CIRRHOSIS

● Chronic progressive disease of the liver

● Cells attempt to regenerate but are disorganized
● Results in abnormal architecture, overgrowth of
fibrous connective tissue, and impeded blood flow
● Eventually results in decreased functioning of
liver
● Insidious, prolonged course Eighth leading cause
of death in United States
● Twice as common in men
Case Study
Biliary cirrhosis
● D.L. is a 35-year-old woman admitted from the ED ● Associated with chronic biliary
with a diagnosis of hepatic encephalopathy. inflammation and obstruction
● Review of old medical records indicate a diagnosis Cardiac cirrhosis
of fatty liver disease at age 29 and cirrhosis at age ● From long-standing severe right-sided
31. heart failure
● She accepts treatment only during crises.
Case Study
● What else would you look for in D.L.'s past
medical history that might be a precipitating ● For what late clinical manifestations of
factor in her liver disease? cirrhosis would you assess D.L.?

Etiology and Pathophysiology

Clinical Manifestations
● Specific cause not always known
● Most common causes in United States are chronic ● Onset is insidious
hepatitis C and alcohol-induced liver disease ● Fatigue may be early symptom
- Protein malnutrition ● Many patients have no symptoms until
- Environmental factors late
- Chronic inflammation and cell necrosi%) ● Later manifestations
- Synergistic factors accelerate damage - Jaundice, peripheral edema,
ascites
- Skin, hematologic, endocrine,
and neurologic disorders
Jaundice
● Functional derangement of liver cells
● Compression of bile ducts by
overgrowth of connective tissue
● Decreased ability of liver cells to
conjugate and excrete bilirubin
● Severity varies

1 Jayrah Joy A. Uy BSN 3 - J

Skin lesions ○ Upper portion of stomach
● Due to increase in circulating estrogen caused by ● Peripheral edema
inability of liver to metabolize steroid hormones ○ ↓Colloidal oncotic pressure from
● Spider angiomas (telangiectasia or spider nevi) impaired liver synthesis of
● Palmar erythema albumin
Hematologic disorders ○ ↑Portacaval pressure from
● Thrombocytopenia portal hypertension
● Leukopenia ○ Occurs as ankle/presacral edema
● Anemia ● Ascites
● Coagulation disorders ○ Accumulation of serotJS fluid in
Endocrine disorders peritoneal or abdominal cavity
● Secondary to decreased metabolism of hormones ○ Abdominal distention with
● Gynecomastia, loss of axillary and pubic hair, weight gain
testicular atrophy, impotence and loss of libido ○ Common manifestation of
(men) cirrhosis
● Amenorrhea or vaginal bleeding
● Hyperaldosteronism in both sexes
Peripheral neuropathy
● Dietary deficiencies of thiamine, folic acid, and
cobalamin (vitamin B12)
● Sensory symptoms predominate
Complications
● Compensated cirrhosis
● Decompensated cirrhosis
○ Portal hypertension
○ Esophageal and gastric varices
○ Peripheral edema and ascites
○ Hepatic encephalopathy
○ Hepatorenal syndrome
● Portal hypertension
○ Increased portal venous pressure
○ Splenomegaly
○ Large collateral veins
○ Ascites
○ Gastric and esophageal varices
● Esophageal varices
○ Complex of tortuous veins at lower end of
esophagus Case Study
○ Very fragile ● What might be causing D.L.'s current
○ Bleed easily; bleeding can be life- episode of hepatic encephalopathy?
threatening
● Gastric varices
 ● What specific clinical manifestations related to
hepatic encephalopathy would you expect D.L. to
have?

Complications
Hepatorenal syndrome
● Renal failure with azotemia, oliguria, and
intractable ascites
● No structural abnormality of kidneys
● Portal hypertension → vasodilation → renal
vasoconstriction
● Treat with liver transplantation
Hepatic encephalopathy
● Neurotoxic effects of ammonia
● Abnormal neurotransmission
● Astrocyte swelling
● Inflammatory cytokines
- Liver unable to convert increased ammonia
Case Study
- Ammonia crosses blood-brain barrier
● What diagnostic tests would you expect
● Changes in neurologic and mental
the health care provider to order for
responsiveness
D.L.?
● Impaired consciousness and/or
inappropriate behavior Diagnostic Studies
● Sleep disturbances to lethargy to coma ● Liver enzyme tests
● Asterixis ● Total protein, albumin levels
● Fetor hepaticus ● Serum bilirubin, globulin levels
● Cholesterol levels
● Prothrombin time
● Liver ultrasonography
● Liver biopsy
● Analysis of ascitic fluid
Case Study
● D.L.’s laboratory values are as follows:
○ Total bilirubin 11 mg/dL
○ AST 80 U/mL
○ ALT 70 U/mL
○ LDH 700 U/mL
○ Serum ammonia 220 mg/dL
○ WBC 21,450/μL
 ● D.L. is thin and malnourished with ascites and ● Mechanical compression of varices
marked edema on lower extremities. ● Sengstaken-Blakemore tube
● Both her liver and spleen are palpable. ● Minnesota tube
● Jaundice and spider angiomas are present. ● Linton-Nachlas tube
● There is evidence of bruising throughout her
body.
● What would be your priorities of care for D.L.?
Collaborative Care
● Rest
● Administration of B-complex vitamins
● Avoidance of alcohol, aspirin, acetaminophen,
and NSAIDs

- Deflate balloon for 5 minutes every 8 to

Case Study
12 hours per institutional policy to
● What specific treatment measures might be used
prevent tissue necrosis
to treat D.L.’s ascites?
Supportive measures for acute bleed
Collaborative Care ● Fresh frozen plasma
Ascites ● Packed RBCs
● Sodium restriction ● Vitamin K (AquaMEPHYTON)
● Albumin ● Proton pump inhibitors (e.g.,
● Diuretics pantoprazole)
● Tolvaptan (Samsca) ● Lactulose (Cephulac) and rifaximin
● Paracentesis (Xifaxan) may be started to prevent
● Transjugular intrahepatic portosystemic shunt hepatic encephalopathy from
(TIPS) breakdown of blood and the release of
Esophageal and gastric varices ammonia in the intestine
● Prevent bleeding/hemorrhage ● Antibiotics to prevent bacterial infection
- Avoid alcohol, aspirin, and irritating foods Long-term management
- Screen for presence with endoscopy ● Nonselective β-adrenergic blockers
- Nonselective β-blocker ● Repeated band ligation
● If bleeding occurs, stabilize patient, manage ● Portosystemic shunts
airway, provide IV therapy and blood Shunting procedures
● Drug therapy ● Used more after second major bleeding
- Octreotide (Sandostatin) episode
- Vasopressin (VP, terlipressin) with ● Nonsurgical: transjugular intrahepatic
nitroglycerin (NTG) portosystemic shunt (TIPS)
● Endoscopic therapy ● Surgical: portacaval and distal
- Band ligation splenorenal shunt
- Sclerotherapy
Balloon tamponade
 Nutritional Therapy
● Diet for patient without complications
- High in calories (3000 cal/day)
- ↑ Carbohydrate
- Moderate to low fat
- Protein restriction rarely justified
● Protein supplements for protein-calorie
malnutrition
● Low-sodium diet for patient with ascites
and edema
Nursing Assessment & Management
Subjective data
● Past health history
- Hepatitis
- NASH
- Chronic biliary obstruction and
infection
- Severe right-sided heart failure
Medications
● Adverse reactions
● Anticoagulants, aspirin, NSAIDs,
acetaminophen
Subjective data: functional health patterns
Case Study ● Chronic alcoholism
● What specific treatment measures would you ● Weakness, fatigue
expect the health care provider to order for D.L.’s ● Anorexia, weight loss
encephalopathy? ● Dyspepsia
● Nausea and vomiting
Collaborative Care
● Gingival bleeding
Hepatic encephalopathy
● Dark urine
● Reduce ammonia formation
● Decreased output
○ Lactulose (Cephulac), which traps
● Light-colored or black stools
ammonia in gut
● Flatulence
○ Rifaximin (Xifaxan) antibiotic
● Change in bowel habits
○ Prevent constipation
● Dry, yellow skin
● Treatment of precipitating cause
● Bruising
○ Control GI bleeding
● RUQ or epigastric pain
○ Remove blood from GI tract
● Numbness, tingling
● Drug therapy
● Pruritus
○ Not specific for cirrhosis
● Impotence
○ Used to treat symptoms and complications
● Amenorrhea
of advanced liver disease
Objective data ● Minimal to no complications
● Fever, cachexia, wasting of extremities ● Return to as normal a lifestyle as
● Icteric sclera, jaundice possible
● Petechiae, ecchymoses Nursing Implementation
● Spider angiomas, palmar erythema
Health promotion
● Alopecia, loss of axillary and pubic hair
● Reduce or eliminate risk factors
● Peripheral edema
● Treat alcoholism
● Respiratory: shallow, rapid respirations, epistaxis
● Maintain adequate nutrition
● Gastrointestinal: abdominal distention, ascites,
● Identify and treat acute hepatitis
distended abdominal wall veins, palpable liver
● Bariatric surgery for morbidly obese
and spleen, foul breath; hematemesis; black, tarry
Acute intervention
stools; hemorrhoids
● Rest needs
● Neurologic: Altered mentation, asterixis
- Prevent complications
● Reproductive: Gynecomastia and testicular
- Modify schedule
atrophy (men), impotence (men), loss of libido
● Nutritional needs
(men and women), amenorrhea or heavy
- Oral hygiene
menstrual bleeding (women)
- Between-meal nourishment
● Possible diagnostic findings: anemia,
- Food preferences
thrombocytopenia; leukopenia; ↓ serum albumin
- Explanation of dietary
level, ↓ potassium level; abnormal liver function
restrictions
studies; ↑ INR, ↑ ammonia level, and ↑ bilirubin
● Assess for jaundice
levels; abnormal abdominal ultrasound study or
● Measures to relieve pruritus
MRI
- Cholestyramine or hydroxyzine
Nursing Diagnosis - Baking soda or Alpha Keri baths
● Imbalanced nutrition: less than body - Lotions, soft or old linen
requirements related to anorexia, nausea, - Temperature control
impaired utilization and storage of nutrients - Short nails; rub with knuckles
● Impaired skin integrity related to peripheral ● Monitor color of urine and stools
edema, ascites, and pruritus ● Accurate I/O recording
● Excess fluid volume related to portal ● Daily weight measurement
hypertension and hyperaldosteronism ● Extremities measurement
● Ineffective self-health management related to ● Abdominal girth measurement
ineffective coping and abuse of alcohol ● Paracentesis
● Dysfunctional family processes related to abuse - Patient voids immediately before
of alcohol and inadequate coping skills as - High Fowler’s position or sitting
evidenced by deterioration in family relationships, on side of bed
family denial, neglected obligations, inability to - Monitor for fluid and electrolyte
accept and receive help appropriately imbalances
- Monitor dressing for
Planning
bleeding/leakage
Overall goals
● Relief of dyspnea
● Relief of discomfort
- Semi- or high Fowler’s position
 ● Skin care - Close observation for signs of
- Special mattress bleeding
- Turning schedule, at least every 2 hours - Balloon tamponade care
● ROM exercises ● Explanation of procedure
● Coughing/deep breathing exercises ● Check for patency
● Elevate lower extremities/scrotum ● Position of balloon
verified by x-ray
Question
A patient with advanced cirrhosis who has ● Balloon tamponade
ascites is short of breath and has an - Monitor for complications (i.e.,
increased respiratory rate. The nurse should aspiration pneumonia)
a. Initiate oxygen therapy at 2 L/min to - Scissors at bedside
increase gas exchange. - Semi-Fowler’s position
b. Notify the health care provider so that
- Oral/nasal care
a paracentesis can be performed.
c. Ask the patient to cough and breathe
deeply to clear respiratory secretions. Case Study
d. Place the patient in Fowler’s position
● What nursing measures would you
to relieve pressure on the diaphragm.
Answer: D prioritize in caring for D.L. in relation to
Rtionale: her encephalopathy?
Dyspnea is a frequent problem for the patient
Nursing Implementation
with ascites, and a semi-Fowler’s or Fowler’s
position allows for maximal respiratory Acute intervention
efficiency. ● Hepatic encephalopathy
a. Oxygen administration is not indicated; - Maintain safe environment
SpO2 level less than 90% would be an - Assess carefully
indication for oxygen. The respiratory
● Level of responsiveness
distress is caused by ascites (not by
respiratory secretions); coughing and ● Sensory and motor
deep breathing will not alleviate the abnormalities
respiratory distress. ● Fluid/electrolyte
b. A paracentesis may be performed to imbalances
remove ascitic fluid; however, this ● Acid-base balance
procedure provides only temporary ● Effects of treatment
relief and is reserved for severe
measures
respiratory distress or abdominal pain.
● Hepatic encephalopathy
Nursing Implementation - Perform neurologic assessment
Acute intervention every 2 hours
● Monitor for fluid and electrolyte disturbances - Prevent constipation
- Hypokalemia - Encourage fluids
- Fluid volume excess - Control factors known to
● Observe for bleeding disorders precipitate encephalopathy
● Assess patient’s response to altered body image Case Study
- Supportive listening
● Bleeding varices
 ● D.L. recovers from her hepatic encephalopathy ○ M>F Age 40-50
and is ready to be discharged from the hospital. ○ F>M Ages 50-70
● What teaching would you provide for D.L. and her ○ F>>M Ages > 70
family?
● How might a social worker help you with D.L.’s Anatomic location of diverticuli varies with the
discharge planning? geographic location
Ambulatory and home care ● “Westernized” nations (North America,
● Supportive measures Europe, Australia) have predominantly
- Proper diet left sided diverticulosis
- Rest ○ 95% diverticuli are in sigmoid
- Avoidance of hepatotoxic OTC drugs colon
- Abstinence from alcohol ○ 35% can also have proximal
● Caring attitude always diverticuli
● Community support programs ○ 4% have only right sided
● Symptoms of complications diverticuli
● When to seek medical attention ● Asia and Africa diverticulosis in general
● Written instructions with adequate explanations is rare and usually right sided
for patient/family ○ Prevalence < 0.2%
● Referral to community or home health nurse ○ 70% diverticuli in right colon in
Japan
Evaluation
What exactly is a diverticulum?
● Maintenance of food/fluid intake to meet needs
● True diverticulum contains all layers of
● Maintenance of skin integrity
the GI wall (mucosa to serosa)
● Normalization of fluid balance
● Colonic pseudo-diverticulum more like a
● Treatment for substance abuse
local hernia
○ Mucosa-submucosa herniates
DIVERTICULAR DISEASE OF THE through the muscle layer
COLON (muscularis propria) and then is
only covered by serosa
Nomenclature
● Diverticulum = sac-like protrusion of the colonic
Pathophysiology
wall
● Diverticuli develop in ‘weak’ regions of
● Diverticulosis = describes the presence of
the colon. Specifically, local hernias
diverticuli
develop where the vasa recta penetrate
● Diverticulitis = inflammation of diverticuli
the bowel wall
Epidemiology
● Increases with age
○ Age 40 <5%
○ Age 60 30%
○ Age 85 65%
● Gender prevalence depends on age
○ M>>F Age less than 40
 ● However, a significant minority of
patients will complain of cramping,
bloating, irregular BMs, narrow caliber
stools
○ IBS?
○ Recent studies demonstrate
motility abnormalities in pts with
‘symptomatic’ uncomplicated
diverticulosis
● Treatment: Fiber
○ Bulk content reduces colonic
pressure preventing underlying
pathophysiology that lead to
Lifestyle factors associated with diverticular disease
diverticulosis
● Low fiber diverticular disease
○ 20 to 30 g fiber per day is
○ Not absolutely proven in all studies but
needed; difficult to get with diet
strongly suggested
alone
○ Western diet is low in fiber with high
prevalence of diverticulosis
○ In contrast, African diet is high in fiber Diverticulitis
with a low prevalence of diverticulosis ● Diverticulitis = inflammation of
● Obesity associated with diverticulosis – diverticuli
particularly in men under the age of 40 ● Most common complication of
● Lack of physical activity diverticulosis
● Occurs in 10-25% of patients with
diverticulosis
Pathophysiology of Diverticulitis
● Micro or macroscopic perforation of the
diverticulum subclinical inflammation to
generalized peritonitis
● Previously thought to be due to fecaliths
causing increased diverticular pressure;
Uncomplicated diverticulosis this is really rare
● Usually an incidental finding at time of
colonoscopy

● Considered ‘asymptomatic’
● Erosion of diverticular wall from increased ● Barium enema is contraindicated due to
intraluminal pressure →inflammation→ focal risk of perforation.
necrosis →perforation
● Usually inflammation is mild and microperforation
is walled off by pericolonic fat and mesentery

Diagnosis of Diverticulitis
Treatment of Diverticulitis
● Classic history: increasing, constant, LLQ
abdominal pain over several days prior to ● Complicated diverticulitis = Presence of
presentation with fever macroperforation, obstruction, abscess,
○ Crescendo quality – each day is worse or fistula
○ Constant – not colicky ● Uncomplicated diverticulitis = Absence
○ Fever occurs in 57-100% of cases of the above complications
● Previous of episodes of similar pain
● Associated symptoms Uncomplicated diverticulitis
○ Nausea/vomiting 20-62% ● Bowel rest or restriction
○ Constipation 50% ○ Clear liquids or NPO for 2-3 days
○ Diarrhea 25-35% ○ Then advance diet
○ Urinary symptoms (dysuria, urgency, ● Antibiotics
frequency) 10-15% ○ Coverage of fecal flora
● Right sided diverticulitis tends to cause RLQ ■ Gram negative rods,
abdominal pain; can be difficult to distinguish anaerobes
from appendicitis ○ Common regimens
● Physical examination ■ Cipro + Flagyl x 10 days
○ Low grade fever ■ Augmentin x 10 days
○ LLQ abdominal tenderness ● Monitoring clinical course
■ Usually moderate with no ○ Pain should gradually improve
peritoneal signs several days (decrescendo)
■ Painful pseudo-mass in 20% of ○ Normalization of temperature
cases ○ Tolerance of po intake
■ Rebound tenderness suggests free ● If symptoms deteriorate or fail to
perforation and peritonitis improve with 3 days, then Surgery
● Labs : Mild leukocytosis consult
○ 45% of patients will have a normal WBC ● After resolution of attack → high fiber
● Clinically, diagnosis can be made with typical diet with supplemental fiber
history and examination ● Follow-up: Colonoscopy in 4-6 weeks
● Radiographic confirmation is often performed ● Purpose:
● Abdominal CT is analysis of choice ○ Exclude neoplasm
 ○ Evaluate extent of the diverticulosis ○ Small abscesses too small to
● Prognosis after resolution drain percutaneously (< 1cm) can
○ 30-40% of patients will remain be treated with antibiotics alone
asymptomatic ○ These pts behave like
○ 30-40% of pts will have episodic uncomplicated diverticulitis and
abdominal cramps without frank may not require surgery
diverticulitis ● Fistulas
○ 20-30% of pts will have a second attack ○ Occurs in up to 80% of cases
○ Second attack requiring surgery
■ Risk of recurrent attacks is high ■ Major types
(>50%) ■ Colovesical fistula
■ Some studies suggest a higher rate 65%
(60%) of complications (abscess, ■ Colovaginal
fistulas, etc) in a second attack and 25%
a higher mortality rate (2x ■ Coloenteric, colouterine
compared to initial attack) 10%
○ After a second attack elective surgery Symptoms
○ Some argue in the elderly recurrent ● Passage of gas and stool from the
attacks can be managed with medications affected organ
○ Some argue elective surgery should be ● Colovesical fistula:
considered after a first attack in ○ pneumaturia, dysuria,
■ Young patients under 40-50 years fecaluria
of age ○ 50% of patients can have
■ Immunosuppressed diarrhea and passage of
urine per rectum
● Diagnosis
Complicated Diverticulitis ○ CT: thickened bladder
● Peritonitis with associated colonic
○ Resuscitation diverticuli adjacent and
○ Antibiotics air in the bladder
■ Ampicillin + Gentamycin + ○ BE: direct visualization of
Metronidazole fistula track only occurs in
■ Imipenem/cilastin 20-26% of cases
○ Emergency exploration ○ Flexible sigmoidoscopy is
○ Mortality 6% purulent peritonitis and 35% low yield (0-3%)
fecal peritonitis ○ Some argue cystoscopy
Complicated Diverticulitis: helpful
● Abscess ● Surgery
○ Occurs in 16% of patients with acute ○ Resection of affected
diverticulitis colon (origin of the
○ Percutaneous drainage followed by single fistula)
stage surgery in 60-80% of patients
 ○ Fistula tract can be “pinched off” ○ Accurate localization
most of the time ■ 30-47% sensitive
○ Suture closure for larger defects ■ 100% specific
○ Foley left in 7-10 days ○ Need brisk active bleeding: 0.5-1
Surgical Treatment of Diverticulitis mL/min
● Elective single stage resection is ideal, ~6 weeks ○ Offers therapy: embolization,
after episode vasopressin
● Two stage procedure (Hartmann procedure) ■ 20% risk of intestinal
Diverticular bleeding infarction
● Most common cause of brisk hematochezia (30-
50% of cases)
● 15% of patients with diverticulosis will bleed
● 75% of diverticular bleeding stops without need INFLAMMATORY BOWEL DISEASE
for intervention Inflammatory – inflammation
● Patients requiring less than 4 units of PRBC/ day Bowel – involvement of the GI system
99% will stop bleeding
 An idiopathic inflammatory intestinal
● Risk of rebleeding 14-38%
disease resulting from an inappropriate
● After second episode of bleeding, risk of immune activation to host intestinal
rebleeding 21-50% microflora.
Localization
● Right colon is the source of diverticular bleeding
in 50-90% of patients
● Possible reasons
○ Right colon diverticuli have wider necks
and domes exposing vasa recta over a
great length of injury
○ Thinner wall of the right colon
● Colonoscopy after rapid prep
Different types of IBD
○ Can localize site of bleeding
1. Ulcerative Colitis
○ Offers possible therapeutic intervention Inflammation of colon
(cautery, clip, etc)  Mucosal inflammation
○ Often limited by either brisk bleeding  Involves colon only
obscuring lumen OR no active bleeding  Continuous inflammation from anal verge
upwards
with clots in every diverticuli  Bloody diarrhea
● Tagged red blood cell scan  Increased risk of colon cancer
○ Can localize bleeding source
■ 97% sensitivity 2. Crohn’s Disease
Inflammation of GI tract
■ 83% specificity
 Transmural segment inflammation
■ 94% PPV  Involves any portion of GI tract (most
○ Can detect bleeding as slow as 0.1 mL/min commonly ileo-cecal region)
○ Often not particularly helpful  Leads to strictures and fistula formation
(with peri-anal disease)
● Angiography
  More abdominal pain and diarrhea, less bleeding  Bloody diarrhea
 Crampy abdominal pain
3. Indeterminate Colitis  Tenesmus
(If the patient could not be identifies as either the two both  Fever
Ulcerative colitis and crohn’s disease)
 Symptoms must be present for at least 3-4
weeks, thus making UC a diagnosis of
exclusion.

Epidemiology
 Has a Bimodal distribution
o UC: 3rd decade and 7th decade
o Crohn’s: 15-30 yo and 60 -70 yo
 Common in Northern Europe and in Caucasians
 Highest rate in Jewish Population
 UC>Crohn’s
o UC: 8-15 per 100,000
o Crohn’s: 1-5 per 100,000
Etiology Pathology
 Multifactorial
 Mucosal Process
o Environmental
o Colonic Mucosa and submucosa are
 Diet (increase intake of refined sugars)
 OCP infiltrated with inflammatory cells
 Alcohol drinking and smoking o Involves only the colon
o Genetics
 NOD2 (Nucleotide-binding
Oligomerization Domain containing
protein 2)
 ATG16L1 gene
 IRGM gene
ULCERATIVE COLITIS
Pathogenesis

a.
b. Proctosigmoiditis -involves the rectum and the
sigmoid colon
c. Distal Colitis – left side of the colon.
d. Pancolitis –(universal colitis) – entire colon

Backwash colitis - Descent 2-3 cm into the terminal

ileum

Clinical Manifestations Diagnostic Finidings

 Inactive or Quiescent to Low grade disease to  Friable mucosa
Fulminant disease
  With multiple inflammatory cell infiltrates and pseudo
polyps Pathology
 Diffuse superficial ulcerations  Transmural inflammatory process
 With continuous involvement of rectum and colon  Occurs anywhere in the GI system (from
mouth to anus)
Complications  Most commonly found in the terminal ileum
 Toxic Megacolon  With rectal sparing in 40% of patients
 Increased risk for colon cancer
 Massive hemorrhage Diagnostic Findings

Treatment: Medical
 Aminosalicylates
 Corticosteroids
 More potent immunomodulators (Azathioprine,
Cyclosporin, Tacrolimus)
 Biologic Agents (Anti-tumor necrosis factor)

Treatment: Surgical
 Total Abdominal colectomy with end ileostomy
 Indications for emergent surgery:
o With massive life-threatening hemorrhage
o Toxic megacolon
o Fulminant colitis who failed to respond rapidly
to medical therapy
o Deterioration in clinical condition or failure to
improve within 24 to 48 hours.
 Total Proctocolectomy with end ileostomy
 Indications for elective surgery
o Intractability despite maximal medical therapy
o High-risk development of major complications
of medical therapy such as aseptic necrosis of Characteristic pathologic findings
joints secondary to chronic steroid use  Mucosal Ulcerations
o Significant risk of developing colorectal  An inflammatory cell infiltrates
carcinoma.  Noncaseating granulomas
Complications
CROHN’S DISEASE  Fistula, abscess and stricture formation
Epidemiology  Risk for colorectal carcinoma, if with
 Bimodal incidence pancolitis
 1-5 per 100,000 in North European and Caucasian
populations. Treatment: Medical
 Amniosalicylates
Clinical manifestation  Corticosteroids
 Diarrhea  More potent immunomodulators
 Crampy abdominal pain (Azathioprine, cyclosporin, tacrolimus)
 Fever  Biologic agents (anti-tumor necrosis factor)
 Weight loss  Antibiotics
 Perianal disease or mouth ulcers
 Megaloblastic anemia Treatment: Surgical
 Not curative in Crohn’s disease
  Percutaneous Draining of abscess
 Simple closure of secondary fistula site Corticosteroids
 Removal of diseased segment of bowel  A key treatment for an acute exacerbation
 Resection of stricturoplasty of stricture of IBD
 A topical preparation effective in mild to
Indications for surgery: moderate distal colonic disease
 Internal fistula or abscess  Oral preparation needed for more proximal
 Obstruction or extensive disease
 Fibrotic strictures  IV preparation for severely ill patients
 Useful for induction of remission but not for
maintenance
Extraintestinal manifestation  Significant side effects with long term use

Hepatobiliary involvement Immunomodulating agents (Azathioprine or 6-MP)

 Fatty infiltration of the liver  Immunosuppressive medications interfere
 Cirrhosis with nucleic acid synthesis and decrease
 Primary sclerosing cholangitis proliferation of inflammatory cells)
 Pericholangitis  Used in
 Bile duct carcinoma o ASA failure
o Corticosteroid dependent/ refactory
Joint/ bone involvement  Long half-life and onset of action (6-12
 Arthritis weeks)
 Sacroiliitis  Side effects
 Ankylosing spondylitis o Pancreatitis
o Hepatitis
Skin involvement o Bone marrow suppression
 Erythema nodosum
 Pyoderma gangrenosum Immunomodulating agents (Cyclosporine)
 Immunosuppressive medications (interfere
Eye involvement T Lymphocyte function)
 Uvelitis  Used to treat acute flare of ulcerative colitis
 Iritis and exacerbations of Crohn’s disease
 Episcleritis  Side effects:
 Conjunctivitis o Nephrotoxicity
 Macular Degenerative, hyperpigmented Epithelium o Hirsutism
(CHRPE) o Gum hypertrophy

Non-operative treatment Immunomodulating agents (Methotrexate)

5 – ASA  Folate antagonist (cause impaired DNA
 EX: Sulfasalazine & Mesalamine synthesis)
 1st line agents for mild to moderate IBD  Side effects:
 Acts by inhibiting lipoxygenase pathway of arachidonic o Leukopenia
acid in the gut mucosa o Hepatic fibrosis
 More effective in colonic than ileal disease
 Side effects Antibiotics
o Nausea, rash, hair loss, hemolysis  Ciprofloxacin and metronidazole commonly
o Pancreatitis, hepatitis, aplastic anemia used for Crohn’s Disease
 Not useful in UC
  Side effects: Ulcerative colitis
o Lingterm use of Metronidazole is associated Nursing considerations
with peripheral neuropathy and disulfiram -  Teach & Educate
like effects o Early recognition
o Ciprofloxacin is associated with tendinitis or o Monitor hydration and keep food
tendon rupture journal
o Stool chart
Anti-TNF therapy o Weight monitoring
 Monoclonal antibody directed against TNF-alpha  Support
 3 preparations available in US o Emotional Support
o Infliximab  Collaborative care
o Adalimumab o Infection control nurse
o Certolizumab o Dietitian
 Better response in Crohn’s disease o Gastroenterologist & surgeon
 Used both for induction and maintenance of remission
 Increased risk of serious infection, including TB and
lymphoma

Nutrition
 Parenteral nutrition
 Colostomy (Diversion of fecal stream)

Crohn’s Disease
Nursing considerations
 Teaching & Educations
o Stress management techniques
o Medication therapies
o Diet management & exercise
o Diagnostic testing and procedures
 Support
o Understanding the disease
o Body image
 Collaborate
o Dietitian
o Gastroenterologist & surgeon
o Smoking cessation programs
 Gastrointestinal System
 Stomach – located in the upper portion of
the abdomen
o Under the left lobe of the liver and
diaphragm
o Overlaying most of the pancreas

o Hollow muscular organ with a

capacity of approx. 1500 ml
o Stores food during eating, secretes
digestive fluids
o Propels the partially digested food
or chyme, into small intestine

DISORDERS OF THE STOMACH

 Median & lateral borders of the stomach are

curved
o Lesser (shorter concave medial
surface of the stomach – the
 angular notch junction of the body on the Prevention
pyloric region.  Wash your hands, utensils and food surfaces
o greater curvature (forms the long convex often
lateral border of the stomach arising the  Keep raw foods separate from ready to eat
cardic noch and arching backwards and foods
passing inferiorly to the left.  Cook foods to a safe temperature
FOOD POISONING  Refrigerate or freeze perishable foods
 Food poisoning also called foodborne illness, is illness promptly
cause by eating contaminated food. Infectious  Defrost food safely.
organisms -including bacteria, viruses, and parasites or  When in doubt, throw it out
their toxins are the most common causes of food
poisoning. Complications
 Infectious organisms or their toxins can contaminate  The most common serious complications of
food at any point of processing or production. food poisoning is dehydration -a severe loss
Contamination can also occur at home if food is of water and essentials salts and minerals
incorrectly handles or cooked.  Infants, older adults and people with
 Food poisoning symptoms, which can start within suppressed immune system or chronic
hours of eating contaminated food, often include illnesses may become severely dehydrated
nausea , vomiting or diarrhea. when they lose more fluids that they can
replace. In that case, they may need to be
Signs & Symptoms hospitalized and receive intravenous fluids.
 Nausea In extreme cases dehydration can be fatal.
 Vomiting – signs or symptoms of dehydration –
excessive thirst, dry mouth, little or no urination, Nursing Diagnosis with Nursing intervention
severe/ weakness, dizziness or lightheadedness
 Watery or bloody diarrhea
 Abdominal pain and cramps
 Fever
 Neurological symptoms such as blurry vision, muscle
weakness and tingling in the arms

Causes
 Contamination of food can happen at any pont of
production, growing, harvesting, processing, storing
shipping or preparing .
 Cross-contamination – the transfer of harmful
organisms from one surface to another – id often the
cause. This is especially troublesome for raw, ready to
eat foods such as salads or other produce. Because
these foods aren’t cooked, harmful organisms aren’t
destroyed before eating and can cause food poisoning.
Risk factors
 Wheter you become ill after eating contaminated food
depends on the organism, the amount of exposure
your age and your health. High risk groups include:
o Older adults.
o Pregnant women
o Infants and young children
o People with chronic disease
 Signs and symptoms
 Epigastric discomfort or pain
 Nausea and vomiting
 Dyspepsia
 Bleeding causing hematemesis “coffee
ground” vomiting and melaena
 Iron deficiency anemia (due to constant
bleeding)

PEPTIC ULCER
 Involves ulceration of the mucosa of the stomach
(gastric ulcer) or the duodenum (duodenal ulcer)
 Duodenal ulcers are more common.

Management
 Peptic ulcer are diagnosed by endoscopy.
During endoscopy a rapid urease test (CLO
test) can be performed to check for H. pylori
(UBT)
 Biopsy should be considered during
Pathophysiology endoscopy to exclude malignancy as cancers
The stomach mucosa is prone to ulceration from can look similar to ulcers during the
 Breakdown of the protective layer of the stomach and procedure
duodenum  Medical treatment is the same as with
 Increase in stomach acid GERD, usually with high dose proton pump
There is a protective layer in the stomach comprised of mucus inhibitors. Endoscopy can be used to
and bicarbonate secreted by the stomach mucosa. This monitoring the ulcer to ensure it heals and
protective layer can be broken down by: to assess for further ulcers.
 Medication (steroids or NSAIDS) Complications
 Helicobacter pylori  Bleeding from the ulcer is a common and
potentially life threatening complications
 Perforation resulting in an acute abdomen
and peritonitis. This required urgent surgical
repair (usually laparoscopic)
 Scarring and strictures of the mucosa. This can lead to
a narrowing of the pylorus (exit of the stomach)causing
difficulty in emptying the stomach contents. This is
known as pyloric stenosis. This presents with upper
abdominal pain, distention, nausea and vomiting,
particularly after eating.