II. Etiology
A. Pathophysiologic mechanisms may include one or several of these mechanisms:
1. Increased absorption.
2. Decreased secretion.
3. Decreased peristalsis.
B. Decreased oral intake of both fluids and fiber with resultant dehydration.
C. Decreased physical activity related to hospitalization, generalized weakness, fatigue, or lethargy can reduce neurologic stimulus to pass stool.
D. Depression and anxiety can result in decreased oral intake or decreased physical activity. Antidepressant medications may also enhance the risk of constipation.
E. Carcinomas of the bowel may alter normal bowel function or cause lumen obstruction.
F. Surgical Procedures
1. Any operative manipulation of the bowel will slow peristalsis.
2. Anesthetic agents used for surgery slow peristalsis.
3. Surgical procedures involving the GI tract may affect any component of normal absorption, secretion, or peristalsis.
G. Chemotherapeutic Agents
1. Vinca alkaloids (eg, vincristine, vinblastine) cause autonomic neuropathy in about 30% of patients that can result in constipation or paralytic ileus that peaks in incidence 3 to 7 days after chemotherapy administration (
Brown et al., 2001).
2. Thalidomide
1. Incidence is 45% to 98% of patients receiving regular regimen of opioids.
2. Dose related.
I. Medical Disorders
1. Addison’s disease.
2. Cushing’s disease.
3. Diabetes mellitus causes autonomic neuropathy.
4. Hypothyroidism.
5. Spinal cord compression between T8 and L3 can cause relaxation of the anal sphincter and fecal retention.
J. Other Medications
1. Aluminum-containing antacids
2. Antiemetics
3. Anticholinergics (eg, loperamide, medications to treat bladder spasms)
4. Antihypertensives—Calcium channel blockers, centrally acting agents (eg, clonidine)
5. Calcium or iron supplements
6. Diuretics
7. Phenothiazines
8. Sympathetic stimulation—Antidepressants, antiparkinson agents
9. Sleep medications
10. Tricyclic antidepressants
K. Electrolyte Disturbances
1. Hypokalemia causes decreased intestinal motility and paralytic ileus due to neuromuscular irritability.
2. Hypercalcemia impedes the transmission of stimuli causing atony of the GI tract and constipation.
L. Increased Sympathetic Tone
1. Chronic pain or stress
2. Use of sympathetic stimulating agents: Dopamine, antidepressants
M. Older age may be the most important adjunctive risk factor in patients receiving medications known to cause constipation.
N. Changes in routine that disrupt normal bowel toileting
1. Travel.
2. Lack of time—When bowel evacuation is delayed from initial urges, the stimulation and sensation of having to defecate weaken.
3. Lack of privacy.
III. Patient Management
A. Assessment
1. Patient history
a. Risk factors
b. Normal bowel habits
c. Diet history—Fluid, fiber, caffeine
d. Medication history for risk factors
e. Use of laxatives
f. Activity level
2. Patient complaints
a. Frequency of stool.
b. Consistency of stool.
c. Associated symptoms—Lower back discomfort, feeling of fullness, rectal pressure, abdominal pain, abdominal cramping or gas, abdominal distention, anorexia, nausea, headache.
3. Physical findings
a. Performance status and ability to increase activity level
b. Bowel sounds
c. Abdomen firmness, tenderness to palpation
d. Manual detection of stool in rectum
B. Diagnostic Parameters: There are no definitive diagnostic tests for constipation; it is a diagnosis made by clinical evidence.
C. Treatment
1. Lifestyle alterations
a. Diet—Increase fluid, increase fiber
b. Exercise—Increase aerobic exercise
2. Complementary therapies
a. Herb teas—1 tsp of substance in boiling water; dried dandelion blooms, licorice root, mullein, slippery elm, raspberry leaves, rhubarb root tincture, guelder rose bark tincture (
Brown, 2001)
b. Aloe vera juice several times a day
c. Flax or linseed seeds crushed into a porridge or chewed
3. Surgical therapy
b. Laparoscopy-assisted bowel resection
D. Nursing Diagnoses
1. Constipation related to cancer, cancer treatment, or adverse effects
a. Problem: Constipation can be caused by multiple factors and is often the result of several interacting risk factors. Constipation can result in bowel obstruction, reabsorption of metabolic toxins, and discomfort.
b. Interventions—Will vary based on causative factors and the patient’s ability to comply with some interventions, and should, therefore, be individualized. The following interventions are listed in the order they are usually initiated, from least invasive to most comprehensive.
(1) Increase fluid intake (2 to 3 L daily). Warm fluids may act as a peristaltic stimulant and assist with evacuation.
(2) Increase fiber intake. High-fiber foods include whole grains, bran, fresh raw fruits and vegetables, nuts, coconuts, corn, popcorn, raisins, dates, and prunes.
(3) Avoid caffeine because it can act as a diuretic, decreasing water volume.
(4) Avoid cheese products and refined grains.
(5) Increase physical activity, which will increase gut motility. If confined to bed, contract and relax abdominal muscles and move lower extremities.
(6) Provide for regular toilet habits, including:
(a) Consistent daily toilet time (after breakfast is a time when gut motility is naturally high)
(b) Privacy
(c) A bedside commode rather than a bedpan when possible
(7) Anticipate treatment regimens likely to cause constipation and implement preventive stool softeners or bulk producers. Regimens to reduce opioid-induced constipation include both a stool softener and a peristaltic stimulant.
(a) Senna 1 to 2 tablets daily at bedtime.
(b) Docusate 1 to 2 tablets daily in the morning.
(c) If patients do not move their bowels at least once per day, each can be increased by 1 tablet daily until a maximum of 4 tablets three times a day is reached, or 3 to 4 days without a bowel movement.
(8) Add bulk producers and stool softeners as needed (see
Table 23-1).
(9) Additional pharmacologic interventions (see
Table 23-1).
(10) Participate in referral for surgical management of bowel obstruction when indicated.
(a) Possible candidates: Tumor-associated constipation and luminal obstruction, or severe high fecal impaction.
(b) Diagnostic tests defining location and extent of fecal obstruction include abdominal flat plate and lateral x-rays, abdominal computed tomography (CT) scan, or abdominal ultrasound.
(c) Serum ammonia levels may aid in determining severity of toxic metabolic waste absorption.
(11) Teach the patient pelvic Kegel exercises to enhance rectal muscle tone.
c. Desired outcomes
(1) Patient will maintain regular, comfortable passage of soft, formed stool.
(2) Patient will have fewer complaints of discomfort or constipation.
(3) Patient will have decreased need for laxatives or other interventions.
2. Potential for infection due to bowel obstruction or rupture.
a. Problem: Severe and intractable constipation can lead to bowel obstruction and possible rupture. If the large bowel ruptures, peritoneal sepsis will ensue.
b. Interventions
(1) Frequent abdominal assessment when the patient has known constipation.
(a) Bowel sounds.
(b) Abdominal pain—Report rebound tenderness immediately.
(c) Abdominal distention.
(2) Vital sign monitoring every shift or ambulatory visit. Investigate possible abdominal sepsis if the patient is febrile.
(3) Serial abdominal circumferences if distention is present.
(4) If acute obstruction or rupture is suspected, prepare for:
(a) Stat abdominal flat plate x-ray.
(b) Wide open infusion of intravenous (IV) fluids and possible transfer to an intensive care unit for vasopressors.
(c) Stat IV antibiotics that usually include metronidazole or a fluoroquinolone.
(d) NPO until it is determined whether the patient is a candidate for surgery.
(e) Frequent vital signs and intake and output measurement.
(f) Laboratory specimens for serum chemistry, amylase, and lactate.
c. Desired outcome: Constipation is resolved before abdominal crisis occurs.