1. Collaborative Care
1.1. Complementary/ Alternative Treatment
1.1.1. Probiotic
1.1.1.1. yogurt, supplements, buttermilk, kefir, tempeh, miso, sauerkraut, kim chi, brewer's yeast (Crohn's and Colitis Canada, n.d.)
1.1.2. Prebiotics
1.1.2.1. raw chicory root, jerusalem artichoke, dandelion greens, raw garlic, leek; raw and cooked onion; raw asparagus, wheat bran, cooked whole wheat flour, raw banana (Crohn's and Colitis Canada, n.d.)
1.1.3. Nutritional Therapy (Crohn's and Colitis Canada, n.d.)
1.1.3.1. high calorie
1.1.3.2. lactose free
1.1.3.3. low fat
1.1.3.4. low fiber
1.1.3.5. low salt
1.1.3.6. eat smaller meals more often
1.1.4. Enteral Nutrition
1.1.4.1. nutrition given through a nasogastric (NG) tube
1.1.4.2. Indications
1.1.4.2.1. severe cases
1.1.4.2.2. small bowel fistulas or short bowel syndrome (Crohn's and Colitis Canada, n.d.)
1.1.4.2.3. give before and after surgery to promote wound healing, reduce complications and speed up recovery (Crohn's and Colitis Canada, n.d.)
1.1.5. Elemental Diet (Crohn's and Colitis Canada, n.d.)
1.1.5.1. high calorie
1.1.5.2. high nitrogen
1.1.5.3. no residue substrate
1.1.5.4. no residue substrate
1.2. Surgical Therapy (NIDDK, 2017)
1.2.1. indications for surgery
1.2.1.1. treat fistulas
1.2.1.2. bleeding that is life threatening
1.2.1.3. intestinal obstructions
1.2.1.4. side effects from medication provided
1.2.1.5. treat the symptoms when medications have failed
1.2.2. small bowel resection
1.2.2.1. remove part of small intestine when disease is severe or there is an obstruction (NIDDK, 2017)
1.2.2.1.1. laparoscopic
1.2.2.1.2. open surgery
1.2.3. subtotal colectomy
1.2.3.1. large bowel resection
1.2.3.1.1. laparoscopic
1.2.3.1.2. open surgery
1.2.3.2. removes part of the large intestine if there is an obstruction, a fistula or the disease is severe (NIDDK, 2017)
1.2.4. protocolectomy
1.2.4.1. removes entire colon and rectum (NIDDK, 2017)
1.2.5. ileostomy
1.2.5.1. is a stoma or opening in abdomen
1.2.5.2. created from part of the ileum
2. Clinical Manifestations/ Nursing Interventions
2.1. Primary symptoms
2.1.1. Diarrhea
2.1.1.1. Considerations (Cedars Sina, 2019)
2.1.1.1.1. Onset, number of stools per day, and characteristics (amount, consistency, odour, and colour)
2.1.1.1.2. Steatorrhea
2.1.1.1.3. Other precipitating factors
2.1.1.2. Interventions (Schmelzer, 2014)
2.1.1.2.1. Perform Abdominal Assessment
2.1.1.2.2. Promote Bedrest
2.1.1.2.3. Possible restriction of food and fluids that precipitate diarrhea
2.1.1.2.4. Promote clear fluid intake
2.1.2. Cramping Abdominal Pain (Vera, 2013)
2.1.2.1. Considerations
2.1.2.1.1. Typically confined to the lower quadrants for Crohn's Disease
2.1.2.2. Interventions
2.1.2.2.1. Perform Pain Assessment
2.1.2.2.2. Pharmacological Treatment
2.1.2.2.3. Non-Pharmacological Treatment
2.2. Secondary symptoms
2.2.1. Intermittent Low Grade Fever (Vera, 2013)
2.2.1.1. Considerations
2.2.1.1.1. Consistency and severity of symptom
2.2.1.2. Interventions
2.2.1.2.1. Assess Temperature
2.2.1.2.2. Monitor and Assess for additional symptoms that would indicate causation
2.2.1.2.3. Pharmacological Treatment
2.2.1.2.4. Non-Pharmacological Treatment
2.2.2. Deficient Fluid Volume (Schmelzer, 2014)
2.2.2.1. Considerations
2.2.2.1.1. Possible causations for Excessive Fluid Loss
2.2.2.2. Interventions
2.2.2.2.1. Monitor vital signs, skin turgor, capillary refill, and I&O with urine for normal concentration and amount
2.2.2.2.2. Assess integumentary system and mucous membranes
2.2.2.2.3. Monitor for unintentional weight loss
2.2.2.2.4. Monitor laboratory studies for electrolyte values (especially potassium and magnesium)
2.2.3. Unintentional Weight Loss (Schmelzer, 2014)
2.2.3.1. Considerations
2.2.3.1.1. Possible Causation
2.2.3.1.2. excessive weight loss puts the patient at risk for:
2.2.3.1.3. severe weight loss can be fatal
2.2.3.2. Interventions
2.2.3.2.1. Encouragement to keep a daily food diary (with calorie estimates)
2.2.3.2.2. Referral to nutritionist
2.2.3.2.3. Promote small frequent meals with increased fluid intake
2.2.3.2.4. Depending on severity of malnutrition, administration of a parenteral feed may be ordered
2.2.4. Malabsorption and Nutrition Deficiency
2.2.4.1. Considerations (Vera, 2013)
2.2.4.1.1. Contributing factors include:
2.2.4.1.2. Fat soluble vitamins A, D, E, and K will be affected
2.2.4.1.3. increased risk of steatorrhea
2.2.4.2. Interventions (Cedars Sina, 2019)
2.2.4.2.1. Oral Vitamin supplements
2.2.4.2.2. Increased oral intake depending on deficiency
2.2.4.2.3. Treat the underlying cause (i.e. controling the increased diarrhea)
2.2.4.2.4. Intravenous feeding (depending on severity of deficiency)
2.2.5. Anxiety, Depression and Stress (Golik et al., 2014)
2.2.5.1. Considerations
2.2.5.1.1. Can be difficult to cope with the recurrent and unpredictable nature of the disease
2.2.5.1.2. the consistency and severity of symptoms
2.2.5.2. Interventions
2.2.5.2.1. Provide a calm and restful environment
2.2.5.2.2. help patient to identify coping mechanisms and support systems available to patient
2.2.5.2.3. encourage verbalization of feelings
2.2.5.2.4. monitor depression/anxiety for severity
2.3. Anemia (Reinisch, Staun, BhandarI & Munoz, 2013).
2.3.1. Considerations
2.3.1.1. Vitamin B12 is primarily absorbed in the terminal ileum
2.3.1.1.1. Terminal ileum is the primary site of inflammation process for Crohn's Disease
2.3.1.1.2. Lack of B12 can cause megaloblastic anemia
2.3.1.2. if inflammation affects the duodenum
2.3.1.2.1. risk exists for iron deficiency anemia
2.3.2. Interventions
2.3.2.1. Oral Iron supplement
2.3.2.2. Blood transfusion (based on severity) (Cedars Sina, 2019)
2.4. Possible Complications
2.4.1. Obstructions (Cedars Sina, 2019)
2.4.1.1. Considerations
2.4.1.1.1. scaring and stricture can occur from inflammation
2.4.1.2. Interventions
2.4.1.2.1. Surgical correction
2.4.2. Fistulas (Cedars Sina, 2019)
2.4.2.1. Considerations
2.4.2.1.1. Abnormal openings between two adjacent hollow organs
2.4.2.1.2. bowel-bladder fistulas are most common for patients with Crohn's Disease
2.4.2.1.3. Create high risk scenarios for UTI, peritonitis or abscesses (depending on location)
2.4.2.2. Interventions
2.4.2.2.1. Draining of the abscess in or near fistula
2.4.2.2.2. Surgical corrention
3. Risk Factors
3.1. Genetic (Mazal, 2014)
3.1.1. Sibling/ first degree relative also has Crohn's
3.1.2. Sex
3.1.2.1. Females slightly more affected than males
3.2. Environmental (Mazal, 2014; Silva, 2016)
3.2.1. High Socioeconomic status
3.2.1.1. Theorized over sanitation decreasing exposure to antigens and leaving the immune system susceptible.
3.2.2. Geographical
3.2.2.1. Northern Europe: 27-48 cases per 100 000
3.2.2.2. United States:3 to 5 cases per 100 000
3.3. Nutritional (Mazal, 2014)
3.3.1. Diet high in animal based proteins is positively correlated with diagnosis while diet high in vegetables is negatively correlated.
3.4. Race (Mazal, 2014)
3.4.1. White - 43.6 per 100 000
3.4.2. African American-29.8 per 100 000
3.4.3. Hispanic-4.1 per 100 000
3.4.4. Asian- 5.6 per 100 00
4. Treatment Goals (Schmelzer, 2014)
4.1. Resting the Bowel
4.2. Controllling Inflammation
4.3. Combating potential infection
4.4. Correcting Malnutrition
4.5. Alleviating Stress
4.6. Providing Symptomatic Relief
4.7. Improving Quality of Life
5. Common Medication Classes used for Treatment
5.1. Prescribed based on the stage of the disease process, level of disease activity and evidence of penetrating behaviour (Mazal, 2014)
5.1.1. Aminosalicylates
5.1.2. Immunosuppressants
5.1.3. Biological therapy
5.1.4. Corticosteriods
5.1.5. Antimicrobials
6. Pathogenesis
6.1. Persistent inflammation of the mucosa of the entire GI tract due to inappropriate immune responses (Mazal, 2014; Silva, Rodrigues, Ayrizono & Leal, 2016).
6.1.1. "Leaky Bowel"- Increased Epithelial permeability allows pathogens to pass through epithelial barrier
6.1.2. Reduced TLR-3 and TLR-5 receptors increase sensitivity to normal flora
6.1.3. Inability to suppress active inflammatory process
6.1.3.1. Decreased T-Cell apoptosis
7. Co-morbitites (Mazal, 2014)
7.1. Ankylosing Spondylitis
7.2. Pancreatitis
7.3. Pyoderma Gangrenosum
7.4. Myocarditis
7.5. Sacroilitis
7.6. Pleuritis
8. Presentation of Disease
8.1. Trans-mural Inflammation (Mazal, 2014; Silva et al., 2016)
8.1.1. Involves all five layers of the lumenal mucosa
8.2. Phenotypes (Mazal, 2014)
8.2.1. Terminal Ileum- 47%
8.2.2. Colon- 28%
8.2.3. Ileo Colon- 21%
8.2.4. Upper GI- 3%
8.3. Presence of Skip lesions (Mazal, 2014; Lewis, Heitkemper, Dirksen, Bucher & Camera, 2014).
8.3.1. Area of inflammation followed by unaffected area
8.4. Bi-modal (Mazal, 2014)
8.4.1. HIgh Occurance in second and third decade of life
8.4.2. Minor incidence peak between sixth and seventh decade of life
8.5. Cobble stone appearance (Lewis et al., 2014)
8.5.1. Deep, longitudinal ulcerations cut between inflamed mucosa separating the inflamed tissue
8.6. Periods of exacerbation and remission
9. Diagnostics
9.1. Patient Hx (Mazal, 2014)
9.1.1. Cheif complaints
9.1.1.1. Diarrhea
9.1.1.1.1. Presence of blood in stool
9.1.1.2. Malaise
9.1.1.3. Low grade fever
9.1.1.4. Weight loss
9.1.1.4.1. Number of watery stools
9.1.1.4.2. Presence of pain with digestion
9.1.1.4.3. Vitamin deficiency
9.1.1.5. Abdominal cramping
9.1.1.5.1. Location of pain
9.1.1.5.2. Use of pain scale- 10 point scale
9.1.2. Onset and varying severity of symptoms
9.1.2.1. Symptoms could be present for months/ years before patient seeks medical care for worsening symptoms
9.1.3. Timing between flare ups
9.1.3.1. increased time in between flare ups indicative of worsening Crohns
9.1.4. Genitourinary Symptoms
9.1.4.1. Indicates fistulae formation
9.1.4.1.1. UTI's
9.1.4.1.2. Blood and/ or fecal matter in urine
9.1.5. Nutrition/ Lifestyle
9.1.5.1. Eating habits- fruits, vegetables, lactose
9.1.5.2. Cigarette Smoking
9.1.5.3. Use of NSAIDS
9.1.6. Immunization Records
9.1.6.1. Hypothesis that attenuated live measles, mumps and rubella vaccine contribute to IBD
9.2. Physical Exam (Mazal, 2014)
9.2.1. Vital Signs: BP, resp. rate, heart rate and temp.
9.2.2. Observation
9.2.2.1. Abdominal distention
9.2.2.1.1. Prolonged bloating
9.2.2.1.2. Intestinal obstruction
9.2.2.2. Fistula formation between intestinal tract and dermal layer most often at site of surgical scars (Penetrating Crohns)
9.2.2.3. Rippling of abdomen
9.2.2.3.1. Peristalsis visible due to intestinal obstruction
9.2.3. Auscultation
9.2.3.1. Should precede Percussion- Alters intensity/ number of bowel sounds
9.2.3.2. Minimum five minutes and include all four quadrants
9.2.3.3. High pitched tinkling sounds
9.2.3.3.1. Indicates fluid/ air under pressure and possible obstruction
9.2.3.4. Borborygmi- Long, pronged gurgles
9.2.3.4.1. Possible obstruction
9.2.4. Percussion
9.2.4.1. Dull sounds over organs may indicate potential masses associated with obstruction
9.2.5. Palpation
9.2.5.1. Associated tenderness
9.2.5.1.1. Fistula formation
9.2.5.2. Palpable masses
9.2.5.2.1. Thickened/ matted bowel loops (usually in lower abdomen)
9.2.6. Rectal Exam
9.2.6.1. Pernianal skin tags
9.2.6.2. Fistulae
9.2.6.3. Fissures
9.3. Lab Tests (Mazal, 2014; Lewis et al., 2014).
9.3.1. WBC
9.3.1.1. Indicates infection, inflammation, tissue necrosis
9.3.2. Tests to confirm non- specific inflammatory processes
9.3.2.1. CRP
9.3.2.2. ESR
9.3.2.3. Leukocytes
9.3.2.4. Platelets
9.4. Diagnostic Procedures (NIKKD, 2017)
9.4.1. Intestinal Endoscopy (most accurate)
9.4.1.1. Colonoscopy
9.4.1.1.1. endoscope is used to look inside rectum and colon (NIDDK, 2017)
9.4.1.2. Upper GI Endoscopy
9.4.1.2.1. doctor inserts endoscope down the esophagus and into stomach and duodenum (NIDDK, 2017)
9.4.1.3. Upper GI Enteroscopy
9.4.1.3.1. examines small intestine with longer endoscope
9.4.1.4. Capsule Endoscopy
9.4.1.4.1. patient swallows capsule that has camera; therefore able to see inside entire digestive tract (NIDDK, 2017)
9.4.2. Upper GI Series
9.4.2.1. x-ray
9.4.2.2. fluoroscopy
9.4.2.3. barium (chalky liquid)
9.4.3. CT Scan