfusion. • ii) Cervical incision • Oesophagus mobilised and resected. Colon graft delivered via oesophageal bed and is anastomosed proximally and distally. • Primary colocolonic anastomosis.

16. Gastric pull-up • Right thoracotomy • Mobilise the oesophagus. • Upper midline abdominal incision • Mobilise the stomach and examine gastroepiploic supply, ligation of distal oesophagus. • Left cervical incision with dissection of oesophagus, pull up of gastric conduit and anastomosis.

17. Outcomes Orringer et al (Ann Surg 2007) reviewed 482 pts undergoing transhiatal oesophagectomy for benign disease. Mortality 2% Long-term follow-up (median at 41 months) showed 96% had a fair to excellent response5. Curet-Scott et al (Surgery 1987) reviewed 83 pts undergoing oesophagectomy and colonic interposition for benign disease6. Mortality 3.8% Follow-up (average 5 years) showed 75% rated as good or excellent results

18. Outcomes continued Watson et al (J Thorac Cardioasc Surg 1998) studied 104 patients with benign disease who underwent oesophageal reconstruction over 21 year period7. Colon in 85 pts, stomach in 10, jejenum in 9. Mortality was 2%. 98% reported resolution or improvement at 1 year.

19. Conclusions Achalasia is considered end-stage when medical, endoscopic, and myotomy procedures fail to alleviate symptoms. Oesophagectomy is the definitive end-stage treatment. Stomach is usually the preferred graft but colon makes a very acceptable substitute.

20. References 1. Williams VA, Peters JH. Achalasia of the esophagus: a surgical disease. J Am Coll Surg 2008; 208 (1): 151-162. 2. Watson TJ, Jones CE, Litle VR. Benign diseases of the esophagus. Curr Probl Surg 2009; 46(3): 195-259. 3. Mayberry JF. Epidemiology and demographics of achalasia. Gastrointest Clin N Am 2001; 11: 253-248. 4. Campos GM, Vittinghoff E, Rabl C et al. Endoscopic and surgical treatments for achalasia. Ann Surg 2009; 249(1): 45-57. 5. Orringer MB, Marshall B, Chang AC, Lee J, Pickens A, Lau CL. Two thousand transhiatal esophagectomies: changing trends, lessons learned. Ann Surg 2007; 246: 363-374 6. Curet-Scott MJ, Ferguson MK, Little AG, Skinner DB. Colon interposition for benign esophageal disease. Surgery 1987; 102: 568-574 7. Watson TJ, DeMeester TR, Kauer WK, Peters JH, Hagen JA. Esophageal replacement for end-stage benign esophageal disease. J Thoracic Cardiovasc Surg 1998; 115: 1241-1247