Ulcerative Colitis

Introduction:

An inflammatory disease of the large intestine that affects the mucosal layer begin-
ning in the rectum and colon and spreading into the adjacent tissue. There are ulcer-
ations in the mucosal layer of the intestinal wall, and inflammation and abscess
formation occur. Bloody diarrhea with mucous is the primary symptom. There are
periods of exacerbations and remissions. Symptom severity may vary from mild to
severe. The exact cause is unknown, but there is increased incidence in people with
northern European, North American, or Ashkenazi Jewish origins. The peak inci-
dences are from mid-teen to mid-twenties and again from mid-fifties to mid-sixties.

PROGNOSIS

Patients with ulcerative colitis may have an increase in symptoms with each flare-
up of the disease. Malabsorption of nutrients can cause weight loss and health
problems. Some patients will need surgery to resect the affected area of the large
intestine, resulting in a colostomy, ileal reservoir, ileoanal anastomosis, or ileoanal
reservoir. There is an increased risk of colon cancer in patients with ulcerative coli-
tis. The patient is also at risk for developing toxic megacolon or perforating the
area of ulceration.

SIGNS AND SYMPTOMS
• Weight loss
• Abdominal pain
• Chronic bloody diarrhea with pus due to ulceration
• Electrolyte imbalance due to diarrhea
• Tenesmus—spasms involving the anal sphincter; persistent desire to empty
bowel

TREATMENT
• Keep stool diary to identify irritating foods.
• Low-fiber, high-protein, high-calorie diet.
• Administer antidiarrheal medications:
• loperamide
• diphenoxylate hydrochloride and atropine
• Administer salicylate medications to reduce inflammation within the intes-
tinal mucosa:
• sulfasalazine
• mesalamine
• olsalazine
• balsalazide
• Administer corticosteroids during exacerbations to reduce inflammation:
• prednisone
• hydrocortisone
• NPO for bowel rest during exacerbations.
• Administer anticholinergics to reduce abdominal cramping and discomfort:
• dicyclomine
• Surgical resection of affected area of large intestine.

NURSING DIAGNOSES

• Acute pain
• Diarrhea
• Impaired skin integrity

NURSING INTERVENTION

• Monitor intake and output.
• Monitor stool output, frequency.
• Weigh patient regularly.
• Sitz bath.
• Vitamin A & D ointment or barrier cream applied to skin.
• Witch hazel to soothe sensitive skin.
• Monitor for toxic megacolon (distended and tender abdomen, fever, elevated
WBC, elevated pulse, distended colon).
• Teach home care for new ostomy patients or refer to enterostomal therapist
for education:
• Teach proper skin care of perianal area to avoid skin breakdown.
• Avoid fragranced products which can be irritating.
• Teach dietary modification, and which foods to avoid.
• Teach medication use, schedule, and side effects.
• Teach importance of follow-up care.
• Teach wound care for postoperative patients.
• Disturbed body image

Peptic Ulcer Disease (PUD)

Introduction:

An ulcer develops when there is erosion of a portion of the mucosal layer of either
the stomach or duodenum. The ulcer may occur within the stomach (gastric
ulcer), or the duodenum (duodenal ulcer). A break in the protective mucosal lin-
ing allows the acid within the stomach to make contact with the epithelial tissues.
Gastric ulcers favor the lesser curvature of the stomach. Duodenal ulcers tend to
be deeper, penetrating through the mucosa to the muscular layer. Helicobacter
pylori infection has been associated with duodenal ulcers. Stress ulcers are asso-
ciated with another acute medical condition or traumatic injury. As the body
attempts to heal from the other physical condition (for example, major surgery),
small areas of ischemia develop within the stomach or duodenum. The ischemic
areas then ulcerate.

PROGNOSIS

The ulcerated areas may develop bleeding or may perforate. Depending on the
location of the ulceration, a vessel may become exposed to the effects of the stom-
ach acids. Damage to these vessels may result in significant bleeding. Perforation
of the ulcer can occur as the ulcer continues to erode more deeply into the tissue.
Perforation permits the contents of the stomach or duodenum to enter the peri-
toneum, leading to peritonitis, paralytic ileus, septicemia, and shock. This patient
will need emergency surgery due to a life-threatening condition.


SIGNS AND SYMPTOMS

• Sudden, sharp pain
• Tender, rigid, board-like abdomen
• Knee-chest position reduces pain
• Hypovolemic shock
• Weight changes
• Loss with gastric ulcer
• Gain with duodenal ulcer

TREATMENT
• Administer antacids
• Administer histamine-2 blockers:
• famotidine, ranitidine, nizatidine
• Administer proton pump inhibitors:
• omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole
• Administer mucosal barrier fortifiers:
• sucralfate
• Administer prostaglandin analogue:
• misoprostol
• Adjust diet.
• Treat H. pylori infection if present with combination therapy:
• Proton pump inhibitor plus clarithromycin plus amoxicillin or
• Proton pump inhibitor plus metronidazole plus clarithromycin or
• Bismuth subsalicylate plus metronidazole plus tetracycline.

NURSING DIAGNOSES

• Acute pain
• Risk for imbalanced nutrition: less than what body requires
• Risk for imbalanced nutrition: more than what body requires

NURSING INTERVENTION

• Monitor vital signs.
• Monitor intake and output.
• Assess abdomen for bowel sounds, tenderness, rigidity, rebound pain, guarding.
• Monitor stool for change in color, consistency, blood.
• Teach patient about home care:
• Diet modification to avoid acidic foods, caffeine, peppermint, alcohol.
• Eat more frequent, small meals.
• Avoid nonsteroidal anti-inflammatory medication.
• Stop smoking.

Peritonitis

Introduction:

Peritonitis is an acute inflammation of the peritoneum, which is the lining of the
abdominal cavity. Peritonitis may be primary or secondary to another disease
process. It typically occurs due to bacterial presence within the peritoneal space.
The bacteria may have passed from the gastrointestinal tract or the rupture of an
organ within the abdomen or pelvis. After the introduction of the bacteria into the
abdominal area, an inflammatory reaction occurs.

PROGNOSIS

It is a life-threatening disease process. Patients may develop septicemia from the
bacteria within the abdomen that enter the bloodstream.

SIGNS AND SYMPTOMS

• Fever
• Tachycardia
• Abdominal distention
• Abdominal pain—may be localized or generalized
• Rebound pain (pain when quickly removing pressure during palpation of
abdomen)
• Rigid abdomen
• Nausea, vomiting, loss of appetite
• Decreased bowel sounds
• Decreased urine output

TREATMENT
• Intravenous fluids.
• Administer broad-spectrum antibiotics.
• Surgical intervention may be necessary to correct cause of peritonitis.
• Pain management postoperatively.

NURSING DIAGNOSES

• Acute pain
• Impaired tissue integrity
• Impaired skin integrity

NURSING INTERVENTION
• Weigh daily.
• Monitor vital signs.
• Monitor intake and output.
• NPO to avoid irritation of intestinal tract, further stress on abdominal organs
• Position for comfort, head of bed elevated.
• Assess for return of bowel sounds postoperatively.
• Teach patient about home care:
• Pain management.
• Wound care, drains, etc.
• Monitor for signs of infection.

Pancreatitis

Introduction:

Pancreatitis is an inflammation of the pancreas which causes destructive cellular
changes. It may be an acute or a chronic process. Acute pancreatitis involves auto-
digestion of the pancreas by pancreatic enzymes and development of fibrosis. Blood
glucose control may be affected by the changes to the pancreas. Chronic pancreatitis
results from recurrent episodes of exacerbation, leading to fibrosis and a decrease in
pancreatic function. Presence of gallstones blocking a pancreatic duct, chronic use
of alcohol, post-abdominal trauma or surgery, or elevated cholesterol are associated
with an increased risk of pancreatitis.

PROGNOSIS

Acute pancreatitis may be life-threatening. Pleural effusion may develop as a com-
plication of acute pancreatitis; older patients have a greater risk of also developing
pneumonia. Disseminated intravascular coagulation is another complication that
may occur, affecting the body’s ability to clot due to depleted clotting factors in
the development of small thrombi.

SIGNS AND SYMPTOMS

• Epigastric pain due to inflammation and stretching of pancreatic duct
• Boring abdominal pain may radiate to back or left shoulder in acute pan-
creatitis
• Gnawing continuous abdominal pain with acute exacerbations in chronic
pancreatitis
• Patient in knee-chest position for comfort—reduces tension on abdomen
• Nausea and vomiting
• Bluish-gray discoloration of periumbilical area and abdomen (Cullen’s sign)
• Bluish-gray discoloration of flank areas (Turner’s sign)
• Ascites
• Weight loss
• Blood glucose elevation
• Fatigue

TREATMENT

• NPO during acute stage to reduce release of pancreatic enzymes.
• Intravenous fluids for hydration.
• Total parenteral nutrition.
• Administer vitamin supplementation.
• Pain management with narcotics during acute stage.
• Avoid morphine that may increase pain due to spasm of the sphincter of Oddi
at the opening to the small intestine from the common bile duct.
• Intravenous, patient-controlled analgesia or transdermal delivery preferable
to intramuscular.
• Acute:
• NG tube connected to suction if vomiting.
• Surgical intervention for abscess or pseudocyst.
• Chronic:
• Blood glucose control with insulin.
• Administer pancreatic enzymes with meals.
• Surgical intervention for pain control, abscess.

NURSING DIAGNOSES

• Acute pain
• Imbalanced nutrition: less than what body requires

NURSING INTERVENTION

• Assess vital signs for elevated temperature, elevated pulse, and changes in
blood pressure.
• Assess pain level.
• Monitor intake and output.
• Assess abdomen for bowel sounds, tenderness, masses, ascites.
• Monitor fingerstick blood glucose.
• Assess lung sounds for bilateral equality.
• Frequent oral care for NPO patients.
• Teach patient about home care:
• Avoid alcohol and caffeine.
• Bland, low-fat, high-protein, high-calorie, small, frequent meals.
• Use of blood glucose meter.
• Medication management, schedule, side effects.
• Plan rest periods until strength returns.

Hiatal Hernia

Introduction:

This is also known as a diaphragmatic hernia. A part of the stomach protrudes up
through the diaphragm near the esophagus into the chest. Patients may be asymp-
tomatic or have daily symptoms of gastroesophageal reflux disease (GERD). The
hernia may be a sliding hiatal hernia which allows movement of the upper portion
of the stomach including the lower esophageal sphincter up and down through
the diaphragm. These patients typically have symptoms of GERD. Another type
of hiatal hernia is a rolling hernia in which a portion of the stomach protrudes up
through the diaphragm, but the lower esophageal sphincter area remains below the
level of the diaphragm. These patients do not generally suffer from reflux.

PROGNOSIS

Lifestyle modifications may help control the symptoms of hiatal hernia. Some
patients who do not get adequate control of symptoms or are refractory to treat-
ment may need surgery to correct the movement through the diaphragm.

SIGNS AND SYMPTOMS

• Sliding hernia:
• Heartburn
• Difficulty swallowing (dysphagia)
• Burping (eructation)
• Chest pain
• Rolling hernia:
• Chest pain
• Shortness of breath after eating
• Feeling of fullness after eating

TREATMENT

• Administer antacids for patients with reflux symptoms:
• Maalox, Mylanta, Tums, Gaviscon
• Administer histamine type 2 (H2) blockers to reduce stomach acid:
• ranitidine, nizatidine, famotidine, cimetidine
• Administer proton pump inhibitors to reduce the production of acid:
• omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole
• Avoid lying down after eating.
• Modify eating schedule; small, frequent meals.
• Elevate head of bed.

NURSING DIAGNOSES

• Acute pain
• Chronic pain

NURSING INTERVENTION

• Monitor vital signs.
• Assess abdomen for distention, bowel sounds.
• Teach patient about lifestyle modifications:
• Medication management.
• Avoid clothing that is tight around the waist.
• Not to lie down after eating.
• Elevate head of bed.
• Avoid wearing clothing that is tight at waist.
• Avoid acidic foods (citrus, vinegar, tomato), peppermint, caffeine, alcohol.
• Stop smoking.
• Lose weight if overweight.

Hepatitis

Introduction:

Hepatitis is an inflammation of the liver cells. This is most commonly due to a
viral cause which may be either an acute illness or become chronic. The disease
may also be due to exposure to drugs or toxins.
Hepatitis A is transmitted via an oral route, often due to contaminated water or
poor sanitation when traveling; it is also transmitted in daycare settings and resi-
dential institutions. It can be prevented by vaccine.
Hepatitis B is transmitted via a percutaneous route, often due to sexual contact,
IV drug use, mother-to-neonate transmission or possibly blood transfusion. It can
be prevented by vaccine.
Hepatitis C is transmitted via a percutaneous route, often due to IV drug use or,
less commonly, sexual contact. There is currently no vaccine available.
Hepatitis D is transmitted via a percutaneous route and needs hepatitis B to
spread cell to cell. There is no vaccine available for hepatitis D.
Hepatitis E is transmitted via an oral route and is associated with water con-
tamination. There is no known chronic state of hepatitis E and no current vaccine
available.
Hepatitis G is transmitted via a percutaneous route and is associated with chronic
infection but not significant liver disease.
Exposure to medications (even at therapeutic doses), drugs, or chemicals can
also cause hepatitis. Onset is usually within the first couple of days of use, and may
be within the first couple of doses. Hepatotoxic substances include acetamino-
phen, carbon tetrachloride, benzenes, and valproic acid.


PROGNOSIS

Hepatitis may occur as an acute infection (viral type A, E) or become a chronic
state. The patient with chronic disease may be unaware of the illness until testing
of liver function shows abnormalities and further testing reveals presence of hep-
atitis. The chronic (viral type B, C) disease state creates the potential development
of progressive liver disease. Some patients with chronic disease will need liver
transplant. Recurrence rate post-transplant is high. Liver cancer may develop in
those with chronic disease states.

SIGNS AND SYMPTOMS

• Acute hepatitis:
• Malaise
• Nausea and vomiting
• Diarrhea or constipation
• Low-grade fever
• Dark urine due to change in liver function
• Jaundice due to liver compromise
• Tenderness in right upper quadrant of abdomen
• Hepatomegaly
• Arthritis, glomerulonephritis, polyarteritis nodosa in hepatitis B
• Chronic hepatitis:
• Asymptomatic with elevated liver enzymes
• Symptoms as acute hepatitis
• Cirrhosis due to altered liver function
• Ascites due to decrease in liver function, increased portal hypertension
• Bleeding from esophageal varices
• Encephalopathy due to diminished liver function
• Bleeding due to clotting disorders
• Enlargement of spleen


TREATMENT
• Avoid medications metabolized in the liver.
• Avoid alcohol.
• Remove or discontinue causative agent if drug-induced or toxic hepatitis.
• Intravenous hydration if vomiting during acute hepatitis.
• Activity as tolerated.
• High-calorie diet; breakfast is usually the best tolerated meal.
• Administer interferon or lamivudine for chronic hepatitis B.
• Administer interferon and ribavirin for hepatitis C.
• Administer prednisone in autoimmune hepatitis.
• Liver transplantation.

NURSING DIAGNOSES

• Fatigue
• Risk for injury
• Impaired tissue integrity

NURSING INTERVENTION

• Monitor vital signs.
• Assess abdomen for bowel sounds, tenderness, ascites.
• Plan appropriate rest for patient in acute phase.
• Monitor intake and output.
• Assess mental status for changes due to encephalopathy.
• Assist patient to:
• Plan palatable meals; remember that breakfast is generally the best toler-
ated meal.
• Avoid smoking areas—intolerance to smoking.

Gastritis

Introduction:

Gastritis is an inflammation of the stomach lining due to either erosion or atrophy.
Erosive causes include stresses such as physical illness or medications such as
nonsteroidal anti-inflammatory drugs (NSAIDs). Atrophic causes include a his-
tory of prior surgery (such as gastrectomy), pernicious anemia, alcohol use, or
Helicobacter pylori infection.

PROGNOSIS
Gastritis may cause changes within the cells of the stomach lining leading to mal-
nutrition, lymphoma, or gastric cancer. Hospitalized patients, especially in criti-
cal care settings, should have preventive medications to avoid the development
of gastritis.

SIGNS AND SYMPTOMS

• Nausea and vomiting
• Anorexia
• Epigastric area discomfort
• Epigastric tenderness on palpation due to gastric irritation
• Bleeding from irritation of the gastric mucosa
• Hematemesis—possible coffee ground emesis due to partial digestion of blood
• Melena—black, tarry stool

TREATMENT

• Administer antacids:
• Maalox, Mylanta, Tums, Gaviscon
• Administer sucralfate to protect gastric lining.
• Administer histamine 2 blockers:
• ranitidine, famotidine, nizatidine, cimetidine
• Administer proton pump inhibitors:
• omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole
• Eradicate Helicobacter pylori infection if present.
• Diet modification.
• Monitor hemoglobin and hematocrit.

NURSING DIAGNOSES

• Risk for imbalanced nutrition: less than what body requires
• Risk for imbalanced fluid volume

NURSING INTERVENTION

• Monitor vital signs.
• Monitor intake and output.
• Monitor stool for occult blood.
• Assess abdomen for bowel sounds, tenderness.
• Teach patient about:
• Diet restrictions: avoid alcohol, caffeine, acidic foods.
• Medications.
• The need to avoid smoking.
• The need to avoid NSAIDs.
• Nausea

Gastrointestinal Bleed

Introduction:

Bleeding from the gastrointestinal tract may cause significant blood loss. The bleed-
ing may be from either the upper or lower gastrointestinal tract. Upper gastrointesti-
nal bleeds are commonly from ulcers, esophageal varices, neoplasms, arteriovenous
malformations, Mallory-Weiss tears secondary to vomiting, or anticoagulant use.
Lower gastrointestinal bleeds are commonly due to fissure formation, rectal trauma,
colitis, polyps, colon cancer, diverticulitis, vasculitis, or ulcerations.

PROGNOSIS

The amount and speed of blood loss coupled with the patient’s age and co-
morbidities account for the prognosis. The greater the loss of blood, the harder it
is for the system to overcome the stress. Multiple transfusions to replace the lost
blood increase the patient’s risk for a reaction. Patients with blood-clotting disor-
ders have a greater risk of a significant bleed. Patients may go into shock if the
amount of blood loss is great, as they become hemodynamically unstable.

SIGNS AND SYMPTOMS

• Hematemesis—vomiting of blood (red, maroon, coffee ground)
• Melena—black, tarry stool
• Hematochezia—red or maroon blood rectally
• Orthostatic changes—drop in BP of at least 10 mmHg with position changes
• Tachycardia as body attempts to circulate lesser blood volume
• Pallor due to decrease in circulating blood volume
• Lightheadedness

TREATMENT
• Maintain IV access.
• Administer isotonic fluids like normal saline.
• Monitor serial hemoglobin and hematocrit levels.
• Type and cross match for 3 to 6 units depending on amount of blood loss.
• Transfuse packed RBCs, type-specific when possible (type O negative when
type-specific unavailable—no time to get results back from lab yet).
• May need to administer albumin or fresh frozen plasma, depending on amount
of units transfused and comorbidities such as cirrhosis or clotting disorders.
• Endoscopic procedures to treat ulcer topically, with injectable or laser treatment.
• Esophageal varices may be treated by tamponade with Blakemore-Sengstaken
tube.
• Surgery indicated when bleeding uncontrolled.

NURSING DIAGNOSES

• Deficient fluid volume
• Decreased cardiac output

NURSING INTERVENTION

• Monitor vital signs for changes—drop in BP, increase in pulse or respiration.
• Monitor intake and output.
• Replace volume lost.
• Monitor abdomen for bowel sounds, tenderness, distention.
• Maintain large bore IV (14- to 18-gauge) access.
• Assess IV site for signs of redness or swelling.
• Monitor lab results—drop in lab values may lag behind blood loss.
• Monitor during blood transfusion as per institution protocol for checking
blood unit, patient identity, frequency of vital signs, and documentation
• Anxiety

Gastroesophageal Reflux Disease (GERD)

Introduction:

The reflux of stomach acid and contents into the esophagus. This typically causes
symptoms because the lining of the esophagus is not protected against the acid that
is normally found only in the stomach. The pain that is produced is often referred to
as heartburn, or may be mistaken for cardiac pain. The pain may also be referred
to the back. The pain occurs more frequently in men, people who are obese, smok-
ers, and those who use alcohol or medications that lower the muscle tone of the
lower esophageal sphincter. The pain due to acid refluxing into the esophagus is
worse after eating or when lying down. Patients with a hiatal hernia may also
experience reflux due to the increased pressure that exists from a portion of the
stomach protruding upward through the diaphragm.

PROGNOSIS
Control of symptoms is possible through lifestyle modification and use of med-
ications to reduce acid production within the stomach. There has been no correla-
tion shown between the severity of patient symptoms and the degree of damage
being done to the tissue of the esophagus. Patients with ongoing symptoms should
have an upper endoscopy to allow for visualization and biopsy of the area to mon-
itor for the possibility of cancer of the esophagus developing due to long-term
reflux. Barrett’s esophagus is a premalignant condition of the esophagus that
occurs due to reflux, where cellular changes have occurred and the patient needs
to be monitored for progression to a malignant cell type. Some patients may
develop trouble with swallowing due to the development of scarring from long-
term exposure to acid. These patients may develop strictures over time. Procedures
can be performed to help stretch the lumen of the esophagus to aid in swallowing.

SIGNS AND SYMPTOMS
• Epigastric burning, worse after eating
• Heartburn
• Burping (eructation) or flatulence
• Sour taste in mouth, often worse in the morning
• Nausea
• Bloating
• Cough due to reflux high in the esophagus
• Hoarseness or change in voice

TREATMENT
• Administer antacids to neutralize acid; these medications act quickly:
• Maalox, Mylanta, Tums, Gaviscon
• Administer H2 (histamine type 2) blockers to decrease the production of acid:
• ranitidine, famotidine, nizatidine, cimetidine
• Administer proton pump inhibitors to reduce the production of acid:
• omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole
• Have patient eat six small meals rather than three large ones to reduce intra-
abdominal pressure.
• Surgery or endoscopic procedures may be performed to prevent the reflux
from occurring.

NURSING DIAGNOSES

• Risk for imbalanced nutrition: less than what body requires
• Risk for imbalanced nutrition: more than what body requires
• Acute pain
• Chronic pain

NURSING INTERVENTION

• Monitor vital signs.
• Assess abdomen for distention, bowel sounds.
• Teach about medication management.
• Teach patient about lifestyle modifications:
• Not to lie down after eating.
• Elevate head of bed.
• Avoid wearing clothing that is tight at waist.
• Avoid acidic foods (citrus, vinegar, tomato), peppermint, caffeine, alcohol.
• Stop smoking.
• Lose weight if overweight

Gastroenteritis

Introduction:

An acute inflammation of the gastric and intestinal mucosa which is most com-
monly due to bacterial, viral, protozoal, or parasitic infection. It may also be caused
by irritation due to chemical or toxin exposure or allergic response. Viral exposure
is more likely in winter; bacterial exposure is more common in summer when
food-borne illness exposure is likely.

PROGNOSIS

Symptoms may be self-limiting or may need prescription medication to resolve the
illness. Older or debilitated patients may have more severe symptoms or require
hospitalization due to dehydration.

SIGNS AND SYMPTOMS

• Nausea and vomiting due to gastric irritation
• Diarrhea—watery, soft, may be mixed with mucous or blood
• Abdominal pain due to intestinal irritation
• Abdominal distention
• Fever due to infection
• Anorexia due to gastric irritation
• Malaise due to infection
• Headache due to viral illness
• Signs of dehydration—dry, flushed skin and mucous membranes, decreased
urine output, tachycardia, poor skin turgor, orthostatic blood pressure changes

TREATMENT

• Monitor intake and output.
• Replace fluids lost.
• Administer antiemetic medication for symptom relief:
• prochlorperazine
• trimethobenzamide
• Administer antidiarrheal medications for symptom relief:
• loperamide
• diphenoxylate
• kaolin-pectin
• bismuth subsalicylate
• Need to allow organism one way out of gastrointestinal system (either anti-
emetic or antidiarrheal, not both).
• ciprofloxacin
• metronidazole
• Intravenous fluids to correct dehydration.
emetic or antidiarrheal, not both).

NURSING DIAGNOSES

• Risk for imbalanced nutrition: less than what body requires
• Deficient fluid volume
• Altered bowel elimination
• Diarrhea
• Fatigue

NURSING INTERVENTION

• Monitor vital signs for changes.
• Monitor intake and output.
• Replace fluids lost.
• Assess skin and mucous membranes for signs of dehydration.
• Assess abdomen for bowel sounds, tenderness

Diverticulitis Disease

Introduction:

Small out-pouchings called diverticula develop along the intestinal tract. Diverti-
culosis is the condition of having these diverticula. Any part of the large or small
intestine may be involved. The area of the intestinal tract that most commonly
develops diverticula is the lower portion of the large intestine. Certain types of
undigested foods can become trapped in the pouches of the intestine. Bacteria mul-
tiply in the area, causing further inflammation. Diverticulitis is an inflammation of
at least one of the diverticula. Diets that have a low fiber content, seeds, or nuts
have been implicated in the development of diverticulitis. Perforation of the diver-
ticula is possible when they are inflamed.

PROGNOSIS

Inflammation in diverticulitis increases the risk of perforation of the intestine.
Peritonitis will develop from bacterial contamination after perforation of a diver-
ticula. Bleeding from the intestinal mucosa in the area of inflammation can also
occur. The presence of diverticula and repeated periods of inflammation may allow
development of fistula formation from the diverticula to other areas within the
abdomen, such as the intestine or bladder. Patients needing surgery may have a
colostomy postoperatively. Depending on the location of the diverticulitis and the
reason for the surgery, the colostomy may be reversible after healing has occurred.


SIGNS AND SYMPTOMS

• Asymptomatic in diverticulosis
• Change in bowel habits
• Bloating, increased gas
• Abdominal pain most often in the left lower quadrant with diverticulitis
• Rectal bleeding due to inflammation with diverticulitis
• Fever with diverticulitis
• Nausea, vomiting
• Tachycardia due to fever
• Peritonitis if diverticula ruptures

TREATMENT

• Administer antibiotics:
• ciprofloxacin
• metronidazole
• trimethoprim-sulfamethoxazole
• Administer adequate intravenous hydration.
• Manage pain as needed.
• NPO or clear liquids (depending on order) during acute inflammation to rest
intestinal tract.
• Surgical intervention to correct perforation of diverticula, abscess formal-
tion, bowel obstruction, fistula formation.
• NG tube postoperatively.

NURSING DIAGNOSES

• Acute pain
• Altered bowel elimination
• Disturbed body image

NURSING INTERVENTION

• Monitor vital signs for fever, increased heart rate, and decreased blood pressure.
• Assess abdomen for distention, presence of bowel sounds.
• Monitor intake and output.
• Postoperatively check:
• Stoma at colostomy site
• Wound site for drainage or signs of infection
• Peripheral circulation, swelling due to increased risk of clot formation
• Teach patients:
• Eat low-residue foods during flare-ups.
• Eat high-fiber diet when asymptomatic, fresh fruits and vegetables, whole
wheat breads, bran cereals.
• Avoid laxatives and enemas due to increased irritation and intra-abdominal
pressure.
• Avoid lifting during exacerbation.
• Avoid eating nuts and seeds.

Cirrhosis Prognosis Sign and Symptoms

Introduction

Injury to the cellular structure of the liver causes fibrosis due to chronic inflamma-
tion and necrotic changes, resulting in cirrhosis. There are nodular changes to the
liver. The bile ducts and blood vessels through the liver may become blocked due
to both the nodular changes and fibrosis. These changes to the liver cause enlarge-
ment of the organ and change in texture. There is increased pressure within the
portal vein. This causes resistance to blood flow throughout the venous system in
the liver and also backs up venous blood to the spleen, causing enlargement of this
organ also. Damage to the liver may be reversible if the cause if identified early and
removed. The most common causes of cirrhosis include chronic alcohol use, liver
damage secondary to exposure to drugs or toxins, viral hepatitis (especially hepati-
tis B, hepatitis C, and hepatitis D in those already infected with hepatitis B), fatty
liver (steatohepatitis), autoimmune hepatitis, cystic fibrosis, metabolic disorders
(excess iron storage—hemachromatosis), or genetic causes.

PROGNOSIS

As cirrhosis progresses, the patient may develop encephalopathy and coma. Early
signs and symptoms of encephalopathy include altered level of consciousness,
neuromuscular changes, and elevated serum ammonia levels.

SIGNS AND SYMPTOMS
• Initially asymptomatic
• Weakness, fatigue due to chronic disease
• Muscle cramps
• Weight loss
• Anorexia
• Nausea with possible vomiting
• Ascites—the accumulation of fluid within the abdominal cavity due to por-
tal hypertension
• Abdominal pain
• Portal hypertension
• Pruritus (itching)
• Ecchymosis (bruises) or petechiae (small, pinpoint, round, reddish purple
marks)
• Coagulation defects due to problems with vitamin K absorption, causing
problems with production of clotting factors
• Amenorrhea
• Impotence due to inactivity of hormones
• Gynecomastia
• Jaundice due to problems with excretion of bilirubin
• Hepatomegaly (enlarged liver) in over one-half of the patients

TREATMENT

• Low-sodium diet; adequate calorie intake.
• Restrict fluid intake if hyponatremic (low serum sodium) or fluid overloaded.
• Restrict alcohol intake to prevent further damage.
• Administer vitamin supplements—folate, thiamine, multivitamin.
• Administer diuretics to reduce excess fluids:
• furosemide
• spironolactone
• Paracentesis to remove ascitic fluid.
• Monitor electrolytes for imbalance.
• Monitor coagulation profile (PT, PTT, INR).
• Administer lactulose to promote removal of ammonia in the gut.
• Administer antibiotics to destroy the normal GI flora which decreases pro-
tein breakdown and the rate of ammonia production:
• neomycin sulfate
• metronidazole
• Shunt placement:
• Peritoneovenous—moves ascitic fluid from abdomen to superior vena
cava.
• Portocaval—diverts venous blood flow from liver to decrease portal and
esophageal pressures.
• Transjugular intrahepatic portal systemic—nonsurgical procedure per-
formed in interventional radiology—sheath placed into jugular and hepatic
vein; needle threaded through sheath and pushed into portal vein through
the liver; balloon enlarges the tract and stent maintains.
• Gastric lavage.
• Esophagogastgric balloon tamponade for control of bleeding from esophageal
varices.
• Administer blood products as needed for patients with bleeding esophageal
varices.
• Sclerotherapy for esophageal variceal bleeding.

NURSING DIAGNOSES

• Ineffective breathing pattern
• Excess fluid volume
• Risk for infection

NURSING INTERVENTION

• Monitor intake and output.
• Monitor vital signs.
• Weigh patient daily.
• Measure abdominal girth—making sure to measure at level of umbilicus for
consistency; marks are typically made at sides of abdomen to align tape meas-
ure on subsequent days.
• Assess peripheral edema.
• Assess heart and lung sounds for excess fluid.
• Elevate head of bed 30 degrees or greater to ease breathing.
• Elevate feet to decrease peripheral edema.
• Monitor for signs of bleeding or bruising.
• Monitor level of consciousness, orientation, recent and remote memory, be-
havior, mood, and affect.

Cholecystitis

Introduction:

An inflammation of the gallbladder, often accompanied by the formation of gall-
stones (cholelithiasis), is cholecystitis. The inflammation may be either acute or
chronic in nature. In an acute cholecystitis, the blood flow to the gallbladder may
become compromised which in turn will cause problems with the normal filling and
emptying of the gallbladder. A stone may block the cystic duct which will result in
bile becoming trapped within the gallbladder due to inflammation around the stone
within the duct. Blood flow to the inflamed area will be minimized, localized
edema develops, the gallbladder distends due to retained bile, and ischemic changes
will occur within the wall of the gallbladder. Chronic cholecystitis occurs when
there have been recurrent episodes of blockage of the cystic duct, usually due to
stones. There is chronic inflammation. The gallbladder is often contracted, which
leads to problems with storing and moving the bile. Patients may develop jaundice
due to back-up of bile or obstructive jaundice. They will exhibit a yellowish tone to
skin and mucous membranes. If patients have a naturally dark pigmentation to their
skin, check palms and soles. Icterus is the yellow color change seen in the sclera
(white) of the eye.
There is increased risk for gallbladder inflammation and development of gall-
stones with increasing age, being female or overweight, having a family history of
gallbladder disease, people on rapid weight loss diets, and during pregnancy.

PROGNOSIS

The ischemic changes of the gallbladder wall increase the risk of perforation of the
organ or development of gangrene. Peritonitis is a potential risk in patients if a sig-
nificant area of gallbladder perforates or there is associated infection or abscess
that spreads. A small percentage of patients will develop cancer of the gallbladder.
There is increased surgical risk for older patients or patients with comorbidities.

SIGNS AND SYMPTOMS

• Upper abdominal, epigastric, or right upper quadrant abdominal pain which
may radiate to right shoulder
• Right upper quadrant (RUQ) pain increases with palpation of right upper
abdomen during inspiration (Murphy’s sign) causing the patient to stop tak-
ing deep breaths
• Nausea and vomiting, especially following fatty foods
• Loss of appetite
• Fever
• Increased air in intestinal tract (eructation, flatulence)
• Pruritis (itching) of skin due to build-up of bile salts
• Clay-colored stools due to lack of urobilinogen in gut (normally converted
from bilirubin which was blocked with bile flow)
• Jaundice—yellowish skin and mucous membrane discoloration
• Icterus—yellowish discoloration of sclera (white of eye)
• Dark, foamy urine as kidneys attempt to clear out bilirubin

TREATMENT

• Low-fat diet.
• Intravenous fluid replacement for vomiting.
• Administer antiemetics for control of nausea and vomiting:
• prochlorperazine
• trimethobenzamide
• Replace fat-soluble vitamins (A, D, E, K) as needed.
• Administer analgesics for adequate pain control:
• avoid morphine (may cause spasm of sphincter of Oddi, increasing pain).
• Administer antibiotics for acute symptoms.
• Placement of stent into gallbladder if the patient is not a candidate for surgery.
• Ultrasound-guided aspiration of gallbladder.
• Surgical removal of gallbladder:
• Laparoscopic cholecystectomy
• Open cholecystectomy

NURSING DIAGNOSES

• Acute pain
• Chronic pain
• Risk for imbalanced nutrition: less than what body requires
• Nausea

NURSING INTERVENTION

• Monitor vital signs for changes in temperature, pulse rate, respiratory rate,
and blood pressure.
• Assess abdomen for bowel sounds, distention, and tenderness.
• Assess pain level for adequate pain control.
• Assess postoperative wound for drainage, signs of infection.
• Monitor T-tube drainage in postoperative open cholecystectomy patients;
empty and record at least every 8 hours.
• Advance diet to low-fat diet postoperatively as tolerated.
• meperidine

Appendicitis

Introduction:

Inflammation of the vermiform appendix (a blind pouch located near the ileocecal
valve in the right lower quadrant of the abdomen) is known as appendicitis. It may
be due to obstruction from stool. The mucosal lining of the appendix continues to
secrete fluid, which will increase the pressure within the lumen of appendix, caus-
ing a restriction of the blood supply to the appendix. This decrease in blood sup-
ply may result in gangrene or perforation as the pressure continues to build. Pain
localizes at McBurney’s point, located midway between the umbilicus and right
anterior iliac crest. Appendicitis may occur at any age, but the peak occurrence is
from the teenage years to 30.

PROGNOSIS

Rupture of the appendix is more likely to occur in acute appendicitis within the
first 36 to 48 hours. Symptoms of peritonitis (inflammation of the peritoneum—
the membrane lining the abdominal cavity) may occur as a complication of appen-
dicitis. Rapid diagnosis and surgical intervention are necessary to avoid rupture of
the appendix.

SIGNS AND SYMPTOMS

• Rigidity of the abdomen (abdomen feels more firm when palpating)
• Fever due to infection
• Nausea, vomiting, loss of appetite
• Right lower quadrant pain that improves with flexing the right hip suggests
perforation

TREATMENT

• Surgical removal of the appendix—appendectomy (may be done via laparo-
scopy or open laparotomy).
• NPO—nothing by mouth to avoid further irritation of the intestinal area, and
prep for surgery.
• Intravenous fluids until diet resumed.
• Pain medications after surgery as needed; pain medication is used cautiously
preoperatively to maintain awareness of increase in pain due to possible rup-
ture of appendix.
• Antibiotics postoperatively if needed.

NURSING DIAGNOSES

• Acute pain
• Hyperthermia
• Nausea

NURSING INTERVENTION

• Monitor vital signs for fever, increased heart rate, respiratory rate, and decrease
in blood pressure.
• Assess pain level for changes.
• Monitor surgical site for appearance of wound, drainage.
• Monitor abdomen for distention, presence of bowel sounds.
• Monitor intake and output.
• Monitor bowel function.

How the Gastrointestinal System Works

The gastrointestinal system includes the alimentary canal (mouth, esophagus,
stomach, small intestine, large intestine, rectum) and accessory organs (salivary
glands, liver, pancreas, gallbladder) and ducts. The alimentary canal is a hollow
tube lined with mucous membrane. The gastrointestinal tract functions to digest
food, absorb nutrients, propel the contents through the lumen, and eliminate the
waste products.
Digestion of food has both mechanical and chemical components. Both pro-
cesses begin in the mouth. Chewing, movement through the gastrointestinal tract,
and churning within the stomach are parts of the mechanical process. Saliva,
hydrochloric acid, bile, and other digestive enzymes all contribute to the chemical
process of digestion.
The esophagus extends from the oropharynx to the stomach. At the top of the
esophagus is the upper esophageal sphincter (UES) to prevent the influx of air into
the esophagus during respiration. At the bottom of the esophagus is the lower
esophageal sphincter (LES) to prevent the reflux of acid from the stomach into the
esophagus.
The contents of the esophagus empty into the stomach through the cardiac
sphincter. The stomach secretes gastrin, which promotes secretion of pepsinogen
and hydrochloric acid, pepsin, and lipase, all of which aid digestion and mucous
which helps protect the stomach lining.
The liver is a very vascular organ located in the right upper quadrant of the
abdomen under the diaphragm. It has two main lobes that are comprised of smaller
lobules. The liver stores a variety of vitamins and minerals. It metabolizes pro-
teins; synthesizes plasma proteins, fatty acids, and triglycerides; and stores and
releases glycogen. The liver detoxifies foreign substances such as alcohol, drugs,
or chemicals. The liver forms and secretes bile to aid in digestion of fat. Bile will
release into the gall bladder for storage or into the duodenum if needed for diges-
tion if the sphincter of Oddi is open due to secretion of the digestive enzymes
secretin, cholecystokinin, and gastrin. The gall bladder is a small receptacle that
holds bile until it is needed. It is located on the inferior aspect of the liver.
The pancreas is located retroperitoneally in the upper abdomen near the stom-
ach and extends from just right of midline to the left toward the spleen. The pan-
creas has both endocrine and exocrine functions. The endocrine functions include
secretion of insulin in response to elevations in blood glucose from the beta cells
of the islets of Langerhans and glucagon in response to decrease in blood glucose
from the alpha cells. The exocrine function includes secretion of trypsin, lipase,
amylase, and chymotrypsin to aid in digestion.
The small intestine is comprised of the duodenum, jejunum, and the ileum. The
duodenum attaches to the stomach, is about one foot long and C-shaped, and
curves to the left around the pancreas. The common bile duct and pancreatic duct
enter here. The jejunum is between the duodenum and ileum and is about eight
feet long. The last portion of the small intestine is the ileum which is up to twelve
feet long, depending on the size of the patient. The ileocecal valve separates the
ileum from the large intestine. The appendix is found at this juncture. The large
intestine can be broken down into the ascending colon, transverse colon, descend-
ing colon, and sigmoid colon. The sigmoid colon joins the rectum and ultimately
the anal canal.