Managing patients with gastrointestinal disorders, Part 1 By Linda Self

1
Managing patients with gastrointestinal
disorders, Part 1By Linda Self
2
Obtain history

• ?GI painduration, pattern, frequency, location,
  referred pain
• Dyspepsia
• Changes in bowel habits
• Stool characteristics,
• Medications
• Previous surgeries
• Use of alcohol, NSAIDs, tobacco
• Changes in eating habits

3
Physical Examination

• Assess
• General appearance
• Oral cavity
• Skin color and turgor
• Abdomensize, shape, symmetry, bowel sounds, for
  borborygmi, for tympani or dullness, and for
  tenderness or guarding

4
Diagnostics

• CBC, CMP, PT, TG, LFTs, amylase, lipase, CEA ,
  AFP
• Carcinoembryonic antigencancer antigen
  reflective of GI cancers, somewhat non-specific
• CA-19 levelsprotein that exists on surface of
  cells and is shed by tumor cells, tumor marker.
  CA-19 levels are elevated in advanced pancreatic
  cancer, colorectal, lung and GB cancers,
  gallstones, pancreatitis, CF and liver disease

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Diagnostics continued

• Many studies require clear liquid diets, fasting,
  ingestion of a liquid bowel preparation, use of
  laxatives and even ingestion or injection of
  contrast dys
• Stool testsleukocytes, fat, nitrogen, parasites,
  pathogens, food residues. Fecal occult blood.
• Breath testsurea breath tests detect presence of
  Helicobacter pylori

6
Diagnostics

• Abdominal ultrasoundnoninvasive, reliable,
  inexpensive, no ionizing radiation
• Endoscopic ultrasonography
• DNA testing for risk for certain
  diseaseshereditary adenomatous polyposis
• UGIbarium
• Barium enema
• CT, MRIcontrast given

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Diagnostics

• EGD
• Colonoscopy
• Manometry measures changes in intraluminal
  pressures and the coordination of muscle activity
  in the GI tractdetects motility problems such as
  achalasia, esophageal spasm, scleroderma, GERD
• Gastric analysis, gastric acid stimulation and pH
  monitoring (NPO for 8-12h) used to diagnose
  pyloric or duodenal obstruction, atrophic
  gastritis or even Zollinger-Allison syndrome.

8
Gerontologic considerations

• Atrophy of taste buds, decreased saliva
  production
• Decreased esophageal motility, weakened gag
  reflex, decreased resting pressure of LES
• Atrophy of gastric acids and digestive enzymes.
  Decreased motility and emptying of stomach.
• Thinning of villi, atrophy of muscle of small
  intestine
• Decrease in mucous secretion of large intestine,
  decreased tone of sphincters, duller nerve
  impulses in rectal area

9
Hiatal hernia

• Opening of the diaphragm through which the
  esophagus passes, becomes enlarged, part of
  stomach moves up into lower thorax.
• Sliding and paraesophageal. 90 are sliding.
  Paraesophageal actually is when entire stomach
  pushes through the diaphragm beside the esophagus.

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Hiatal hernias

• Implicated in reflux, s/s of dyspepsia,
  esophageal fullness
• Tx with small frequent feedings
• Do not recline for at least one hour after eating
• Elevate HOB to prevent hernia from sliding
• Surgery may be indicated (Nissan fundoplication)

11
GERD

• Backflow of gastric or duodenal contents into the
  esophagus
• Caused by incompetent lower esophageal sphincter
• S/Spyrosis, dyspepsia, regurgitation,
  odynophagia (pain on swallowing), esophagitis.
• Assessmentendoscopy, esophageal pH monitoring,
  bilirubin monitoring for bile reflux patterns

12
Management of gerd

• Low fat diet
• Avoid caffeine, tobacco, beer, milk, mint and
  carbonated beverages
• Avoid eating or drinking 2 hours before bedtime
• Maintain normal body weight
• Avoid tight fitting clothes
• Elevate HOB
• Antacids, H2 receptor antagonists, PPIs
• Prokinetic meds like Reglan, Urecholine
• Nissen fundoplication

13
Barretts Esophagus

• Condition whereby the lining of the esophageal
  mucosa is altered
• Chronic reflux causes changes in esophagus from
  squamous to precancerous cells
• c/o frequent heartburn
• EGD
• Determine if high grade dysplasia
• Options are photodynamic therapy (laster
  ablation)
• Prophylactic transhiatal esophagectomy

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Cancer of the Esophagus

• Adenocarcinoma or squamous cell
• Risk for adenocarcinoma is GERD that progresses
  to Barretts
• Risk for squamous chronic hot liquids,
  nutritional deficiencies, chronic etoh and
  tobacco exposure, nitrosamines in food

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Clinical manifestations

• Dysphagia
• Sensation of something in their throat
• Painful swallowing
• Substernal pain
• Regurgitation
• Weight loss
• Foul breath

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Assessment

• EGD with biopsy
• Imaging such as CT, PET, exploratory laparoscopy

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Medical managment

• Surgery, radiation, chemotherapy
• Resection of esophagus
• May have a jejunal graft transfer (tumor excised,
  graft of jejunal tissue, segment of colon, or
  stomach can be elevated
• High mortality due to infection, pulmonary
  complications and leaky anastomosis
• Palliation may be accomplished with a stent,
  dilation of esophagus or laser therapy

18
Nursing Management

• May need to be on enteral or parenteral feeding
  initially
• Chest tube drainage
• NG tube and gastric intubation
• Often in ICU post-op
• Low Fowlers position to prevent aspiration
  pneumonia

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Nursing Management

• Monitor for regurgitation and dyspnea
• Rigorous pulmonary plan of care incl. incentive
  spirometry, sitting up in chair
• Close monitoring of temperature
• Watch for drainage from cervical neck wound,
  evidence of esophageal leak
• Atrial fibrillation 2ndary to vagal nerve
  irritation

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Nursing management

• Protect NG tubewill remove 5-7 days after
  surgery
• Introduce water and advance diet to soft
  gradually
• As food and fluid intake increases, will
  gradually decrease parenteral fluids
• After each meal, patient remains upright for at
  least two hours to allow food to travel down the
  GI tract
• Avoid Boost and Ensure as they promote the
  vagotomy syndrome (dumping syndrome)
• Education is key before dischargediet, s/s
  aspiration, prevention of aspiration, comfort
  measures, s/s for prompt follow-up

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Post-Vagotomy or dumping syndrome

• Caused from interruption of vagal nerve fibers.
  Alters storage function of stomach and pyloric
  emptying mechanism.
• Results in large amounts of osmotically active
  content rapidly dumping into duodenum. Results
  in severe cramping, followed by diarrhea, may or
  may not be associated with diaphoresis, rapid
  heart rate /or rapid respirations.
• Usually improves with time provided patient
  follows prescribed diet.

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Dumping syndrome

• Unpleasant set of vasomotor and GI s/s.
• Foods high in CHO and lytes need dilution before
  entering the jejunum, however, food passes too
  quickly for this to happen. The hypertonic
  material causes rapid influx of fluid to occur.
• S/Sweak, faint, dizzy, diaphoresis, palpitations
• Thereafter, rapid increase in BS, surge of
  insulin so reactive hypoglycemia

23
Gastritis

• Condition whereby gastric mucous membranes become
  inflamed. Result is superficial erosion.
• Causes include dietary indiscretions, excessive
  NSAID use, excessive alcohol intake, bile reflux
  bisphosphanate use and radiation therapy.
• Chronic gastritis can be caused by benign or
  malignant ulcers of the stomach caused by H.
  pylori. Also associated with autoimmune disorders
  such as pernicious anemia.

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Clinical manifestations

• Characterized if acute or chronic
• Anorexia, heartburn, nausea and vomiting
• Food intolerances
• May result in B12 deficiencies

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Assessment

• UGI
• Endoscopy with biopsy
• Check for H. pylori

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Management

• Nonspicy foods
• Antacids
• Prostaglandin analogue Cytotec
• PPIsPrevacid, Aciphex, Nexium
• H2 receptor antagonists
• Avoid alcohol and NSAIDs
• Tx for H. pyloritwo antibiotics and anti-acid
  med (see text)

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Peptic ulcer disease (PUD)

• Gastric, duodenal or esophageal ulcers
• Is an excavation that forms on the mucosal wall
  of the stomach, pylorus, duodenum, or esophagus
• Erosion may extend as deeply as the muscle layers
  and peritoneum
• Occurs more frequently in those between 40-60
  years of age

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PUD

• Frequently caused by H. pylori
• Excess acidity
• Familial
• Those with O type blood
• Zollinger-Ellison syndrometumor that causes
  excess secretion of gastrin. May consist of
  peptic ulcers, gastric hyperacidity and gastrin
  secreting benign or malignant tumors

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Comparison of duodenal and gastric ulcers

• Duodenal ulcer
• Age 30-60
• Male to female 2-31
• 80 of peptic ulcers are duodenal
• Possible weight gain
• Pain 2-3h after eating, food relieves pain
• Melena
• Risk factors H. pylori, stress,
  alcohol,,smoking, cirrhosis

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Comparison cont.

• Gastric ulcers
• Usually in 50 and over
• Male to female 11
• 15 of peptic ulcers are gastric
• Weight loss
• Hyposecretion of acid
• Pain ½ to 1 hour after a meal
• Vomiting is common
• Hemorrhage more likely
• RisksH.pylori, stress, etoh, smoking,NSAIDS

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Presentation of pud

• Epigastric tenderness
• Gnawing pain
• Pyrosis
• Diarrhea or constipation
• Bleeding as manifested by melena

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Assessment/dx

• Physical exam
• Stools for occult blood
• Endoscopy is the gold standard
• H. pylori
• Gastric secretory studies
• biopsy

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Medical management

• Eradicate H. pylori, manage gastric acidity
• Combination of antibiotics, PPIs or H2 receptor
  antagonists or bismuth
• Maintenance of PPIs or H2 RA possible for up to
  one year
• Stress reduction
• Reduction of smoking and alcohol intake
• Dietary modificationdecrease caffeine, milk
  products,

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Surgical management in pud

• Indicated for those with intractable ulcers
  (those who do not heal within 12-16 weeks)
• In those with hemorrhage, perforation or
  obstruction
• Vagotomy to decrease acidity
• Billroth I (gastroduodenostomy)
• Billroth II (gastrojejunostomy)

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Nursing management

• Relieve pain
• Explain all procedures to reduce anxiety
• Maintain optimal nutrition
• Monitor for bleeding, infection
• Educate patient post-procedure of need to avoid
  alcohol, coffee, tea, colas need to eat regular
  meals, smoking cessation.
• Stress need for f/u care.

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GI Bleed

• Distinctivehematemesis and melena
• Large bore IV, saline or LR
• Frequent vitals
• Type and crossmatch blood
• Monitor CBC
• NG tube
• Foley
• Possible trendelenburg as BP mandates

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GI Bleed

• Transendoscopic coagulation by laser
• Interventional radiology with selective
  embolization
• If s/s of bleeding tachycardia, tachypnea,
  hypotension, change in LOC, thirst and oliguria
  are present, has had tx and blood and rebleeding
  occurs, may need surgery

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Perforation and penetration

• Erosion of the ulcer through the gastric serosa
  into the peritoneal cavity w/o warning
• Need immediate surgery
• Presents with back and epigastric pain not
  relieved by meds that were prev. effective

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Perforation cont.

• s/ssudden, severe upper abdominal pain, may be
  referred in shoulders due to phrenic irritation
• Vomiting and collapse
• Rigid abdomen, hypotension and tachycardia
• Warrants immediate attention! Becomes an
• Acute abdomen

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Morbid obesity

• People who are more than two times their ideal
  weight or whose BMI exceeds 30kg/m2
• Or, body weight that is more than 100 pounds
  greater than the ideal weight
• Much higher risk for diabetes, heart disease,
  stroke, hypertension,gallbladder disease,
  osteoarthritis, sleep apnea and some forms of
  cancer (uterine, breast, colorectal, kidney and
  GB).

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Medical management

• Weight loss program
• Behavioral modification
• Exercise
• antidepressants

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Pharmacologic management

• Xenicalprevents absorption of fats
• Meridiaaffects serotonin and norepinephrine
• Rarely result in more than 10 loss of body
  weight
• More often regain weight

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Surgical managment

• Performed only after nonsurgical options have
  been exhausted
• Bariatric surgical procedures work by
• Restricting a patients ability to eat
• Interfering with ingested nutrient absorption
• Average amount of weight lost with these
  procedures is 61
• Co-morbid conditions show radical improvement

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Patient selection

• Body weight
• Unsuccessful weight reduction
• Long history of obesity
• Absence of endocrine disorders that cause morbid
  obesity
• Psychological stabilityno drug/alcohol abuse,
  aware of mechanism of action, aware not a
  guarantee, ability to comply w/tx plan

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Surgical procedures for morbid obesity

• Vertical banded gastroplasty
• Gastric banding10-15ml capacity
• Roux-en- Ypouch of only 20-30cc. Good for long
  term weight loss
• Biliopancreatic diversion.
• May need body recontouring after weight loss

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Complications

• Infection secondary to leaking from anastomosis
  site
• Bleeding
• Nutritional deficiencies
• Blood clots, incisional hernias, bowel
  obstructions

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Nursing management

• Monitor for usual post-op complications
  especially respiratory, DVT, peritonitis
• With return of bowel sounds, introduce diet. 6
  small feedings totaling 600-800 calories/day
• Ensure satisfactory fluid intake
• Teach dietary compliance to avoid n/v, diarrhea
• Discharged after 4-5 days
• Teach long-term SE wt. gain,gallstones and
  nutritional deficiencies

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Dietary guidelines for the patient who has had
bariatric surgery

• Avoid liquid calories like alcohol and sodas
• Eat three meals per day, protein and fiber rich
• Two protein snacks per day
• Restrict meal size to less than cup
• Eat slowly and chew thoroughly
• Eat only foods packed with nutrients
• Drink plenty of water 90 after meals to 15
  before meals
• Do not eat and drink at the same time
• Walk for at least 30 minutes per day

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Irritable bowel syndrome

• 12 of adults in US have this disorder
• ? Cause
• More common in women
• Factors such as heredity, depression, anxiety,
  diet high in fact, alcohol consumption, and
  smoking may be contributive
• Results from a functional disorder of intestinal
  motility, Segments of peristaltic waves and
  intensity of propulsion seem affected

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IBS

• Presents with constipation, diarrhea, or
  combination
• Pain, bloating, abdominal distention also occur
• Frequently relieved with defecation
• Diagnosis of exclusiondo ESR, barium enema, EMG
  to measure intraluminal pressures

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Medical management

• Identify foods that trigger s/s
• High fiber diet
• Antispasmotics and hydrophilic colloids
• Antidepressants
• anticholinergics

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Acute inflammatory intestinal disorders

• Diverticulosis/diverticulitishigh fiber,low fat
  antispasmotics, demerol, abx (Flagyl, Bactrim,
  Cipro), possible bowel resection
• Peritonitisinflammation of the serous membrane
  lining the abdominal cavity common bacteria
  areKlebsiella, Proteus, E. coli and Pseudomonas
• Inflammation and paralytic ileus are the results
  of the infection

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Peritonitis cont.

• Common causes include stab injuries, from
  appendicitis, perforated ulcer, diverticulitis
  and bowel perforation, abdominal surgical
  procedures, peritoneal dialysis, others

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Peritonitis

• s/sdiffuse pain,more intense at origin, muscles
  become rigid,rebound tenderness, paralytic ileus,
  n/v, fever
• Dx findings elevated WBCs, electrolyte
  abnormalities xray will show air and fluid
  levels CT will show abscess peritoneal
  aspiration shows organisms
• Complications sepsis
• Txfluid replacement, analgesics, antiemetics,
  NG, O2, possible vent, antibiotics, surgery--

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Peritonitis

• Two primary postsurgical complications are
  evisceration and abscess formation
• Eviscerationcover wound w/saline gauze
• Raise to Fowlers position
• Fluids IV
• Prepare for surgery

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Nursing management

• Usually ICU
• VS
• Analgesia
• Positioning
• IO
• Monitoring for return of normal bowel sounds
• Wound, drain care

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Ulcerative colitis and crohns disease

• Oral fluids, low residue, high protein, high
  calories diet with vitamins and iron. Restore
  fluid and lytes
• May need to avoid milk
• Sedatives, anti-diarrheals
• Steroids
• Immunomodulators like methotrexate and
  cyclosporine monoclonal antibodies like Remicade
• Parenteral nutrition may be indicated
• Possibly surgery-colectomy with ileostomy

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Paralytic ileus

• Also called adynamic ileus or nonmechanical
  obstruction
• In ileus, bowel contents accumulate above area
  of obstruction or dysmotility. Intestinal
  distention ensues. To compensate, peristalsis
  increases in effort to move contents along.
  Increase in peristalsis stimulates more
  secretions, more distention.
• Edema of bowel and capillary permeability result

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Paralytic ileus cont.

• Now have edematous bowel with increased capillary
  permeability
• Plasma leaking into the peritoneal cavity and
  fluid trapped in intestinal lumen decrease
  absorption of fluid and lytes into vascular
  space. Reduced circulatory blood volume and
  electrolyte imbalances occur. Hypovolemia can be
  profound.

60
Paralytic ileus cont.

• Can result following abdominal surgery or trauma
• Can result from handling of intestines during
  abdominal surgery
• Other contributors include vascular
  insufficiency, electrolyte disturbances, result
  of peritonitis, MI

61
Paralytic ileus

• Decreased or no bowel sounds
• Vomiting of gastric contents
• Abdominal distention
• Obstipation
• May have increased WBC, HH, creatinine and BUN
  fr. Dehydration
• Flat plate and upright will show distended bowel
  loops in small intestine, no gas in colon

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Paralytic ileus

• NPO
• NG
• Abdominal girth
• Replace fluid and electrolytes
• Opioids not initially so as not to slow motility
• Possibly exploratory laparatomy

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Mechanical causes of obstructions

• Adhesions
• Tumors
• Volvulus
• Hernia
• tumor