GERD HIATUS HERNIA

PEPTIC ULCER DISEASE

MAY 2011

Upper GI Stucture

GERD

• Presence of gastric secretions into the lower esophagus

• Affects 7% of adults; common in children

• Not a disease but a syndrome

• Frequency and severity of S/S determines the outcome

Etiology and Pathophysio• No single cause, several contributing factors

• Lower esophageal sphincter (LES) damaged /weakened allows gastric content to enter into esophagus esophagitis

• Pepsin and bile salts corrode esophageal lining

• Severity depends on weakness of LES, and amount and duration of acid refluxed into the esophagus

GERD Risk Factors• Predisposing conditions: incompetent LES,

impaired esoph motility, hiatal hernia, defective mucosal defense, decreased gastric emptying

• Diet: Citrus, pineapple, tomato, coffee and tea, caffeinated drinks, hot/cold foods, spices

• Smoking, alcohol

• Age

Exacerbating foods:

• Acid producing foods, fatty foods (increase the time food remains in the stomach), chocolate, mint, coffee, alcohol

Clinical Manifestation• Pyrosis (heartburn): Burning tight sensation

that spreads to jaw and throat.Mild S/S for 5+ years, linked w/ difficulty swallowing, or more severe/often (>once/week)

• Sudden awaken at night with dyspnea

• Respiratory problems: wheezing, coughing

• Autolaryngologic S/S: hoarseness, sore throat, choking, ‘lump’ in the throat, regurgitation

• Early satiety, PC bloating, N&V

Clinical manifestations in PEDS• Spitting up (in infants)• Projectile vomiting• Weight loss, failure to thrive• Gagging or choking at the end of feeding• Respiratory problems• Hematemesis: vomiting of blood• Melena: black, tarry stool• Anemia• Heartburn/irritability• Apnea

GERD Complications• Esophagitis, esophageal ulcerations• Esophageal stricture• Dysphagia• Barrett’s Syndrome: serious change in the

cells lining the esophagusMay lead to esophageal cancer

• Respiratory: bronchospasm, laryngeospasm, aspiration pneumonia

• Dental erosions• Anemia

Diagnostic Tests• Upper GI endoscopy**• Biopsy• Barium Swallow• Manometry Studies• Radionucleid tests• Spinctigraphy(detects radioactive substance

in the esophagus after feeding of a compound, it also assesses gastric emptying

• Medical History

Treatment

Collaborative Care AdultGOALS: to reduce reflux damage to esophageal

lining and lifestyle changes in the adult.

Elevate head of the bed with block 4-6” high.• PPI• H2 receptor blockers• Cholinergic drugsOther meds such as Reglan tighten the LESuseful at night when reflux often occurs.Avoid lying down immediately after eating. Avoid late

evening snacks. • Avoid tight clothing and bending over after eating.

Therapeutic Mgmt – Peds

• Depends on the severity

• None if infant is thriving

• Diet changes

• High Fowler’s when eating

• Small frequent meals with frequent burping for infants

Sx Intervention: Nissen Fundoplication

• Fundus of stomach wrapped and sutured around distal portion of the esophagus

• Restores normal pressure to LES and prevents acid from refluxing into the esophagus.

• The patient is usually started on clear liquids the first day after surgery and discharged later that day

• The patient is given a general anesthesia. Then the abdomen is inflated with carbon dioxide

• The laparoscope, a thin tube carrying the video camera, is inserted.

• Four pinpoint incisions are then made in the upper abdomen through which needle-like instruments are inserted

Post OP Nsg Care – Adult • Resp assessment

• Fluid/electrolyte balance

• Chest tubes (if done via open approach)

• Clear fluids

• I/O, N/G tube

• Pain management

Post OP Nsg Care – Peds• Ongoing assessment of infants • Educating parents re: positioning, feeding &

meds• Appropriate care post op• Coping strategies• Fluid & electrolyte imbalance• Prevention of infection• N/G tube patency

Nissen Complications• Internal bleeding or infection

• Gas-bloat: Since the LES muscle has been tightened, the patient may be unable to belch, resulting in a feeling of bloating and discomfort.

• A common but usually short-term problem

• Tx: Sit pt up, provide meds for gas allevation, assure pt that bloating is temporary

Hiatus HerniaHiatus Hernia• Sliding of part of the stomach through the

diaphragm (muscular sheet that separates the lungs and chest from the abdomen)

• Also known as diaphragmatic/esophageal hernia • Often causes no symptoms, but can cause pain

and heartburn. • It is not usually a serious condition, often needs

no treatment.• Most S/S can usually be treated with drugs, or if

severe, a surgical intervention (Nissen).

Hiatal Hernia

Etiology and Patho

• Etiology unknown, • Weaken of the muscle in the diaphram and the

espgogastric opening. • Increased intra abdominal pressure • Wearing of Tight corset, • Pregnancy• Obesity• Ascites• Tumors• Lifting of heavy objects continuously

Other Predisposing Factors

• Trauma• Old age • Poor nutrition• Prolonged illness, (that confines patient to

bed in a constant recombinant position)• Congenital• A rare form of hiatus hernia may be present at

birth due to incorrect development of the diaphragm or stomach

Types of hiatus hernia

1) Sliding hiatus hernia: the lower esophageal sphincter slides up through the diaphragm•Most common type of hiatus hernia.

2) Paraesophageal or rolling hernia: esophagogastric junction remains in a normal position, but the fundus and greater curvature of the stomach rolls up into the diaphragm and causes a pocket to form beside the esophagus.

Clinical Manifestations

Usually similar to GERD•Bleeding (from erosions)•Stenosis •Ulcerations•Strangulation: cuts off supply of blood flow tissue necrosis•Non-radiating pain and discomfort behind the breastbone (sternum). If severe, this can feel similar to a heart attack

Diagnostic Test

• Barium swallow

• Endoscopic visualisation of lower esophagus

• Other tests the same as GERD

Collaborative ManagmentSimilar to GERD•Lifestyle modification•Decrease intrabdominal pressures•Avoid lifting Heavy Object, straining•Avoid alcohol and smoking•Elevate head of the bed•Same medications as for GERD•Weight Loss

•Small frequent meals rather than fewer large meals•Avoid bending over or lying down after a meal

DietAvoid (or use in moderation) foods and substances that increase reflux of acid into the esophagus: •nicotine (cigarettes) •caffeine •chocolate •fatty foods •peppermint •alcohol •spearmint

Meds /Surgical Intervention

Rare, but if a hiatus hernia causes such severe symptoms or complications then surgery is recommended.

• Niessen Fundoplication

• Laporoscopic

• Traditional

Peptic Ulcer Disease• Erosion on the lining of the stomach or

duodenum from the digestive action of HCL and pepsin.

• Common – 2000 Cdn die each year from PUD

PUD Etiology• Hypersecretion NOT the primary mechanism by

which most ulceration occurs. • Certain factors disrupt the normal mucosal defense

and repair, making the mucosa more susceptible to the attack of acid.

• Cancerous tumors in the stomach or pancreas• Not caused by stress or eating spicy food, but are

contributing factors.• Usually develop in the presence of an acid env’t or

people with pernicious anemia

PUD Risk factors• Overproduction of acids, bile salts

• Meds: ASA, NSAIDs

• Alcohol

• Ischemia• **Bacterial infection (H. pylori) – Responsible

for the majority of peptic ulcers• Common in the US, 20% of people <40 and

50% >60 are affected (by orofecal contamination)

Types

• Peptic ulcers are classified as acute or chronic depending on the degree and or duration of mucosal involvement, and gastric or duodenal and according to the location.

• Gastric and Duodenal Ulcers

Gastric vs. Duodenal Ulcers

Gastric Ulcers

• Lesions are superficial with smooth margins round, oval or cone shaped.

• Antrum, body and fundus of the stomach affected.

• Gastric secretions are usually normal of decreased.

• Greater in women fifty to sixty years old

Gastric Ulcers• Low socioeconomic status• Unskilled labourers• Smokers• Alcoholics• Weak or incompetent pyloric sphincter• Individuals with bile reflux• Head trauma (affects CNS control of cortisol

levels)• Major surgery• H. pyloria

Clinical Manisfestation

• Burning or gaseous pressure in the left epigastris region abdomen and back.

• Pain 1 to 2 hours after meals

• Nausea/vomiting and weight loss.

Clinical Manisfestation

• Symptoms of gastric ulcer often do not follow a consistent pattern (eg, eating sometimes exacerbates rather than relieves pain).

• This is especially true for pyloric channel ulcers, (Chronic) which are often associated with symptoms of obstruction (eg, bloating, nausea, vomiting) caused by edema and scarring.

Complications

• Hemorrhage

• Perforation

• Outlet obstructions

• Intractability

• Secondary duodenal ulcers

Duodenal Ulcers

• Devlopment is associated with high HCL• Scretions, • patient with COPD, • Age group 35 years to 45.• Greater in Men• Research shows it is increasing in

females, mainly post menopausal, • Associated with psycological stress

Duodenal Ulcers

• Smoking• Alcohol• Drugs• Chronic Renal Failure• Hyper parthryoidism• Zollinger-Ellison syndrome (is a condition in

which there is increased production of the hormone gastrin. Usually, a small tumor (gastrinoma) in the pancreas or small intestine produces the high levels of gastrin in the blood.

Gastric ulcers• Smooth, superficial

lesions

• Stomach affected

• Normal-low gastric secretions

• More among women

• Burning, gaseous pain 1-2h PC

Duodenal ulcers• **Penetrating lesions• Increased secretions• **Greater among men• Peak 30-45 years• Burning, cramping,

pressure-like pain 2-4h PC and mid-AM, mid-PM, **mid-HS

• **Relieved by antacids and food

Clinical manifestations

SEVERE S/S o duedonal Ulcers• Sharp, sudden, persistent stomach pain

• Bloody or black stools

• Bloody vomitus

• Vomit that resembles coffee grounds

Diagnostic Tests of PUD

• Endoscopy

• Contrast studies

• Tissue specimen, to r/o H-pylori virus

• Urea Breath test – H-pylori detection**

• Stomach Biopsy

• Chest x-rays

• CBC, SMA-14 (to determine coagulation, liver Fx, absorption of nutrients)

Collaborative Care

• Objective is to decrease the production of gastric acidiy

• Enhance mucual defense mechanisms

• And to decrease harmfull effects of on the mucosa

• Rest, physical and emotional support

• Job modifications

• NSAIDS, and COX 2 inhibitors

Collaborative Care Con’t

• PPI and H2 receptor blockers

• Antibiotics

• Antacids

• Anticholinergic (decrease vagal stimulation of HCl and to decrease gastric motility

• Cyto-protective drug therapy (Cytotec)

• Nutritional Therapy

COX-2 inhibitors

Class of drugs which selectively inhibit COX-2, an enzyme involved in the inflammation pathway, while sparing COX-1, thereby reducing gastrointestinal toxicity (Celecoxib)

Cytotec (misoprostol)

• Prostaglandin analog gastric acid secretion– Enhances mucosal resistance to injury

• Uses: prevention and treatment of NSAID related ulcers– NSAIDs inhibit prostaglandins

• Side effects: Nausea, vomiting, abdominal pain• Contraindication: pregnancy miscarriage

– Used therapeutically to induce labor

PUD Complications• Hemorrhage: Most common complication of

PUD.

S/S:

• hematemesis (vomiting of fresh blood or "coffee ground" material); passage of bloody or black tarry stools ( melena), weakness, syncope.

Perforation• Most lethal complication when ulcer

penetrates through the stomach wall, allowing digestive juices and food to leak into the abdominal cavity

S/S:• Sudden severe upper abd pain• Shoulder pain (irritation of phrenic nerve)• Rigid abd muscles• Shallow resp• N/V• Absent bowel sounds• Bacterial peritonitis 6-12hrs

Peptic Ulcer Sx: Indications• Intractability: failure of ulcer to heal or

recurrence

• Hx or increased risk of hemorrhage during Tx

• Prepyloric/pyloric ulcers

• Multiple ulcer sites

• Drug-induced ulcers, potentially malignant ulcer

• Concurrent conditions: severe burns, trauma, sepsis

• Obstruction

Peptic Ulcer Sx: Types1) Partial gastrectomy – distal 2/3 of stomach and

anastomosis to:

– Duodenum – gastroduodenostomy (Billroth I)

– Jejunum – gastrojejunstomy (Billroth II)

2) Vagotomy: severing the vagus nerve to stomach

3) Pyloroplasty: surgical enlargement of pyloric sphincter

Commonly done after vagotomy or dev’t of scar tissue

Gastroduodenostomy / Billroth I Billroth ISx reconstruction procedure that reconnects

the remaining 1/3 of the stomach to the first portion of the small intestine (duodenum) is created.

Gastroduodenostomy / Billroth I Billroth I

Bill Roth II

• The surgical resection of the pylorus to the The surgical resection of the pylorus to the stomach, followed by closure of the cut stomach, followed by closure of the cut

ends of the duodenum and ends of the duodenum and gastrojejunostomy..gastrojejunostomy..

Billroth II anastomosis

Vagotomy

• A vagotomy is the removal of all or some A vagotomy is the removal of all or some of the branches of the vagus nerve.of the branches of the vagus nerve.

• Vagotomy may be used to treat peptic Vagotomy may be used to treat peptic ulceration; it has gradually superseded ulceration; it has gradually superseded partial gastrectomy as the surgical partial gastrectomy as the surgical treatment of choice for chronic duodenal treatment of choice for chronic duodenal ulceration.ulceration.

• Vagotomy can be performed using closed Vagotomy can be performed using closed approach (laparoscopic)approach (laparoscopic)

Vagotomy

• Performed under general anesthesia. The surgeon makes an incision in the abdomen and locates the vagus nerve.

• Either the trunk or the branches leading to the stomach are cut. The abdominal muscles are sewn back together, and the skin is closed with sutures.

• Often, other gastrointestinal surgery is performed (e.g., part of the stomach may be removed) at the same time.

• Vagotomy causes a decrease in peristalsis, and a change in the emptying patterns of the stomach. To ease this, a pyloroplasty is often performed to widen the outlet from the stomach to the small intestine

Post-OP• Patients who have a traditional vagotomy

stay in the hospital for about seven days.• NG suctioning is required for the first three

or four days. • Approximately 6 weeks to fully recover • Sutures can be removed in 7-10 days**• Early ambulation • Pain medication• Stool softeners• Prophylactic antibiotics may be prescribed

following the operation.

Vagotomy Complications

• Gastric or esophageal perforation. May occur from an electrocautery injury or by clipping the branch of the nerve .

• Delayed gastric emptying. Most common after truncal and selective vagotomy, particularly if a drainage procedure is not perform.

Pyloroplasty• The pylorus valve at the lower portion of the

stomach is cut and anastomosed, relaxing and widening the pyloric sphincter into the duodenum

• Surgical enlargement of the pyloric sphincter assist in the flow of the stomach contents.

• Treats patients at high risk for gastric or peptic ulcer disease (PUD).

• Commonly done after vagotomy or to enlarge an opening narrowed as a result of scar tissue

Pyloroplasty

Partial Gastrectomy• Removal of part of the stomach. 

• After the operation the stomach is smaller but the cardiac sphincter between esophagus and stomach remain intact. 

Gastrectomy: Post-op assessment• NG tube (3-4 days) – suction, patency• Drsg – bleeding, odor, drainage• Gastric aspirate:

– Colour – bright red, gradual darkening over 24h; yellow-green within 36-48h

– Amount– Odor

• Peristalsis, comfort in lower abdomen (to prevent bowel obstruction complications)

• VS q4h• Accurate I&O

Post-op care• Drsg cleaning

• If NG tube clogged irrigate /c NS (order req’d)

• Breathing – As incision is high in epigastrium may interfere w/ deep breathing and coughing

Splint w/ pillow, encourage breathing exercises

• NPO, TPN – K+ and vitamin supplements added

Then CL diet PO aspirate stomach within 1-2h to assess qty digested, colour, consistency

Tube removed, increase CL 6 small SF meals QD

Gastrectomy complications• Dumping syndrome: Results fm reduced capacity

of post-gastrectomy bolus of excess hypertonic fluid (chime) enters intestines fluids drawn into lumen plasma volume drops

S/S (onset 15-30 min PC, lasts for 1h): weakness, sweating, palpitations, abd cramps, hyperactive bowel (borborygmi), urge to defecate

• Postprandial hypoglycemia – Bolus w/ high carb levels into intestines excessive rls of insulin

S/S (2h PC): weakness, sweating , tachycardia, anxiety, confusion

• Bile reflux gastritis – Pylorectomy allows bile access back up GI tract damage to gastric mucosaS/S (continuous, increase PC): upper abd pain, frequent heartburn, N&V, wt loss, hoarseness

• Pernicious anemia (total gastrectomy only)Removal/absence of parietal cells intrinsic factor loss Vit-B12 absorption loss anemiaS/S: Fatigue, dizziness, SOB, pallor, arrhythmia, chest pain, cold extremities

Gastrectomy complications

Post-op nutrition• Small, frequent meals (6 per day)

• Avoid fluids within 30-45min before/after meals

• Short rest PC

• Start w/ low-carb, mod-protein and -fat dry diet

• Limit refined sweets: sugar, honey, jam, candy

• If exp. postprandial hypoglycemia sweet fluid

• Bile reflux Questran or alum. hydroxide antacids

• Anemia Vit-B12 supplements for rest of life

Peptic Ulcer: Pt Teaching• Modify diet (to prevent epigastric distress)

• Avoid smoking and alcohol

• Avoid OTC meds unless first approved by MD

Stress Ulcers• A GI mucosal injury related to illness.

• Ulceration may vary from diffuse superficial injuries to deep hemorrhaging ulcerations.

• The development of stress ulceration is not related to a history of PUD or H-pylori infection. The cause is multifactorial and related to hypoperfusion and loss of host defenses.

Causes of stress ulcers• Overproduction of gastric acid, bile and

digestive enzymes. • Mucosal blood flow is diminished, and there is

an imbalance of demand for and supply of oxygen.

• Mucosa is compromised by ischemia and attacked (mostly) by acid.

• Injury and the presence of acid decrease the ability to repair itself (hostile environment)

Risk Factors: Sepsis, Liver failure, Hypotension, Renal failure

Treatment of stress ulcers

• Prevention – focus on reducing the quantity of acid

• Use of H2 receptor antagonists or antacids

• Patients in shock, sepsis, respiratory distress, hepatic or renal failure, or coagulopathy, should all be given stress ulcer prophylaxis meds.

Question

• Client with GERD is having discomfort further teaching is necessary when client states

1- Use antacids between meals and bedtime

• 2-Quit smoking ,but I chew a lot of gum• 3-Sleep with my bed elevated on blocks• 4-Keep my diet low in fat and eat small

meals throughout the day and at bed time

Question

• When teaching client with GERD nurse should teach client to avoid foods that increase pressure in the LES

• 1-Acid and pickled foods

• 2- Coffee tea chocolate

• 3- dairy products (bloats GI)

• 4-Spicy and highly seasoned foods

Question

Client with recurrent heart burn diagnosed with hiatal hernia. Nurse explains to client that this involves•1-Extension of the esophagus through the diaphragm•2-Displacement of the duodenum through the stomach to the esophagus•3-Twisting of the stomach around the esophagus, occluding the esophagus•4-Protrusion of the stomach into the esophagus through an opening the diaphragm