IN SEARCH OF THE OPTIMAL RECONSTRUCTION METHOD AFTER TOTAL GASTRECTOMY. Ph. D. Thesis. Department of Surgery Medical Faculty University of Pécs - PDF

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1 IN SEARCH OF THE OPTIMAL RECONSTRUCTION METHOD AFTER TOTAL GASTRECTOMY Ph. D. Thesis Candidate: Dr. Katalin Kalmár MD Department of Surgery Medical Faculty University of Pécs Consultant: Prof. Dr. Örs

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1 IN SEARCH OF THE OPTIMAL RECONSTRUCTION METHOD AFTER TOTAL GASTRECTOMY Ph. D. Thesis Candidate: Dr. Katalin Kalmár MD Department of Surgery Medical Faculty University of Pécs Consultant: Prof. Dr. Örs Péter Horváth MD, PhD, DSc Department of Surgery Medical Faculty University of Pécs 2006 2 TABLE OF CONTENTS I. Introduction 4 1. Total gastrectomy Physiological Functions of the Stomach Lost by Total Gastrectomy Indications for Total Gastrectomy Method of Total Gastrectomy Physiological Consequences of Total Gastrectomy Postgastrectomy Syndromes 9 2. Techniques of Reconstruction after Total Gastrectomy Types of Reconstructions Importance of Pouch Construction Importance of Duodenal Passage 17 II. The Optimal Reconstruction Method after Total Gastrectomy Objectives of the trials in search of the optimal reconstruction type after total gastrectomy General objectives Endpoints Eligibility criteria, randomisation Patients and Methods Patients Trial-I Trial-II Trial-III Operative Methods Aboral Pouch Aboral Pouch with Preserved Duodenal Passage Oral Pouch with Preserved Duodenal Passage 27 Roux-en-Y reconstruction Methods of Assessment Anthropometric Measures Laboratory Parameters Motility Studies Absorption Studies Quality of Life Test Additional Questionnaire Clinical evaluation Two weeks after surgery , 12 and 24 months after surgery Long term Statistics and Ethics Prospective, Randomised, Controlled Trial to compare Aboral Pouch to the standard Roux-en-Y Reconstruction (Trial-I) Results Discussion Prospective, Randomised Trial to compare Aboral Pouch with Preserved Duodenal Passage, Aboral Pouch and Roux-en-Y Reconstructions after Total Gastrectomy (Trial-II) Results Discussion Long Term Results in comparing Aboral Pouch with Preserved Duodenal Passage, Aboral Pouch and Roux-en-Y Reconstructions after Total Gastrectomy Long Term Results Discussion 53 4 6. Randomised Comparison of Aboral Pouch to Oral Pouch with Preserved Duodenal Passage (Trial-III) Results Discussion 60 III. Gastrointestinal Hormone Production at Different Reconstruction types after Total Gastrectomy Clinical Experiment on a Prospectively Randomised Patient Population to Evaluate Postprandial Glucose, Insulin, Cholecystokinin and Somatostatin response in patients after Total Gastrectomy and Aboral Pouch with Preserved Duodenal Passage, Aboral Pouch or Roux-en-Y Reconstruction (Trial-IV) Objectives, Eligibility Patients Methods of Assessment Statistics Results Discussion 72 IV. New Findings 79 V. Acknowledgements 82 VI. References VII. Publications 5 I. INTRODUCTION 1. Total Gastrectomy 1.1. Physiological Functions of the Stomach Lost by Total Gastrectomy The stomach as a dilated portion of the upper gastrointestinal tract, functions as a reservoir. It transports food from the oesophagus to the small bowel, while mechanically breaking food down and partially digesting it by hydrochloric acid and pepsin. The lower oesophageal sphincter protects the oesophagus from gastric and duodenal juices. When resected in case of a total gastrectomy - this protection is lost. Though recently there are tendencies toward preservation of the lower oesophageal sphincter if it is oncologically possible (1). The fundic region can hold large amounts of food, regulated by vagal reflexes (accommodation and receptive relaxation). Loss of this function results in reduced reservoir capacity, an early fullness feeling during meals, which is often described as epigastric discomfort (2). Tonic contractions of the body and antrum grounds and propels the food towards the duodenum and delivers it in small boluses via the pyloric sphincter. The pylorus controls the emptying of the stomach and prevents duodeno-gastric reflux. The motiliy of the stomach is paced from a distal region at the greater curvature, where smooth muscle cells have the highest intrinsic activity for contraction (2). This grounding of food can partly be replaced by thorough chewing or eating mashed food, however if food remains improperly minced, the digestive process will certainly be less than perfect. The loss of hydrochloric acid production does not necessarily result in any obvious disturbances. Some claim that hydrochloric acid keeps a low number of micro-organisms in the upper gastrointestinal tract, and the lack of it results in bacterial overgrowth, consumption of vitamins and micronutrients (3). There are studies though, which proved 6 no difference in bacterial culture of jejunal aspirates of patients after total gastrectomy, compared to healthy controls (4). The loss of parietal cell mass on the other hand certainly leads to a complete lack of intrinsic factor, which when left unattended leads to pernicious anaemia. Gastrointestinal hormones play a major role in the regulation of gastrointestinal secretions and motility. Removal of the stomach is a rather rude intervention in this sense, which disarranges the harmony in the production of gastrointestinal hormones. The resulted state of disorder is often referred to as pancreatico-cibal asynchrony (5). Gastrin has its most important role in acid secretion. Its production is increased by vagal impulses as well as by protein degradation products in the stomach, the latter raises gastrin level exponentially with a positive feed back (6). Acid appearing in the antrum stops production of gastrin, thus regulating acid release via a negative feed back. Gastrin level is markedly reduced in gastrectomised patients not only because most of it is produced in the stomach, but also because the feed back regulation is lost (7). Cholecystokinin stimulates pancreatic secretion, contracts the gall bladder and slows gastric emptying. The arrival of a bolus to the duodenum increases cholecystokinin output, which in turn increases pancreatic juice production as well as relaxes the fundic region of the stomach and contracts the pylorus (8). Regarding the stimulation of digestive juice production, the nutrients braking down to smaller elements increase cholecystokinin production further, switching on a positive feed back regulation (6). In relation to gastric emptying a negative feed back works. In the lack of stomach, cholecystokinin, however high its level raises, cannot stop the food flowing uncontrolled to the duodenal bulb. Not to mention if duodenum is excluded, and endocrine cells in the duodenum and the Y limb are informed only via neural and hormonal pathways about the fact, that digestion is supposed to be going on. Gallstones are detected at a higher frequency after total gastrectomy (9). And a considerable percentage of these are symptom 7 free. The raised and fairly constant level of cholecystokinin, as well as truncal vagotomy leading to relaxation of the gallbladder are the most important factors involved in the formation of postgastrectomy gallstones (10). The perception of hunger changes significantly after gastrectomy. Some patients feel constant hunger, others never experience the same motivation for eating as before surgery. The blood levels of nutrients and hormones, which have a major role in regulation of eating behaviour, fluctuate much more in the lack of the stomach. The postprandial tension of the gastric fundus via a neural pathway and ghrelin, produced in the stomach via humoral ways, signals to the brainstem to reach the feeling of satiety (11). These are lost in the lack of stomach. Cholecystokinin was repeatedly shown to have an appetitesuppressing effect (12). Its raised levels after gastrectomy might add to the reduced food intake. Glucose homeostasis suffers a special change after removal of the stomach (13). The lack of the stomach results in a shockingly fast absorption of glucose from the small bowel to blood stream resulting is hyperglycaemia. A strong response from the endocrine pancreas yields hyperinsulinaemia. This is magnified by enteroglucagon, which is produced at a higher level because of the excess of sugar in gut lumen (14). The result can be a late postprandial hypoglycaemia, which is the late dumping syndrome itself Indications for Total Gastrectomy Total removal of the stomach is a demanding operation for the surgeon as well as for the patient. There is a considerable operative morbidity ranging between 15-30% and operative mortality between 3-10%. The operative mortality for 345 patients between 1993 and 2002 at the Department of Surgery University of Pécs was 6,9 %.(15). Considering the risks and benefits, it is rare to perform total gastrectomy on a patient without a good reason (occasional profilactic gastrectomies). The overwhelming majority of these patients are operated on for gastric cancer. Some total gastrectomies are performed 8 for bleeding ulcers with or without Zollinger-Ellison syndrome, somewhat more are carried out for nonepithelial gastric tumors, such as GISTs or lymphomas. As a consequence of the above, symptoms seen after total gastrectomy are results of not only the lack of the stomach, but also, to some extent, symptoms of the basic disease Method of Total Gastrectomy Although the laparoscopic technique for total gastrectomy has been elaborated (16), total gastrectomy is routinely performed as an open operation. The access to the stomach is readily available via a midline incision which is supplemented by a transverse incision if necessary for obese patients or more extensive surgery. The most comfortable access to the cardiac region is via a left sided thoracolaparotomy. Some authors feel it inferior to laparotomy with splitting up the diaphragm, for its higher morbidity (17). After exploration of the abdominal organs decision for radical (R0) resection can be made depending on the extent of the disease. The greater omentum is dissected down the transverse colon. The dissection is forwarded onto the transverse mesocolon, to remove the covering peritoneal layer, thus the posterior wall of the lesser sac. This so called bursectomy reduces the chance of peritoneal seeding. Towards the left, the left gastroepiploic artery and the gastro-splenic ligament are divided or in cases of upper third tumour or direct invasion the spleen is removed. The oesophagus is freed in the oesophageal hiatus, the gastro-hepatic ligament is divided closer to the liver. Towards the right the right gastroepiploic vessels, the right gastric artery and the duodenum are divided, the duodenal stump is permanently closed with a linear stapler or only temporarily with clamps, depending on the reconstruction type chosen. D2 lymphadenectomy is performed if the indication is gastric cancer. Lymph node dissection starts at the gastroduodenal artery and a systematic peeling off of all lymphatic tissue is carried out along the primary hepatic artery, common bile duct and portal vein. Dissection follows the upper border of the pancreas by clearing the common hepatic and the splenic artery, dividing the coronary vein and left gastric 9 artery at its origin from the celiac trunk. After dividing few remaining tissues along the diaphragmatic crura between the celiac trunk and the oesophageal hiatus, the stomach is removed. The reconstruction of the continuity of the gastrointestinal tract can be restored following various methods (see chapter 2.) 1.4. Physiological Consequences of Total Gastrectomy The long term consequences of total gastrectomy are weight loss, malabsorbtion, anaemia, disturbed gastrointestinal motility, referred to as dumping (see 1.5.) and alkaline reflux (see 1.5.). The average weight loss after total removal of the stomach is around 15 % of the original healthy body weight (14). The reason for weight loss is partly the malabsorbtion itself, but there is also a reduced initiative for food intake, the background of which needs further clarification. Malabsorbtion of nutrients has also a complex aetiology. The lack of the stomach results in a faster transit of food, a disturbed gastrointestinal hormone production, a reduced stimulation to the pancreas, what is most pronounced if the reconstruction excludes the duodenum from the food passage. Exocrin pancreatic insufficiency is secondary to pancreatico-cibal asynchrony i.e. disharmony in food passage and digestive juice production because of a disturbed order and magnitude of gastrointestinal hormone secretion (6). There is also a primary insufficiency of the pancreas proven by secretin-coerulein test, for which the reason is supposed to be the nerve damage caused by peripancreatic dissection during total gastrectomy (8,18). Anaemia after total gastrectomy originates from B12-vitamin and iron deficiency. B12-vitamin deficiency directly comes from the complete abolishment of intrinsic factor producing gastric mucosa. Iron deficiency is secondary to a malabsorbtion of iron in the duodenum either because of accelerated passage through the duodenum, or in cases of reconstructions excluding the duodenal route because of no passage through the duodenum. Postgastrectomy Syndromes Long term consequences of gastrectomy are commonly summarised as postgastrectomy syndromes (3) (table 1). Only syndromes after total gastrectomy and not ones after partial gastric resection are encountered here, especially for some of the latter (such as afferent and efferent loop syndromes) are rather results of an improper surgical technique, than consequences of loss of the stomach. Table 1: Postgastrectomy syndromes Postgastrectomy syndromes: Reduced reservoir capacity Dumping - Early - Late Alkaline reflux Roux stasis Reduced reservoir capacity is a direct consequence of the fact, that instead of the large, strong-walled, dilated sack of stomach, a finer, narrower organ, the small bowel is sutured to the end of the oesophagus to receive the arriving boluses of food. Guts are sensitive only to tension of their wall. The stomach not only being larger, but also helped by the special vagal reflex of receptive relaxation in the fundic region can accommodate very well to the size of the meal, thus avoid the development of such a tension. A normal size meal cannot fit into the proximal end of the Roux-limb, not even into a pouch of small bowel duplicate, without considerable tension, experienced by the patient as considerable epigastric discomfort. Patients are suggested to ingest small-volume meals more frequently. The receiving small bowel portion dilates with time up to about 400 millilitres (19), which allows larger but still not a normal size of meal to be eaten. Dumping was described by Mix in 1922 as a rapid emptying of gastric content on radiography in patients with this condition (20). It is the most frequently encountered but less well defined syndrome after gastrectomy. Two types can be differentiated, early and late dumping. 11 Early dumping is comprised of vasomotor and / or gastrointestinal symptoms starting minutes postprandially. The reason for it is the sudden appearance of a large volume of high osmolarity (high carbohydrate) liquid in the small bowel, resulting in a fluid shift from the intravascular space to the bowel lumen. The pathophysiological background is supported by experimental evidences of a reduction in packed cell volume, increase in intravascular fluid osmolarity parallel to a fall in blood pressure and elevation in pulse rate in patients experiencing dumping (21). Several gastrointestinal hormones were examined and found to be released during dumping (22, 23, 24). Somatostatin can alleviate or prevent symptoms (21). Vasomotor symptoms are weakness, dizziness, flushing, sweating or palpitation. Gastrointestinal symptoms can accompany vasomotor symptoms or can be present alone, such as fullness, cramps, nausea and sudden diarrhoea. Late dumping is a better defined pathological category, with vasomotor symptoms only, occurring 2-4 hours after a meal. The background is the release of enteroglucagon in response to high carbohydrate load in the small bowel, which brings about excessive amount of insulin release, resulting in a drop of blood sugar. The presenting symptoms are similar to that of hypoglycaemia (25). Resection of the cardia results in free reflux of bowel content into the oesophagus after total gastrectomy. If this content is irritating for the oesophageal mucosa the patient will experience heartburn, maybe nausea and vomiting and in the long term oesophagitis, Barrett metaplasia or even Barrett cancer develops. The noxious content is bile. It is the surgeon s most important task while choosing the reconstruction type after total gastrectomy to avoid any possibility for bilious reflux to the oesophagus. This is why Ω-loop reconstruction is unacceptable and in cases of Roux-en-Y or Longmire reconstructions the jejunal limb has to be long enough (40-50 cm) to prevent alkaline reflux. Roux stasis syndrome occurs in almost one third of patients, undergone total gastrectomy and simple Roux-en-Y reconstruction (3). 12 Symptoms are that of upper gastrointestinal stasis, i.e. early fullness during meal, epigastric discomfort, nausea and regurgitation. The symptoms are the manifestation of a motility disorder thought to develop because the Roux jejunal limb is divided from the duodenal pacemaker (3). Others experienced a positive correlation between the length of the Roux limb and the occurrence of the symptoms (26). Whilst a long limb is preferred as a protection against reflux, a shorter limb reduces the incidence of Roux stasis syndrome. In Roux limbs shorter than 40 cm the symptoms hardly can develop (3). This observation may be explained by the jejunum s ability to pace the contractions of a certain length of small bowel only. 2. Techniques of Reconstruction after Total Gastrectomy 2.1. Types of Reconstructions The first total gastrectomy was attempted by Phineas Conner of Cincinatti in 1884 (27). The first successful one was performed by C. Schlatter of Switzerland in 1897 (28). Since then surgeons tried more than sixty different reconstruction types to re-establish gastrointestinal continuity after removal of the stomach. Zoltán Szabolcs in his excellent monography about gastric cancer published in 1966 had collected 58 different reconstruction types after total gastrectomy as represented in figure 1. The high number indicates that there is no optimal solution found to this problem. Figure 1: Different methods to replace the removed stomach or to reconstruct gastrointestinal continuity after total gastrectomy or fundectomy. Szabolcs Zoltán: A gyomorrák. Akadémiai Kiadó, Budapest To re-establish continuity between the oesophagus and the small bowel, the most straightforward ways are direct oesophagoduodenostomy, as done by Conner or Ω-loop oesophago-jejunostomy 13 (figure 2a,b) as performed by Schlatter. The oesophago-duodenostomy is prone to be under tension, which prevents anastomotic healing, though with a thorough mobilisation of the duodenum and pancreatic head the anastomosis can be performed in almost all cases (Nakayama 1955) (29). Nevertheless oesophago-duodenostomy and omega-loop oesophago-jejunostomy both results in debilitating biliary reflux, thus they are not recommended in surgical practice any longer. In the historical evolution of omega-loop oesophago-jejunostomy, to prevent reflux and postprandial symptoms, an additional jejunojejunal anastomosis a shorter (Hoffmann 1922) (30) or a longer one (Steinberg 1950) (31) - was introduced between the afferent and efferent limbs of the Ω-loop, with still no satisfactory results regarding reflux oesophagitis (figure 2c,d). Others, trying to reconstruct the original anatomical situation, suggested the interposition of a reservoir at the site of the stomach, between the oesophagus and the duodenum. Interposition of a segment of jejunum (Seo 1942, Longmire 1952) (32,3), ileocolon (Hunnicut 1952) (33) and transverse colon (State 1951) (34) was performed (figure 2 e,f,g). The today gold-standard reconstruction, the Roux-en-Y oesophago-jejunostomy is based on Cezar Roux s concept applied after partia
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