Transcript Care of Patient with GERD & Peptic Ulcer

Care of Patient with
GERD & Peptic Ulcer
63-273
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GERD: Background
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Gastroesophageal reflux is a normal physiologic
phenomenon in most people, particularly after a
meal.
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Gastroesophageal reflux disease (GERD) occurs
when the amount of gastric juice that refluxes
into the esophagus exceeds the normal limit
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Causes of GERD
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GERD: Symptoms
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Typical symptoms:
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Heartburn (Pyrosis):
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Regurgitation:
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Most common
Felt as a retrosternal sensation of burning or discomfort
Occurs usually after eating or when lying down or bending over.
Often relieved with milk or water
Effortless return of gastric and/or esophageal contents into the
pharynx.
It can induce respiratory complications if gastric contents spill into
the tracheobronchial tree.
Atypical symptoms
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Cough, dyspnea, hoarseness, and chestpain
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Diagnosis
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Role out other potential causes for the
heartburn:
Cardiac
 Peptic ulcer
 Esophagitis
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Esophageal Endoscopy:
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The gold standard as a definitive diagnosis
Barium swallow
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Not as definitive in mild cases
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Collaborative Care
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Lifestyle modifications
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Nutritional therapy
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Decrease high-fat foods, avoid milk products at night, and
avoid late snacking or meals
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Drug Therapy
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Surgical therapy
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Endoscopic therapy
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GERD: Complications
 Are
related to HCl effect on the
esophageal mucosa
 Esophagitis
 Can
complicate to esophageal ulceration
 Barrett’s
esophagus (esophageal
metaplasia)
 Pre-cancerous
lesion
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Nursing Management
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Avoid factors that cause reflux
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Stop smoking
Avoid acid or acid producing foods
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Elevate HOB ~30°
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Do not lie down 2 to 3 hours after eating
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Patient teaching (see Table 40-10 in textbook)
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Drug therapy
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Evaluate effectiveness
Observe for side effects
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Peptic ulcer
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Erosion or excavation of mucosal wall of the esophagus,
stomach, pylorus, duodenum
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(most common). “Autodigestion”
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Requires acid environment to develop
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Mucosal defenses impaired; cannot protect from effects of
acid/pepsin
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Result from infection with H. pylori or Zollinger-Ellison
syndrome
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Risk factors:
 Alcohol, smoking, and stress, medications
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Three types of peptic ulcer
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Gastric
Duodenal
Stress
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Gastric ulcer
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Most common in the lesser curvature of stomach near
the pylorus
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Mucus and bicarb. generally protect mucosal barrier
from acid
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H. pylori plays a role
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Break in gastric mucosal barrier allows HCl to damage
epithelium via “back diffusion”
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Bile reflux from duodenum may break integrity
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Decreased blood flow
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Duodenal ulcer
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Results from excessive acid
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Associated with protein-rich meals, Ca++, and vagal
stimulation)
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Rapid emptying of food from stomach large acid
load in duodenum
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H. pylori infection plays key role in development
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produces substances that damage the mucosa, and
contributes to higher acid concentrations
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Stress ulcer
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Occurs after acute medical crisis, surgery, or trauma
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Proximal portion of stomach and duodenum are most
common sites
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Ischemia and elevated HCl contribute to evolution of
erosions  ulcerations
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May progress to hemorrhage
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Duodenal versus Gastric ulcers
Gastric
Normal/hypo-secretion of
gastric acid
Pain 1-2 hrs pc meals
Food aggravates pain
Vomiting common
More likely to hemorrhage –
manifests as hematemesis
Duodenal
Hyper-secretion
Pain 2-4 hrs pc meals
Food may relieve pain
Vomiting not common
Less likely to hemorrhage, but if
occurs, likely to manifest as
melena
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Diagnostic tests
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Esphagogastroduodenoscopy
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Fiberoptic endoscope allows
direct visualization of
esophagus, stomach and
duodenum
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Diagnostic tests: Upper GI series
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Patients ingests barium, a thick,
white, milkshake-like liquid, then
multiple X-rays. Can detect structural
disorders
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After the exam, provide plenty of
liquids for 24 to 48 hours.
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The barium may make the stool white
for several days.
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If constipation occurs, the doctor
may recommend a mild laxative.
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Complications of ulcers:
Hemorrhage
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Manifested by:
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Orthostatic hypotension,  BP, HR, cool, clammy skin
overt bleeding
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Hematemesis (bloody vomit) – bright red or coffee
ground (more likely with gastric ulcer)
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Melena (bloody or tarry [black] stool) – more likely with
duodenal ulcer
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 Hgb,  Hct
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Remember: Management during
Haemorrhage includes
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Monitor S/S
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Determine rate amount of blood loss (Hct/hct),
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NGT
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Replace blood, fluid and electrolyte loss
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saline lavage via NGT
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NGT to low intermittent suction
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Prevents distension
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Assess amount/rate of bleeding,
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Medications, oxygen, possible surgery
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Complications: Perforation
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GI contents empty into peritoneal cavity
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Manifested by:
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Sudden, sharp mid-epigastric pain which can shortly spread
to all abdomen
Rigid, tender, board-like abdomen
Patient assumes the fetal position to reduce tension on
muscles
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Can lead to shock
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It is a surgical emergency
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Remember: Management during perforation
includes
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NGT to prevent additional spillage of GI contents in
peritoneum
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Replace blood, fluid, electrolytes
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Antibiotics
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I & O, NPO
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SURGERY: Urgent
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Complications: Pyloric obstruction
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Caused by inflammation or edema of the
pylorus
Stomach cannot empty  abdominal bloating,
N&V
Persistent vomiting  Hypokalemia and
metabolic alkalosis
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Medical Management of ulcers
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Conservative therapy:
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Rest: Both physical and
emotional
Dietary modifications
Elimination of smoking
Long term follow up
care
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Pharmaceutical:
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Antibiotics
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Antiacids
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Initial drugs of choice
Histmaine H2 receptor antagonists
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To eradicate H. Pylori infections
Recurrence of ulcer is 75-90% as high
with infection
Histamine is the final intracellular
activator of HCL secretion
Anticholinergic:
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Stop the cholinergic stimulation of HCl
secretion and slow gastric motility
Not commonly used, if used need to be
used with caution in pts with Glaucoma
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Surgical Management of ulcerations
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Gastroduodenostomy
(Billroth I)
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Removal of the lower
portion of stomach and
small portion of
duodenum and connects
remaining of stomach to
duodenum
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Surgical Management of ulcerations
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Gastojejunostomy
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Removes lower stomach and
small portion of duodenum.
Reconnects stomach to jejunum.
Subtotal gastrectomy
- removal distal third of
stomach, reconnecting to
duodenum or jejunum
Total gastrectomy
removal of stomach; connects
esophagus to jejunum
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Dumping syndrome
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A complication of gastric surgery
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S&S
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occurs after eating
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vertigo, sweating, palpitations, syncope, pallor, tachycardia
D/t rapid emptying of hypertonic stomach contents into small intestine
 fluid shifts into gut abd. distention and cramps and S/S of  plasma
volume.
Later get rapid elevation of blood glucose followed by insulin secretion
and hypoglycemia
Management
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Small frequent meals
 fat,  protein,  CHO meals
liquid between (not with) meals
Lie down after meals
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Nursing diagnoses
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Pain r/t mucosal injury
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Anxiety
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Knowledge deficit
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Risk for fluid volum deficit r/t hemorrhage or
vomiting
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Intervention: Pain
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Medications
 Give antacids after meals and at bedtime to decrease
gastric acidity; buffers the acid.
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Give H2 receptor antagonists as prescribed to decrease acid
secretion
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Diet therapy
 Effectiveness controversial
 Avoid caffeinated beverages
 Exclude foods that cause discomfort
 Provide frequent, small, bland meals
 Avoid smoking, alcohol
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Intervention: Anxiety & Knowledge
deficit
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Anxiety
Provide emotional support
 Teach and provide relaxation techniques
 Identify and manage sources of stress
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Knowledge deficit
Teach re diet, medications,
 Teach the risks associated with continued smoking
 Teach S/S of complications
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