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Role of surgery

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Alternatively, gastrojejunostomy with truncal vagotomy is also an option. Postoperative Complications for Peptic Ulcer surgery Early complication : ... – PowerPoint PPT presentation

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Title: Role of surgery


1
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Introduction
3
Role of surgery
  • Despite advances in medical therapy to inhibit
    acid secretion and to eradicate H. pylori,
    surgery remains important in managing these
    patients. Over the last 2 decades, there has been
    an increase in emergency operations performed for
    complications of peptic ulcers while the number
    of operations for elective indications has
    decreased markedly.
  • An ulcer by definition extends through the
    muscularis mucosa in contrast to an erosion,
    which is superficial to the muscularis mucosa.

4
Etiologies of Duodenal ulcer
  • Duodenal ulcer disease is a disease of multiple
    etiologies. The only absolute requirements are
    secretion of acid and pepsin in conjunction with
    either H. pylori infection or ingestion of
    NSAIDs.

5
Etiologies of gastric ulcers
  • Most of gastric ulcers appear to behave more like
    duodenal ulcers and are associated with excess
    acid.
  • Types I and IV gastric ulcers are defects in
    mucosal protection
  • types II and III are associated with acid
    hypersecretion and behave like duodenal ulcers
  • Gastric cancers ( suspicious ) may ulcerate and
    resemble gastric ulcers.
  • Furthermore, ulcers may be caused by nonacid or
    other peptic disorders such as Crohns disease,
    syphilis, Candida infection, or malignant
    diseases such as Kaposis sarcoma, lymphoma,
    carcinoma, or pancreatic carcinoma.

6
Clinical Manifestations
  • Young and middle-aged patients
  • Pain or one of complication ( perforation ,
    bleeding , obstruction pyloric obstruction ,
    hour glass stomach , penetration , malignant
    transformation in gastric ulcer )

7
ABDOMINAL PAIN
  • The most common symptom is mid-epigastric
    abdominal pain that is usually well localized.
    The pain is usually tolerable and frequently
    relieved by food. Moreover, the pain may be
    episodic, may be seasonal in the spring and fall,
    or may relapse during periods of emotional
    stress. For these reasons and because it is
    relieved, many patients do not seek medical
    attention until they have had the disease for
    many years.
  • When the pain becomes constant, deeper
    penetration of the ulcer, and referral of pain to
    the back is usually a sign of penetration into
    the pancreas.
  • Diffuse peritoneal irritation is usually a sign
    of perforation.

8
PERFORATION
  • Acute Vs subacute
  • Pathology 3 Stages
  • Sudden sever abdominal pain ,assosiated with
    neusia and vomiting , and variable degree of
    shock
  • Peritonitis , frequently accompanied by fever,
    tachycardia, dehydration, and ileus .
  • Abdominal examination reveals tenderness,
    rigidity, and rebound.
  • A hallmark of perforation is the demonstration
    of free air underneath the diaphragm on an
    upright chest radiograph. This complication of
    duodenal ulcer disease represents a surgical
    emergency. Once the diagnosis is made, operation
    should be performed in an expeditious fashion
    following appropriate fluid resuscitation.

9
BLEEDING
  • The most common cause of death in patients with
    peptic ulcer disease is bleeding in patients who
    have major medical problems or are older than 65
    years of age.
  • Because the duodenum has an abundant blood supply
    and the gastroduodenal artery lies directly
    posterior to the duodenum bulb.
  • Most duodenal ulcers present with only minor
    bleeding episodes that are detected by the
    presence of Melina

10
OBSTRUCTION
  • Gastric outlet obstruction manifested by delayed
    gastric emptying, anorexia, or nausea accompanied
    by vomiting.
  • In cases of prolonged vomiting, patients may
    become dehydrated and develop a hypochloremic,
    hypokalemic metabolic alkalosis. Fluid
    resuscitation requires replacement of the
    chloride and potassium deficiencies in addition
    to nasogastric suction for relief of the
    obstructed stomach.
  • In addition to acute inflammation leading to
    functional gastric outlet obstruction , chronic
    inflammation of the duodenum may lead to
    recurrent episodes of healing followed by repair
    and scarring with ultimately fibrosis and
    stenosis of the duodenal lumen. In this
    situation, the obstruction is accompanied by
    painless vomiting of large volumes of gastric
    contents with similar metabolic abnormalities as
    seen in the acute situation. The stomach can
    become massively dilated in this setting, and it
    rapidly loses its muscular tone. Marked weight
    loss and malnutrition are also common in this
    situation.

11
Gastric Ulcer
  • Like duodenal ulcers, gastric ulcers are also
    characterized by recurrent episodes of quiescence
    and relapse. They also cause pain, bleeding, and
    obstruction and can perforate. Hemorrhage occurs
    but the most frequent complication is
    perforation. Most perforations occur along the
    anterior aspect of the lesser curvature. Similar
    to duodenal ulcer, gastric outlet obstruction can
    also occur.

12
Zollinger-Ellison syndrome
  • Zollinger-Ellison syndrome is a clinical triad
    consisting of gastric acid hypersecretion, severe
    peptic ulcer disease, and non-beta islet cell
    tumor of the pancreas. The tumors are known to
    produce gastrin and are referred to as
    gastrinomas.

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Diagnosis
  • History and physical examination
  • Upper GIT endoscopy
  • A serum gastrin level should also be obtained in
    patients with
  • ulcers that are refractory to medical therapy or
    require surgery.
  • An upright chest radiograph is usually performed
    when ruling out perforation.
  • H. pylori testing should also be done in all
    patients with suspected peptic ulcer disease.

15
HELICOBACTER PYLORI TESTING
  • Serology is the test of choice for initial
    diagnosis when endoscopy is not required.
  • If, however, endoscopy is to be performed, the
    rapid urease assay or histology are both
    excellent options.
  • After treatment (only if necessary) the urea
    breath test is the method of choice

16
Treatment
  • Medical Management with exceptions

17
Surgical Procedures for Peptic Ulcer Disease
  • VAGOTOMY
  • TRUNCAL and drainage procedures
  • SELECTIVE VAGOTOMY
  • HIGHLY SELECTIVE VAGOTOMY
  • Gastrectomy

18
Types of VAGOTOMY
19
Heineke-Mikulicz pyloroplasty Vs
gastro-jejunostomy should be associated with
truncal vagotomy or selective vagotomy but not
highly selective vagotomy


20
Hemigastrectomy with Billroth 1 (gastroduodenal)
anastomosis
21
Hemigastrectomy with Billroth II
GASTROJUJINOSTOMY
22
LAPAROSCOPIC PROCEDURES
  • Both parietal cell vagotomy and posterior truncal
    vagotomy with anterior seromyotomy (Taylor
    procedure) can be accomplished laparoscopically
    and represent effective antiulcer operations.

23
Surgical Indications
  • It salvages patients from life-threatening
    complications associated with perforation,
    hemorrhage, and gastric outlet obstruction.

24
Approach to the Patient Bleeding from Peptic
Ulcer Disease
  • Approximately 80 of upper gastrointestinal
    bleeds are self-limited.
  • The initial step in management is adequate
    initial and on going resuscitation.
  • Following resuscitation, endoscopy is performed
    to assess the cause and severity of the bleed.
  • Mortality increases with age ,the severity of the
    initial bleed is also an adverse prognostic
    factor, and this might include the presence of
    shock, a high transfusion requirement, or bright
    red blood in the nasogastric tube or in the
    stool. Recurrent bleeding, concomitant disease
    increased the mortality rate. Also Visible
    vessel was seen during endoscopy

25
  • Endoscopy remains the investigation of choice for
    patients with upper gastrointestinal bleeding
    from peptic ulcer disease.
  • Not only for diagnosis but also therapy.
  • When the bleeding is controlled, long-term
    medical therapy includes antisecretory agents
    usually in the form of a proton-pump inhibitor
    plus testing for H. pylori, with treatment if
    positive.
  • If H. pylori is present, documentation of
    eradication should be performed following
    therapy. If the bleeding continues or recurs,
    surgery may be indicated.

26
Treatment of Bleeding Duodenal Ulcers
  • For those patients who continue to bleed or who
    are referred by the endoscopist , the duodenal
    bleeding is usually controlled by opening the
    duodenum and oversewing the ulcer with a U stitch
    from the vessel, which is usually the
    pancreaticoduodenal artery or gastroduodenal
    artery.
  • As most of these patients are elderly, have bled
    a significant amount, and have some degree of
    hypotension, the more time-consuming parietal
    cell vagotomy is usually not performed. Instead,
    a truncal vagotomy with pyloroplasty is performed.

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Bleeding Gastric Ulcers
  • For bleeding gastric ulcers, a distal gastrectomy
    with Billroth I anastomosis is usually performed.

29
Perforated Duodenal Ulcers
  • Simple patching of a perforated duodenal ulcer
    followed by medical treatment is all that is
    necessary for patients who present with a
    perforated duodenum secondary to peptic ulcer
    disease. Patch closure of the duodenum can be
    performed by either a laparoscopic or open
    procedure.

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Perforated Gastric Ulcer
  • For perforated gastric ulcers that occur in
    hemodynamically stable patients, distal
    gastrectomy with Billroth I reanastomosis is
    usually performed.
  • However, simple patching of the gastric ulcer,
    testing for H. pylori, and treatment if positive
    can also be considered. However, the risk of
    malignancy needs to be ruled out therefore,
    biopsy of the ulcer bed also needs to be
    performed.

32
Gastric Outlet Obstruction
  • The first principle is to categorize the patient
    as either acutely or chronically obstructed.
  • If the patient is acutely obstructed, the
    patient should be treated nonoperatively with
    nasogastric decompression, intravenous fluid,
    nutritional support as needed, and acid
    suppressive therapy. H. pylori should be tested
    for and treated.
  • if the patient has chronic gastric outlet
    obstruction operative therapy is usually
    indicated to open up the gastric outlet. In
    addition, an acid-reducing procedure is
    necessary.

33
Preoperative
  • Nasogastric decompression for several days.
  • Correction of fluid and electrolyte imbalances.
  • Antisecretory therapy.
  • Endoscopy with biopsies.

34
Operative
  • Gastrectomy can be done if technically feasible.
  • Alternatively, gastrojejunostomy with truncal
    vagotomy is also an option.

35
Postoperative Complications for Peptic Ulcer
surgery
  • Early complication bleeding , stomal
    obstruction , duodenal blow-out
  • Postgastrectomy Syndromes Secondary to Gastric
    Resection( Dumping SYNDROME, METABOLIC
    DISTURBANCES,AFFERENT LOOP
  • and EFFERENT LOOP SYNDROME)
  • Postvagotomy Syndromes

36
Postgastrectomy Syndromes
  • DUMPING SYNDROME
  • Dumping syndrome refers to a symptom complex that
    occurs following ingestion of a meal when a
    portion of the stomach has been removed or the
  • normal pyloric sphincter mechanism has become
    disrupted.
  • Dumping syndrome exists in either a late or an
    early form, with the early form occurring more
    frequently.

37
EARLY DUMPING
  • The early form of dumping syndrome usually occurs
    within 20 to 30 minutes following ingestion of a
    meal .
  • The gastrointestinal symptoms include nausea and
    vomiting, a sense of epigastric fullness,
    eructations, cramping abdominal pain, and often
    explosive diarrhea.
  • The cardiovascular symptoms include
    palpitations, tachycardia, diaphoresis, fainting,
    dizziness, flushing, and occasionally blurred
    vision.
  • This occurs because gastrectomy or interruption
    of the pyloric sphincteric
  • mechanism prevents the stomach from
    preparing its contents and delivering them to the
    proximal bowel in the form of small particles in
    isotonic solution. The resultant hypertonic food
    bolus passes into the small intestine, which
    induces a rapid shift of extracellular fluid into
    the intestinal lumen to achieve isotonicity.
  • Following this shift of extracellular fluid,
    luminal distention occurs and induces the
    autonomic responses listed earlier.
  • Dietary measures are usually sufficient to manage
    these patients.

38
LATE DUMPING
  • Appears 2 to 3 hours after a meal.
  • The basic defect in this disorder is also rapid
    gastric emptying. When carbohydrates are
    delivered to the small intestine, they are
    quickly absorbed, resulting in hyperglycemia that
    triggers the release of large amounts of insulin
    to control the rising blood sugar. This results
    in an actual overshooting such that a profound
    hypoglycemia occurs in response to the insulin.
    This activates the
  • adrenal gland to release catecholamines,
    which results in diaphoresis, tremulousness,
    lightheadedness, tachycardia, and confusion.
  • The symptom complex is indistinguishable from
    insulin or hypoglycemic symptom .
  • These patients should be advised to ingest
    frequent small meals and to reduce their
    carbohydrate intake.

39
METABOLIC DISTURBANCES
  • Anemia
  • Iron deficiency anemia a combination of decreased
    iron intake, impaired iron absorption, and
    chronic subclinical blood loss secondary to the
    hyperemic, friable gastric mucosa primarily
    involving the margins of the stoma where the
    stomach connects to the small intestine. In
    general, the addition of iron supplements to the
    patients diet corrects this metabolic problem.
  • Megaloblastic anemiaVitamin B12 deficiency
    occurs secondary to poor absorption ,due to lack
    of intrinsic factor secretion . The patient
    should be treated with intramuscular injections
    of cyanocobalamin every 3 to 4 months
    indefinitely.

40
METABOLIC DISTURBANCES
  • Impaired absorption of fat. On occasion,
    steatorrhea may be seen after gastrectomy and
    Billroth II reconstruction as a result of
    inadequate mixing of bile salts and pancreatic
    lipase with ingested fat because of the duodenal
    bypass.
  • Deficiency in fat-soluble vitamins may also
    occur.
  • In the setting of steatorrhea, pancreatic
    replacement enzymes are often effective in
    decreasing fat loss.

41
METABOLIC DISTURBANCES
  • Both osteoporosis and osteomalacia have also been
    observed following gastric resection and appear
    to be caused by deficiencies in calcium.

42
AFFERENT LOOP SYNDROME
  • Usually occurs when the afferent limb is longer
    than 30 to 40 cm and has been anastomosed to the
    gastric remnant in an antecolic fashion.
  • Following obstruction of the afferent limb, there
    is an accumulation of pancreatic and
    hepatobiliary secretion within the limb,
    resulting in its distention.
  • Pancreatic and hepatobiliary secretion occur in
    response to ingestion of food, accumulation of
    these secretions results in distention, which
    causes epigastric discomfort and cramping. In the
    setting of partial obstruction, the intraluminal
    pressure increases to forcefully empty its
    contents into the stomach, resulting in bilious
    vomiting that is often projectile but offers
    immediate relief of symptoms. There is no food
    contained within the vomitus.
  • If the obstruction has been present for a long
    period, it can also be aggravated by the
    development of the blind loop syndrome.
  • For both forms of afferent loop syndrome, acute
    and chronic, operation is indicated because it is
    a mechanical problem, not a functional problem.

43
EFFERENT LOOP OBSTRUCTION
  • The most common cause of efferent loop
    obstruction is herniation of the limb behind the
    anastomosis in a right-to-left fashion.
  • Operative intervention is almost always necessary
    and consists of reducing the retroanastomotic
    hernia and closing the retroanastomotic space to
    prevent recurrence of this condition.

44
POSTVAGOTOMY DIARRHEA
  • Approximately 30 or more of patients suffer from
    diarrhea after gastric surgery. For most
    patients, it is not severe and usually disappears
    within the first 3 to 4 months. For some
    patients, the diarrhea is part of the dumping
    syndrome. However, vagotomy is also associated
    with alterations in stool frequency
  • Most patients with postvagotomy diarrhea have
    their symptoms resolve over time. In those
    patients who fail to resolve their symptoms,
    cholestyramine, an anionic exchange resin that
    absorbs bile salts and renders them unabsorbable
    and inactive, can significantly diminish the
    severity of diarrhea.

45
STRESS GASTRITIS
  • Stress gastritis has been referred to as stress
    ulcerations, stress erosive gastritis, and
    hemorrhagic gastritis.
  • These lesions may lead to life-threatening
    gastric bleeding and by definition occur after
    physical trauma, shock, sepsis, hemorrhage,
    respiratory failure, or severe burns.
  • They are characterized by multiple, superficial
    (non ulcerating) erosions that begin in the
    proximal or acid-secreting portion of the stomach
    and progress distally.
  • They may also occur in the setting of central
    nervous system disease such as that seen with a
    Cushing ulcer or as a result of thermal burn
    injury involving more than 30 of the body
    surface area (Curling ulcer).

46
Gastric Adenocarcinoma
  • H pylori infection increases the risk of gastric
    cancer
  • Morphologic types ulcerating (15), polypoid
    (25), superficial spreading (15), linitis
    plastica (10), advanced (35)
  • Symptoms and signs include postprandial
    abdominal heaviness early anorexia, with weight
    loss vomiting, often with blood, if pyloric
    obstruction occurs epigastric mass in 25
    hepatomegaly in 10 stool positive for occult
    blood in 50 but melena in a few cases
  • Signs of distant spread metastases to the neck
    (Virchow node) or umbilicus (Sister Mary Joseph
    node), metastases anterior to rectum detectable
    on rectal examination (Blumer shelf), metastases
    to ovaries (Krukenberg tumors)
  • Laboratory findings carcinoembryonic antigen
    is elevated in 65
  • higher levels indicate extensive spread of tumor
  • Endoscopy usually identifies gastric carcinomas
    .

47
Treatment
48
Haematemesis
  • GI bleeding is any blood loss from the GI tract
    (from the mouth to the anus), which may present
    with haematemesis, melaena, rectal bleeding or
    anaemia.
  • Haematemesis is defined as vomiting blood and is
    usually caused by upper GI disease.
  • Melaena is the passage PR of a black
    treacle-like stool that contains altered blood,
    usually as a result of proximal bowel bleeding.

49
Haematemesis
  • Haematemesis is usually caused by lesions
    proximal to the duodenojejunal junction.
  • upper GI lesions can cause frank PR bleeding if
    sever
  • Most tumours more commonly cause anaemia than
    frank haematemesis.
  • In young adults, peptic ulcer disease (PUD)and
    varices are the common causes.
  • In the elderly, tumours, PUD and angiodysplasia
    are the common causes.

50
Gastric causes
  • Erosive gastritis may follow alcohol or NSAID
    intake/stress, history of dyspeptic symptoms.
  • Gastric ulcer possible herald smaller bleeds,
    accompanied by altered blood (coffee grounds),
    history of PUD.
  • Gastric cancer anaemia commoner, associated
    weight loss, anorexia, dyspeptic symptoms.
  • Gastric leiomyoma (rare)
  • Dieulafoys disease (rare) younger patients,
    large bleed.

51
Duodenal causes
  • Duodenal ulcer past history of duodenal ulcer,
    symptoms of back pain, hunger pains, NSAID use.
  • Aortoduodenal fistula (rare) usually infected
    graft post AAA repair, massive haematemesis and
    PR bleed, usually fatal.
  • Cancer ampula of Vater

52
Esophageal causes
  • Bleeding varices sudden onset, painless, large
    volumes, dark red blood, history of (alcoholic)
    liver disease, physical findings of portal
    hypertension.
  • Reflux oesophagitis associated with
    regurgitation.
  • Oesophageal carcinoma (rare) scanty,
    blood-stained debris, rarely significant volume,
    associated with weight loss, anergia,dysphagia.
  • Trauma during vomiting (MalloryWeiss
    syndrome) bright red bloody vomit usually
    preceded by several normal but forceful vomiting
    episodes.

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General (systemic causes)
54
MANAGEMENT
  • Resuscitation
  • Minor bleed observation, scheduled OGD ,monitor
    haemoglobin .
  • Major bleed Continued resuscitation, urgent OGD
  • VaricesEndoscopic therapy, Sengstaken
    tube.,Surgery
  • Peptic ulcer Endoscopic therapy or surgery
  • I.V. PPI treatment, correction of coagulation
    profile , protect aganest hepatic coma if LCF is
    present
  • Early feeding
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