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Thread: Post-Gastrectomy syndromes

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    Post Post-Gastrectomy syndromes

    Diseases of operated stomach include different post gastric resection syndromes. Resection of the part of the stomach with formation of the new relationships between the different organs of the digestive tract may lead to disorder of normal physiological relations of digestive organs and formation of different pathological conditions, which vary from mild to severe.

    Aim of the lesson.
    Based on knowledge of anatomy and physiology of the stomach, the student must know the causes of new pathophysiological relationships, which are formed between the organs of digestive tract after resection of the stomach or gastrectomy and after operation on vagal system (vagotomy), must recognize those syndromes and be able to substantiate the most appropriate tactics and method of treatment.

    Plan of the lesson.
    1) Topographic anatomy of the stomach and duodenum.
    2) Physiology of the stomach and duodenum, regulation of gastric secretion.
    3) Indications for operative treatment of the peptic ulcer, kinds of operative interventions.
    4) Classification of the post gastric resection syndromes.
    5) Etiopathogenesis, classification, clinical presentation, additional methods of investigation, choice of tactics of treatment, prophylactic of the more common organic and functional post gastric resection syndromes and postvagotomy disorders.

    Resection of the stomach disturbs and gastrectomy completely destroys the different functions of the stomach as hydrochloric acid and intrinsic factors production, reduces reservoir capacity, dissolvability function, and increases reflux of bile and rapid empting into the small intestine. Moreover, resection of the stomach by method of Billroth II and gastrectomy exclude the duodenum from direct digestion that also supports appearance of functional disorders.

    Classification of the post gastric resection syndromes
    (A.A.Shalimov, 1972).
    I. Functional disorders:
    a) dumping syndrome;
    b) syndrome of hypoglycemia;
    c) postresection asthenia;
    d) syndrome of the small stomach;
    e) syndrome of the afferent loop (functional);
    f) nutritive allergy;
    g) gastroesophageal and duodenogastral refluxes;

    II. Organic lesions:
    a) recurrence of peptic ulcer;
    b) syndrome of the afferent loop (organic);
    c) gastro-colic fistula;
    d) anastomositis;
    e) scar deformation and stenosis of the anastomosis;
    f) postresection concomitant diseases: pancreatitis, enterocolitis, hepatitis.
    III. Mixed disorders – mostly in combination with dumping syndrome or postvagotomy diarrhea.
    IV. Postvagotomy syndromes:
    a) recurrence of peptic ulcer;
    b) postvagotomy diarrhea;
    c) gastroesophageal reflux;
    d) disorder of the stomach emptying;
    e) dumping syndrome;
    f) reflux-gastritis;
    g) cholelithiasis.

    Dumping syndrome.
    It is common functional complication after stomach resection (10-30%), which is characterized by quick emptying of the stomach stump with quick spread of its contents on the surface of jejunal mucosa.
    Different factors take part in pathogenesis of dumping syndrome: neuro-reflectory, activation of the sympathoadrenal system, secretion of the large amount of biological active substances (serotonin, kinin), osmotic components, which lead to lowering of circulated plasma volume and redistribution of the blood in organism, hyperpotassemia etc. Neurohumoral reactions play the leading role in formation of dumping syndrome together with liberation of some hormones from mucosal membrane of small intestine, which activate the vegetative nervous system and stimulate cholinergic and insulin activities.
    The clinical presentation is characterized by appearance of attack of weakness during the meals or after short period after it. The attack begins from sensation of fullness in epigastric region accompanied with unpleasant sensation of hotness at upper part or at all body. Hyperhidrosis arises, then fatigue, sleepiness, dizziness, disorder of vision and murmur in the ears, tremor of the extremities evolve. Above-mentioned symptoms make the patient to lie. Loss of consciousness is rare and usually during first months after operation. Attacks are accompanied by tachycardia, sometimes dyspnea, headache, paraesthesia in extremities, polyuria, vasomotor rhinitis. Mild pain in epigastrium may be present. Dyspeptic signs during the attack may be variable: hypersalivation or dryness in the mouth, nausea, heartburn, belching. The vomiting usually is absent. Diarrhea is very common at the end of attack or after some period after it.
    Dumping syndrome very commonly may be provoked by specific food as milk, carbohydrate food.
    Dumping tends to be the most severe immediately after an operation and tends to subside spontaneously within about six months
    During the X-ray examination quick evacuation of the barium meal through gastroenteroanastomoses is detected after 5-15 minutes, dilatation of the lumen of the efferent loop, quick passage of the contrast to distal parts of small intestine.
    Classification of the damping syndrome. Depending from severity of dumping syndrome it is divided on:
    I degree or mild form – periodical attacks of weakness with dizziness, nausea, which last no more than 15-20 minutes and occurs mostly after ingestion of the milk and carbohydrate food. During the attack pulse rate raises on 10-15 beats per minute, blood pressure increases or lowers up to 10-15 mm of Hg, VCB (volume of circulated blood) decreases up to 200-300 ml. Deficits of body weight no more than 5 kg. Conservative treatment and diet give positive result.
    II degree or middle form – permanent attacks of weakness with dizziness, painfulness in heart region, sweating, and diarrhea after ingestion of any food last up to 20-40 minutes. During the attack the pulse rate is raised up to 15-20 beats per minute. Blood pressure increases (lowering) up to 15-20 mm of Hg, VCB decreases up to 300-500 ml. Deficits of body weight near 5-10 kg. Conservative treatment gives short relief.
    III degree or severe form – permanent intensive attacks with evolution of syncope condition, diarrhea independent from character and volume of food last near one hour. During the attack pulse rate is raised up to 20-30 beats per minute, blood pressure lowers up to 20-30 mm of Hg, VCB decreases more than on 500 ml. Deficits of body weight more than 10 kg.
    Treatment. Treatment of the patients with dumping syndrome is difficult task. The mild form as usual may undergo to conservative treatment. In case of middle form the conservative treatment usually not so effective and sometimes indication to operative treatment arises. In case of severe form the conservative treatment is used as preparation to surgical treatment.
    Conservative treatment:
    I. Diet – the patient must eat solid food rich in proteins and vitamins by small portions up to 6-8 times per day and avoid eating hypertonic foods such as sugar. The food must be separated from fluids. The preferable position for taking meals is lie down on left side. It delays a quick empting of the stomach stump.
    II. Medical treatment. 1) The drugs, which influence different sites of neuroreflectory arch and lead to delay of the evacuation of the food from the stomach stump: a) local anesthetics per os (novocain, anesthesin); b) ganglioblockers, cholinolitics, anticholinergics – atropine, platiphylline, no-spa, methacin, gangleron, benzohexonium etc; c) sedative drugs, tranquilizators, neuroleptics – elenium, seduxen, aminozinum etc.
    2) Antiserotonin drugs and desensibilisators – reserpin, peritol, tavegil, suprastin, diasolin etc.
    3) Antidiarrheal agents;
    4) Enzymes therapy;
    5) Infusional therapy;
    6) Antianemic therapy;
    7) Insulin therapy;
    Operative treatment is directed on restoration of natural passage of the food (reduodenization). It may be done by different methods, between them the most spread are:
    1) Reconstruction of gastrojejunal anastomosis to gastroduodenal (Billroth II to Billroth I);
    2) Isoperistaltic gastrojejunoplasty by Henley I or Henley II.
    Others kinds of operations may be used. They are directed on delay of the food in the stomach stump or delay of the food passage in intestine such as diminishing of the size of gastroenteroanastomoses, denervation of the efferent loop, antiperistaltic gastrojejunoplasty etc.
    Prophylaxis of dumping syndrome.
    Predisposition to dumping syndrome may be recognized before operation with several tests:
    1) Test of Straford – intrajejunal infusion of 150 ml of 50% solution of dextrose through nasojejunal tube.
    2) Test of Fenger – intraduodenal infusion of 280 ml of 18% solution of dextrose.
    3) Test of Borgstrom (apomorphine test) – subcutaneous injection of 0,5 ml of apomorphine hydrochloride.
    4) Test of Leonhart (consist of three subtests):
    a) comparative evaluation of basic metabolism in sleeping and awake conditions;
    b) double sugar test by Schtaube – Traugott;
    c) test of Schelong (orthostatic test).
    All above-mentioned tests may provoke experimental dumping syndrome before operation in cases if predisposition exists.
    Predisposition to dumping syndrome is assessed by classification of A.V.Nikolaev (1967), which divides 3 types of reactions:
    1. Mild form – slight weakness, sweating, nausea, dizziness. The pulse rate increases not more than on 10 beats per minute, blood pressure rises not more than on 10 mm of Hg. All above mentioned symtoms disappear quickly. The duration of attack is not more than 10-15 minits.
    2. Middle form – expressive weakness, fatigue, sleepiness, wish to lie, sweating. Pulse rate increases on 10-15 beats per minute, blood pressure rises on 10-15 mm of Hg. The duration of attack is near 15- 30 minutes.
    3. Severe form – very extensive weakness, dizziness, headache, murmur in the ears, hyperhidrosis, vomiting, diarrhea. The pulse rate increases on 25 – 30 beats per minute, blood pressure rises on 20-25 mm of Hg. The duration of attack is more than 30 minutes.
    Predisposition to dumping syndrome detected before operation provides possibility to find the most appropriate kind of operation and the route for restoration of digestive tract (the duodenum must be included or may be excluded from digestion of food).

    Syndrome of hypoglycemia.
    This syndrome arises as result of increased secretion of insulin due to quick absorption of the carbohydrates from intestine after meals.
    The attack may develop on an empty stomach or after 1,5 – 3 hours after ingestion of food. The level of serum glucose in this period is lowered up to subnormal values.
    The attack is characterized by all symptoms of hypoglycemia as expressive muscular weakness, fatigue, headache, lowering of blood pressure, sometimes loss of consciousness. Ingestion of the meals preferably sweets improves the condition of the patient.
    By I.V.Kliminsky (1966) syndrome of hypoglycemia depending from expressivity is divided on:
    I degree – the attacks arise after 2-2,5 hours after ingestion of food 2-3 times per week. The clinical presentation usually has mild form.
    II degree – the attacks develop 2-3 times per week. The patients usually foresee these symptoms and prevent them by taking food more often. Those attacks very commonly may be accompanied by other post gastric resection syndromes.
    III degree – the attacks develop every day, the patients eat very often for prevention of these attacks. The patients are permanently bearing the sugar into a pocket.
    Treatment. In cases of mild or moderate forms a treatment as usual conservative (diet, vitamins etc). If conservative treatment is not compensated the disease, appears indication for operative treatment which consist of duodenal inclusion to digestion (reverse operation of Billroth II to Billroth I).




    Post gastric resection (agastral) asthenia.

    It is a result of dysfunction of stomach, pancreas, liver and malabsorbtion of the intestine. Bypass of duodenum, small gastric stump after resection and total gastrectomy decrease secretion of hydrochloric acid and pepsin and lead to decrease stimulation and secretion of the duodenum, pancreatic gland and liver. Hypermotility of the intestine lead to poor mixing, rapid passage of the food with diminishing of quantity of bile and enzymes, decreased transmission time through the intestine, reduced time available for absorption. All above-mentioned factors lead to delay of proteins, fat hydrolysis, vitamins absorption (B1, B2, B6, B12, D, iron). As a result loss of weight, anemia, diarrhea, osteomalacia and other metabolic disorders evolve.
    Clinical presentation. Evidence of post gastric resection asthenia develops after some latent period, which may lasts from some month up to some years. As usual the general weakness, poor appetite, loss of weight, diarrhea, sometimes oedemas, skin and endocrine disorders predominate. Due to reduced host resistance nonspecific (different purulent) or specific (TB) infections are very common.
    Killiot (1951) described 3 degrees of severity of post gastric resection asthenia:
    1) mild;
    2) middle – accompanied by anemia, diarrhea, oedemas with loss of proteins, fats;
    3) severe – accompanied by cachexia, avitaminosis, osteopathy.
    Treatment. For mild form conservative treatment is indicated. If the disease is progressing or there are middle or severe forms of disease operative treatment is indicated.
    The conservative treatment includes: blood, plasma, protein, aminoacids transfusions; restoration of water-electrolyte imbalance, calcium insufficiency, vitaminotherapy, replacement of enzymes etc.
    The operative treatment consists of duodenum inclusion into passage of food.

    Nutritional allergy.
    An allergy is a high sensitivity or reactivity of organism to some substances – allergens. Normally, the proteins under influence of different enzymes are grinded up to polypeptides and aminoacids, which haven’t the antigen property, and then absorbing.
    After resection of the stomach due to maldigestion disorder of proteins absorption may develop. It is supported by: 1) lowering of a proteolyses activity of the intestinal tract, 2) hypermotility of the intestine with diminishing of time for normal digestion, 3) lesion of the intestinal epithelium, erosions of the mucosal membrane, 4) local hyperemia, stasis, inflammatory processes in intestinal tract.
    It means that nutritional allergy develops due to absorption to blood not completely digested proteins (polypeptides), which became allergens.
    After resection of the stomach the patients notes the high sensitivity to milk and milk products, eggs, apples etc, which was not seen before operation.
    Treatment as usual is conservative and must include: prohibition of foods, which are the cause of allergy; administration of enzymes, desensitizing therapy etc.

    Syndrome of afferent loop
    Afferent loop includes remainder part of duodenum and part of jejunum from ligament of Treyz up to gastroenteroanastomosis. Syndrome develops after resection of the stomach by method Billroth II and it is caused by disorder of empting of the afferent loop. The rate of this syndrome is from 4 up to 15% depending from kind of operation.
    Etiological factors of syndrome of afferent loop are divided on 2 groups:
    I. Mechanical: a) long size of afferent loop without enteroenteroanastomosis; b) not correct position of the afferent loop after resection of the stomach by Billroth II in modification of Hofmeyster-Finsterer (retro transversal gastrojejunoanastomosis on short loop); c) postoperative adhesions, invaginations, disorder of evacuation through efferent loop.
    II. Functional: hypertonic dyskinesia of the biliary tract and duodenum, duodenostasis, atony of the duodenum, dyskinesia of the afferent and efferent loops of the small intestine.
    Clinical presentation: sensation of the fullness in right subcostal and epigastric region, which develops after 10-15 minutes after meals and slowly increases. Nausea, bitter taste in mouth, retrosternal burning sensation appears. Than on peak of attack of epigastric pain abundant vomiting with bile sometimes repeated develops. After vomiting all above mentioned symptoms disappear. Some patients note, that the attack may be provoked by ingestion of special food as milk, fat food etc.
    During physical examination slight jaundice of the scleras, sometimes the signs of dehydration may be detected, the painful, elastic mass in epigastric or right subcostal region which disappeared after attack may be palpated.
    3 kinds of syndrome of afferent loop are distinguished: mild, middle and severe.
    The mild form is characterized by vomiting, which arises 1-2 times per month; in middle form vomiting develops 2-3 time per week, there is strong pain syndrome; severe form – daily attack of pain after meals accompanied by bile vomiting.
    X-ray examination shows passage of contrast material through a gastroenteroanastomosis not only to efferent loop but to afferent loop too.
    Conservative treatment as usual is not so effective and include restoration of proteins, water-electrolytes imbalance, spasmolytics, vitamins etc.
    Operative methods of treatment are divided on 3 groups:
    1) operations directed on removal of over bending afferent loop or shortening of it;
    2) draining operations;
    3) reconstructive operations (Billroth II to Billroth I, enteroenteroanastomosis, duodenojejunoanastomosis etc).

    Gastroesophageal reflux
    This syndrome may be result of stomach resection mostly by Billroth I or sometimes as result of vagotomy. Incompetence of cardial sphincter develops and due to it reflux of acid stomach contents to esophagus arises. In case of stomach resection by Billroth I it develops due to overtension of the stomach stump during its connection with duodenum, due to that angle of Hiss from acute becomes dull. In case of vagotomy, mostly truncular, the gastroesophageal reflux develops in late period after operation (2-3 years) and is the result of disorder of innervations of the cardia. The forms of esophagitis may be different: catarrhal, erosive, ulcerative-necrotic. The symptoms are different, but more common the patients complain on burning pain in lower retrosternal region, which arises after 1-2 hours after meals and increases in case of inclination of the body ahead (symptom of laces). The above mentioned clinical presentation may simulate a stenocardia. A common accompanied symptom is hypochromic anemia. Long standing oesophagitis may be the cause of oesophageal stenosis. Diagnosis is established taking into consideration clinical presentation, results of X-ray investigation (examination of the stomach with barium meal in position of Trendelenburg detects reflux of the contrast from stomach’s stump to the oesophagus and indirect sign as reduction or absence of stomach gas-bubble after cough), endoscopic investigation (oedema, hyperemia, bleeding during touching the mucosal membrane, erosions, sometimes ulceration).
    Treatment as usual conservative: diet (avoid spicy, sour, hot foods). The last ingestion of food must be 3-4 hours before sleep. The patient must sleep with elevated head end of the body. Medical treatment includes administration of almagel, H2-blockers, anti-inflammatory drugs. If conservative treatment fails operations directed on restoration of the angle of Hiss are necessary (oesophagofundoplication by Nissen, oesophagophrenofundoplication).
    Duodenogastral reflux.
    Alkaline reflux gastritis is the result of resection of the stomach by Billroth I, pyloroplasty with vagotomy, or duodenostasis.
    The cause of it is affectation of the stomach mucosal membrane by aggressive duodenal contents (bile acids, enzymes of pancreas, lysocitine etc.) due to reflux. Lesion of the stomach’s mucosal barrier with formation of erosions and ulceration develops.
    A clinical presentation is characterized by permanent dull pain in epigastric region, belching, heartburn, sometimes vomiting by bile.
    Diagnosis is made by endoscopy with biopsy.
    Treatment is usually conservative including diet and antacids. In some cases operation is indicated (operation of Roux, transformation of Billroth I resection to Billroth II).

    Peptic ulcer of gastroenteroanastomosis.
    Recurrent peptic ulcer complicates about 2% of gastric resections for duodenal ulcer; it is extremely rare after resection for gastric ulcer. It may be due to inadequate removal of the acid-secreting area of the stomach, or, rarely, because of the Zollinger-Ellison syndrome. As usual the recurrent peptic ulcer is located in area of anastomosis and like any other peptic ulcer may perforate, stenose, penetrate to surrounding structures or bleed.
    It is treated either by vagotomy or higher gastric resection.
    Recurrence of the peptic ulcer may arise after vagotomy with different draining operations. In most cases it is a result of incomplete vagotomy, which may be postoperatively controlled by test of Hollander (insulin test).
    A dose of insulin (15 units intravenously) is sufficient to produce hypoglycemia which produces a brisk vagal reflex secretion of HCl in the normally innervated stomach, this response is abolished if the vagotomy has been complete.
    Treatment in some cases may be conservative (usual antiulcer treatment). If conservative treatment is not effective revagotomy with resection of the stomach is indicated.

    Postvagotomy diarrhea.
    Postvagotomy diarrhea is appearance of fluid stool more than 3 times per day. Rarely a diarrhea arises after selective proximal vagotomy (1-8%), more frequently it appears after selective vagotomy with draining operation (4-20%).
    The reasons are not understood completely, but in evolution of postvagotomy diarrhea disorders of innervation of the digestive tract, liver and biliary tract, and pancreas take part. It leads to disorder of motor function of the stomach and small intestine with formation of gastrostasis and hypochlorhydria, which support evolution of the bacterial flora, maldigestion and malabsorbtion.
    2 forms of diarrhea are distinguished: permanent and episodic. By severity the postvagotomy diarrhea is divided on:
    1. Mild – the fluid stool arises 2-4 times daily
    2. Middle – the fluid stool appears up to 5 times daily
    3. Severe – the fluid stool is present more than 5 times a day
    The clinical presentation is characterized by sudden, without tenesmus, light fluid stool and sudden disappearing of diarrhea.
    The treatment must be complex:
    1. Diet with excluding milk and others food allergens.
    2. Antibiotics – for normalization of the bacterial flora.
    3. Ingestion of the gastric juice.
    4. Administration of enzymes.
    5. The drugs, which activate the function of sympathetic nerves (benzohexonium).
    6. Restoration of the water-electrolyte, protein, vitamin imbalances.
    In severe causes operation is indicated (inverse of the segment of small intestine).


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