CARE OF CLIENT WITH

INFLAMMATORY AND
IMMUNOLOGIC DISORDERS
 Disorder Description
Autoimmunity Normal protective immune response paradoxically
turns against or attacks the body, leading to tissue damage

Hypersensitivity Body produces inappropriate or exaggerated

responses to specific antigens

Gammopathies Overproduction of immunoglobulins

Primary Immune Deficiencies Deficiency results from improper development of

immune cells or
tissues; usually congenital or inherited

Secondary Immune Deficiencies Deficiency results from some interference with an already developed
immune system; usually acquired later in life
INFLAMMATORY DISORDERS
Inflammatory Bowel Disease
• Inflammatory bowel disease (IBD)
represents a group of intestinal disorders
that cause prolonged inflammation of the
digestive tract.
• It is a spectrum of chronic idiopathic
inflammatory condition.
Classification
•Ulcerative colitis: Ulcerative colitis is a disease that causes
mucosal inflammation and sores (ulcers) in the lining of the large
intestine (colon ).
•Chron’s disease: Crohn’s disease is a chronic, relapsing and
remitting inflammatory disease of the gastrointestinal tract, affecting
any site from mouth to anus.
◻ Ulcerative colitis is slightly more common in
males, while Crohn’s disease is more frequent
in women.
◻ Diet, oral contraceptives, perinatal and
childhood infections, or atypical mycobacterial
infections have been suggested, but not
proven, to play a role in developing IBD.
Etiology
•Infectious agents
• Viruses (Measles) Bacteria (Mycobacteria)

•Genetics

•Environmental factors
• Diet Smoking

•Psychological factors
• Stress
• Emotional or physical trauma
Pathophysiology
•ALTERED MUCOSAL IMMUNE RESPONSE
◻ Dietary and bacterial antigens penetrate into
the intestinal wall and activates the immune system.
◻ Thiscauses increased production of pro-
inflammatory mediators which will lead to inflammation of the
mucosal layer.
Pathophysiology
EPITHELIAL
DEFECTS
◻ Variety of epithelial defects have been described in Crohn’s
• disease and Ulcerative Colitis.
◻ Defects in epithelial cells will lead to influx of bacterial components such as
dendritic cells and macrophages which activates CD+4 cells.
◻ Activated CD+4 cells activate other inflammatory cells like B-cells and variable T-cells
or recruit more inflammatory cells by stimulation of homing receptor on
leucocytes and vascular epithelium.
◻ Inflammation in IBD is maintained by an influx of leukocytes from the vascular system
into sites of active disease. This influx is promoted by expression of adhesion
molecules (such as α 4- integrins) on the surface of endothelial cells in the
microvasculature in the area of inflammation.
Clinical Manifestations
◻ Diarrhea
◻ Abdominal pain, cramping & bloating due to bowel obstruction
◻ Hematochezia : Blood in stool
◻ Low fever
◻ Decreased appetite
◻ Weight loss and anorexia
◻ Fatigue
◻ Arthritis
COMPLICATIONS
Includes intestinal obstruction or stricture formation, perineal
disease fluid and electrolyte imbalances, malnutrition from
malabsorption, fistula and abscess formation. the most
common type of small bowel fistula caused by Crohn's disease
is the enterocutaneous fistula (an abnormal opening between
the small bowel and the skin).
OTHER COMPLICATIONS OF IBD
Diagnosis

◻ Physical Examination
◻ Endoscopy
◻ Biopsy
◻ Radiology
◻ Blood Test
 MANAGEMENT OF CHRONIC
INFLAMMATORY BOWEL DISEASE
• MANAGEMENT OF CHRONIC INFLAMMATORY BOWEL DISEASE
• MEDICAL TREATMENT FOR BOTH CROHN’S DISEASE AND
ULCERATIVE COLITIS IS AIMED AT REDUCING INFLAMMATION,
SUPPRESSING INAPPROPRIATE IMMUNE RESPONSES, PROVIDING
REST FOR A DISEASED BOWEL SO THAT HEALING MAY TAKE PLACE.
• MANAGEMENT DEPENDS ON THE DISEASE LOCATION, SEVERITY,
AND COMPLICATIONS
 NUTRITIONAL THERAPY
• ORAL FLUID AND A LOW-RESIDUAL, HIGH PROTEIN, HIGH CALORIC
DIET WITH SUPPLEMENTAL VITAMIN THERAPY AND IRON
REPLACEMENT ARE PRESCRIBED TO MEET NUTRITIONAL NEED.
• FLUID AND ELECTROLYTE IMBALANCE FROM DEHYDRATION ARE
CORRECTED BY THERAPY AS NECESSARY IF THE PATIENT IS HOSPITALIZED
OR BY ORAL FLUIDS FLUID IF THE PATIENT IS MANAGED AT HOME.
• ANY FOOD THAT EXACERBATE DIARRHEA ARE AVOIDED.
• MILK MAY CONTRIBUTE TO DIARRHEA IN THOSE WITH LACTOSE
INTOLERANT.
• COLD FOOD AND SMOKING ARE AVOIDED BECAUSE BOTH
INCREASE INTESTINAL MOTILITY.
• PARENTERAL NUTRITION MAY BE INDICATED
DRUG THERAPY
• SEDATIVE, ANTIDIARRHEAL, AND ANTIPERISTALSIS.
• AMINOSALICYLATES SUCH AS SULFASALAZINE FOR MILD TO MODERATE
INFLAMMATION
• CORTICOSTEROIDS (PREDNISONE, HYDROCORTISONE) USED TO TREAT SEVER
AND FULMINANT
• DISEASE AND CAN BE ADMINISTERED ORALLY
• BUDESONIDE RECTAL ADMINISTRATION.
• AMONG THE NEWEST BIOLOGICAL THERAPIES USING MONOCLONAL
ANTIBODIES ARE NATALIZUMAB (TYSABRI) FOR CROHN’S DISEASE, AND
INFLIXIMAB (REMICADE) FOR ULCERATIVE COLITIS
• ANTICYTOKINE THERAPY USING ANTI-INTERLUKIN TYPE DRUG (E.G. - ANTI-
IL-12) FOR CROHN’S DISEASE.
MANAGEMENT
• SURGICAL MANAGEMENT
• strictureplasty, in which the blocked or narrowed section of the
intestine are widened, leaving the intestine intact.
• in some case a small bowel resection is performed, and diseased segment of
the small intestines are resected and the remaining portions of the intestine
are anastomosed.
• surgical removal of up to 50% of the small bowel usually can be tolerated. in case
of severe crohn’s disease of the colon, a total colectomy and ileostomy may be
the procedure of choice.
• a new surgical procedure developed for patient with severe crohn’s disease is
• intestinal transplant.
• protocolectomy with ileostomy (i.e., complete excision of colon, rectum, and
anus). if the rectum can be reversed, restorative protocolectomy with ileal pouch
anal anastomosis is the procedure of choice
 NURSING MANAGEMENT AND DIAGNOSIS
• the nurse obtains a health history to identify the onset, duration and characteristics of
abdominal pain; the presence of diarrhea or fecal urgency, staining of stool (tenesmus),
nausea, anorexia, or weight loss, and family history of IBD. discus dietary pattern, including
the amount of alcohol, and caffeine, and nicotine containing products used daily and weekly.
• pattern of bowel elimination, character, frequency, and presence of blood, pus, fat, or
mucus.
NURSING DIAGNOSIS
• diarrhea related to inflammatory process
• acute pain related to increase peristalsis and GI inflammation
• imbalance nutrition less than body requirements, related to dietary restrictions, nausea,
and malabsorption
• activity intolerance related to generalized weakness.
• anxiety related to impending surgery.
• ineffective coping related to repeated episode of diarrhea.
• risk for impaired skin integrity related to malnutrition and diarrhea.
PERSONAL EFFECT OF IBD
ULCERATIVE COLITIS

▪ Ulcerative colitis is a recurrent ulcerative & inflammatory

disease of the mucosal & submucosal layers of the colon &
rectum.

▪ The peak incidence is between 30 & 50 years of age.

▪ 10% to 15% of the patients develop carcinoma of the colon.

ETIOLOGY
∙ Genetic predisposition.
∙ Environmental factors may trigger disease (viral or bacterial
pathogens, dietary).
∙ Immunologic imbalance or disturbances.
∙ Defect in intestinal barrier causing hypersensitive
mucosa & increased permeability.
∙ Defect in repair of mucosal injury, which may develop into a
chronic condition.
PATHOPHYSIOLOGY
Etiological factors

superficial mucosa of colon

diffuse inflammations, or shedding of the colonic

epithelium.

Bleeding occurs

Ulcerations.

(The mucosa becomes edematous & inflamed. )

The disease process usually begains in the rectum & spreads proximally to involve
the entire colon.
CLINICAL MANIFESTATIONS:
▪ Diarrhea
▪ painful straining
▪ Increased bowel sounds
▪ There often is weight loss, fever, dehydration, hypokalemia, anorexia, nausea &
vomiting, iron- deficiency anemia
▪ Crampy abdominal pain.
▪ Anal area may be irritated & reddened; left lower abdomen may be tender on
palpation.
▪ There is tendency for the patient experience remissions & exacerbations.
▪ Increased risk of developing colorectal cancer.
▪ May inhibit extracolonic manifestations of eye (irritis), joint (polyarthritis), & skin
complaints (erythema nodosum, pyoderma gangrenosum).
DIAGNOSTIC EVALUATION
Diagnosis is based on a combination of laboratory, radiologic,
endoscopic, & histologic findings.
▪ Laboratory Tests:-
▪ Stool examination to rule out enteral pathogens; fecal analysis
positive for blood during active disease.
▪ Complete blood count- hemoglobin & hematocrit may be low due
to bleeding; WBC may be increased.
▪ Elevated erythrocyte sedimentation rate (ESR).
▪ Decreased serum levels of potassium, magnesium, & albumin
Other Diagnostic Test:

▪ Barium enema to assess extent

of disease & detect
Pseudopolyps, carcinoma, &
strictures.
Other Diagnostic Test:

▪ Flexible proctosigmoidoscopy/colonoscopy findings reveal mucosal erythema &

edema, ulcers, inflammation that begins distally in the rectum & spreads proximally for
variable distances.
▪ CT scan can identify complications such as toxic megacolon.
▪ Rectal biopsy – differentiates from other inflammatory diseases or cancer
MANAGEMENT
General Measures:-
▪ Bed rest, I.V. fluid replacement, clear liquid diet.
▪ For patients with severe dehydration & excessive diarrhea,
fluid may be recommended to rest the intestinal tract &
restore nitrogen balance.
▪ Treatment of anemia- iron supplements for chronic bleeding,
blood replacement for massive bleeding.
Drug Therapy
• Sulfasalazine (Azulfidine)- mainstay drug for acute & maintenance therapy. Given
orally & is systemically absorbed.
• Oral salicylates, such as mesalamine (Pentasa), olsalazine (Dipentum
• Mesalamineenema available for protosigmoiditis; suppository for proctitis.
• Corticosteroids- treated with 5-aminosalicylic acid preparations to benefit from
their potential steroid- sparing effects.
• Immunosuppressive drugs- purine analogues, 6- mercaptopurine, azathioprine
may be indicated when patient is refractory or dependent on corticosteroids.
• Antidiarrheal medications may be prescribed to control diarrhea, rectal urgency &
cramping, abdominal pain; not routinely ordered- treat with caution.
SURGICAL MEASURES

I. Noncurative approaches (possible curative, reconstructive

procedure at later date):
• Temporary loop colostomy for decompression if toxic megacolon
present without perforation.
• Subtotal colectomy, ileostomy, & Hartmann’s pouch.
• Colectomy with ileorectal anastomosis.
SURGICAL MEASURES
II. Reconstructive procedures – curative:
• Total proctocolectomy with permanent end- ileostomy.
• Total proctocolectomy with continent ileostomy
• Total colectomy with ileal reservoir- anal (or ileal reservoir-distal rectal)
anastomosis – procedure of choice. Multiple reservoir shapes can be
surgically created; however, the J-shaped pouch (reservoir) is the easiest
to construct.
• The ultimate surgical goal is to remove the entire colon & rectum to cure
patient
COMPLICATIONS
• Perforation, hemorrhage
• Toxic megacolon- fever, tachycardia, abdominal distention, peritonitis,
leukocytosis, dilated colon on abdominal X-ray – life-threatening
• Abscess formation, stricture, anal fistula
• Malnutrition, anemia, electrolyte imbalance
• Skin lesions (erythema nodosum, pyoderma gangrenosum)
• Arthritis, ankylosing spondylitis
• Colon malignancy
• Liver disease (sclerosing colagitis)
• Eye lesions (conjunctivitis)
• Growth retardation in prepubertal children
• Possible infertility in females.
NURSING MANAGEMENT
• Review nursing history for patterns of fatigue & over-work, tension,
family problems that may exacerbate symptoms.
• Assess food habits & use of any dietary or herbal supplements used as
alternative therapies that may have a bearing on triggering symptoms
(milk intake may be a problem). Many patient use vitamins, herbs &
homeopathic remedies without realizing the effect on bowel function.
• Determine number & consistency of bowel movements, any rectal
bleeding present.
• Listen for hyperactive bowel sounds; assess weight.
NURSING DIAGNOSES
• Chronic pain r/t disease process
• Imbalanced Nutrition: less than body requirement r/t diarrhea, nausea &
vomiting
• Deficient fluid volume r/t diarrhea & loss of fluid & electrolytes
• Risk for infection r/t disease process, surgical procedures
• Ineffective coping r/t fatigue, felling of helplessness, & lack of support
system.
NURSING INTERVENTION
Promoting Comfort :
• Follow prescribe treatment of reducing or eliminating food & fluid & instituting parenteral
feeding or low reside diets to the intestinal tract.
• Give sedatives & tranquilizers, as prescribed, not only to provide general rest , but also to slow
peristalsis.
• Be aware of skin breakdown around anus.
• Cleanse the skin gently after each bowel movement.
• Apply a protective emollient such as petroleum jelly etc.
• Relieve painful rectal spasms
• Report any evidence of sudden abdominal distention
• Reduce physical activity
• Provide commode or bathroom next to bed because urgency of movement may be
problem.
NURSING INTERVENTION
Achieving Nutritional Requirements:
• Maintain acutely ill patient on parenteral replacement of vitamins, fluids, &
electrolytes.
• When resuming oral fluids & food, select those that are nonirritating to the
mucosa.
• Avoid dairy products if patient is lactose intolerant.
• Provide a well-balanced, low-residue, high protein diet to correct malnutrition.
• Determine which foods the patient can tolerate, & modify diet plan
accordingly.
• Possible avoids cold fluids, which may increase intestinal motility.
• Administer prescribed medications for symptomatic relief of diarrhea.
NURSING INTERVENTION
Maintain fluid Balance:
• Maintain accurate intake & output records
• Check weight daily
• Monitor serum electrolytes, & report abnormalities.
• Observer for decrease skin turgor, dry skin, oliguria, decreased
temperature, weakness, increase hemoglobin, hematocrit, BUN, & specific
gravity, which all are signs of fluid loss leading to dehydration.
NURSING INTERVENTION
Minimizing Infection & Complications:
• Give antibacterial drugs as prescribed.
• Administer corticosteroids as prescribed.
• Provide conscientious skin care after severe diarrhea.
• Administer prescribed therapy to correct existing anemia.
• Observe for signs of colonic perforation & hemorrhage – abdominal
rigidity, distention, hypotension, tachycardia.
NURSING INTERVENTION
Providing Supportive Care:
• Recognize psychological needs of the patient.
• Fear, anxiety, & discouragement.
• Hypersensitivity may be evident.
• Acknowledge patient’s complaints.
• Encourage the patient to talk; listen & offer psychological support.
• Answer questions about the permanent or temporary ostomy, if appropriate.
• Initiate patient education about living with chronic disease.
• Include the patient as a part of the health care team to provide continuity of care.
• Offer educational & emotional support to family members
• Refer for psychological counseling, as needed.
Patient Education & Health Maintenance
⚫Teach patient about chronic aspect of ulcerative colitis & each
component of care prescribed.
⚫Encourage self-care in monitoring symptoms, seeking annual
checkup, & maintaining health.
⚫Alert patient to possible postoperative problems with skin care,
aesthetic difficulties, & surgical revisions.
⚫Encourage patient to share experiences with others
undergoing similar procedures.
APPENDICITIS
 APPENDICITIS

APPENDICITIS IS A PAINFUL
SWELLING AND INFECTION
OF THE APPENDIX.
WHAT IS THE APPENDIX?

• The appendix is a fingerlike pouch attached to the

large intestine and located in the lower right area of
the abdomen.
• The inside of the appendix is called the appendiceal
lumen.
WHAT CAUSES APPENDICITIS?
• Obstruction of the appendiceal lumen causes appendicitis. Mucus backs up
in the appendiceal lumen, causing bacteria that normally live inside the
appendix to multiply. The appendix swells and becomes infected. Sources of
obstruction include.
• Feces, parasites, or growth that clog the appendiceal lumen
• Enlarged lymph tissue in the wall of the appendix, caused by infection in the
gastrointestinal tract or elsewhere in the body.
• Inflammatory bowel disease, including Crohn’s disease and ulcerative colitis.
• Trauma to the abdomen.
• An inflamed appendix will likely burst if not removed. Bursting spreads infection
throughout the abdomen-a potentially dangerous condition called peritonitis.
PATHOPHYSIOLOGY
• Obstruction of the appendiceal lumen is the primary
appendiceal lumen leads to distension of the appendix due
to accumulated intraluminal fluid.
• Ineffective lymphatic and venous drainage allows bacterial
invasion of the appendiceal wall and in advanced cases,
perforation and spillage of pus into the peritoneal cavity.
Symptoms
The main symptom of appendicitis is abdominal pain. The abdominal
pain usually:
• Occurs suddenly, often causing a person to wake up at night.
• Occurs before other symptoms
• Begins near the belly button and then moves lower an to the right.
• Is new and unlike any pain felt before
• Gets worse in a matter of hours
• Gets worse when moving around, taking deep breaths, coughing or
sneezing.
Other symptoms of Appendicitis
• Loss of appetite
• Nausea
• Vomiting
• Constipation or diarrhea
• Inability to pass gas
• A low-grade fever that follows other symptoms
• Abdominal swelling
• The feeling that passing stool will relieve discomfort.
Etiology and Risk Factors
• A fecalith ( a fecal calculus, or stone) that occludes the lumen of the
appendix
• Kinking of the appendix
• Swelling of the bowel wall
• Fibrous conditions in the bowel wall
• External occlusion of the bowel by adhesion
• Infection with Yersinia organisms has been found in up to 30% of cases
Diagnostic test
• Blood tests to check for signs of infection

(high white blood cell count)

• Urine test to rule out a urinary tract infection.

• Chest X-ray because of pneumonia in the lower right lung can cause pain
similar to appendicitis

• Ultrasound may be performed to determine if the appendix appears to be

inflamed
Physical Examination
Guarding : Occurs when a person subconsciously tenses the
abdominal muscles during an examination. Voluntary guarding
occurs the moment the doctor’s hand touches the abdomen.
Involuntary guarding occurs before the doctor actually makes
contact.
Rebound tenderness : A doctor tests for rebound tenderness by
applying hand pressure to a patient’s abdomen and then
letting go. Pain felt upon the release of the pressure indicates
rebound tenderness.
Physical Examination

Rovsing’s sign : By applying hand pressure to the lower left side of the
abdomen. Pain on the lower right side of the abdomen upon the
release of pressure on the left side indicates the presence of
Rovsing’s sign.

Psoas sign : The right psoas muscle runs over the pelvis near the
appendix. Flexing this muscle will cause abdominal pain if the
appendix is inflamed. A doctor can check for the psoas sign by
applying resistance to the right knee as the patient tries to lift the
right thigh while lying down.
Physical Examination

Obturator sign : The right obturator muscle alo runs near the
appendix. A doctor tests for the obturator sign by asking
the patient to lie down with the right leg bent at the knee.
Moving the bent knee left and right requires flexing the
obturator muscle and will cause abdominal pain if the
appendix is inflamed.
McBurney’s point
McBurney’s point

Deep tenderness at McBurney's point, known as

McBurney's sign, is a sign of Acute Appendicitis. The
clinical sign of rebound pain when pressure is applied
is also known as Aaron's sign.
Management of Acute Appendicitis
✔Pre-operative care
NPO, IV therapy, close monitoring
Specific pre-operative preparation
✔Emergency operation
Acute appendicitis – appendicectomy
Perforation with peritonitis – laparotomy
Management of Acute Appendicitis
✔Post operative care
Day 1 : Close monitoring vital sign ,oral
by mouth, measuring abdominal
girth and medication
Day 2 : Wound inspection, support patient
to do ADL.
Day 3 : Patient discharged as Doctor
order.
Complications of Acute Appendicitis
▪ Perforation
▪ Appendicular mass
▪ Abscess
▪ Peritonitis
▪ Infection of surgical wound.
Nursing diagnosis for clients with
Acute Appendicitis
• Pre-operative:
Potential complication : perforation related to inflammatory process
Anxiety related to disease process and treatment.
• Post operatives:
Altered comfort related to surgery
High risk for infection of surgical incision.
Diagnosis, Outcomes, Interventions
• Nursing diagnosis
Acute Pain related to inflammation
• Outcomes
Decreased postoperative pain
• Interventions
Medicate as indicated
Assess for abrupt pain changes, which indicate perforation
Diagnosis, Outcomes, Interventions

■ Nursing diagnosis
■ Risk for Infection related to rupture of appendix

■ Outcomes
■ Infection will not develop
Diagnosis, Outcomes, Interventions
• Nursing diagnosis
Risk for Deficient Fluid Volume related to vomiting
Outcomes
• Fluid and electrolyte balance
• Interventions
Administer IV fluids
Careful assessment of intake and output
PANCREATITIS
▪ Acute pancreatitis is an acute
inflammation of the pancreas.
▪ The degree of inflammation varies from
mild edema to severe hemorrhagic
necrosis.
▪ Acute pancreatitis is common in
middle aged men and women.
CAUSES
Two main causes for pancreatitis are
⮚Gallstones (38%)
⮚Alcohol (36%)
Other, less common causes of acute pancreatitis include
⮚Trauma (postsurgical, abdominal)
⮚Viral infections mumps
⮚Coxsackievirus B, HIV
⮚Penetrating duodenal ulcer cysts
CAUSES
⮚Metabolic disorders
⮚Hyperparathyroidism
⮚Hyperlipidemia
⮚Renal failure
⮚Vascular diseases.
⮚Pancreatitis may occur after surgical procedures on the
pancreas, stomach, duodenum or biliary tract.
CAUSES
⮚Abscesses
⮚Cystic fibrosis
⮚Kaposi sarcoma
⮚Certain drugs (corticosteroids, thiazide , diuretics, oral
contraceptives, sulfonamides NSAIDs)
⮚Pancreatitis can also occur after ERCP.
⮚In some cases the cause is unknown (idiopathic)
CLINICAL MANIFESTATION
FEVER
▪ Rarely exceeds 102 degree F

ABDOMINAL FINDINGS
• Rigidity, tenderness, guarding
• Distension
• Decreased or absent peristalsis
CLINICAL MANIFESTATION
ABDOMINAL PAIN
• Steady and severe excruciating
• Located in the left upper quadrant or
in the mid epigastrium may radiate to
the back

• Worsened by lying supine may be

lessened by flexed knee, curved back
positioning
CLINICAL MANIFESTATION
VOMITTING
• Varies in severity but is usually
protacted.
• Worsened by ingestion of food or
fluid.
• Does not relieve the pain.
• Usually accompanied by nausea.
COMPLICATIONS
⚫ Hypotension or shock from hypovolemia or hypoalbuminemia
⚫ Leukocytosis, anemia , disseminated intravascular coagulation from unknown
causes
⚫ Atelectasis, pneumonia, pleural effusion, acute respiratory distress
syndrome
⚫ Gastrointestinal bleeding
⚫ Pancreatic pseudocysts, pancreatic necrosis, pancreatic abscesses, pancreatic
ascites
⚫ Oliguria and acute tubular necrosis
⚫ Hyperglycemia, hypocalcemia, hyperlipidemia
DIAGNOSIS
• History and physical examination
• Liver function tests: elevations commonly seen
• Serum triglycerides
• Serum amylase: Levels elevated within a few hours of disease onset
• Serum lipase: Levels remain elevated up to 7 days after disease onset
• Serum glucose: Hyperglycemia of 500 to 900 mg/d
• Serum calcium: Hypocalcemia from calcium sequestering in abdomen;
hypocalcemia is a poor prognostic sign
DIAGNOSIS
• Abdominal ultrasound
• Endoscopic ultrasound
DIAGNOSIS
• Magnetic Resonance
Cholangiopancreatogr
aphy (MRCP)
DIAGNOSIS
• Endoscopic Retrograde
Cholangiopancreatogr
aphy (ERCP)
COLLABORATIVE CARE
GOALS
• Relief of pain
• Prevention or alleviation of shock
• Reduction of pancreatic secretions
• Correction of fluid and electrolyte imbalances
• Prevention and treatment of infections
• Removal of the precipitating cause
CONSERVATIVE THERAPY

Focused on primary care:

• Aggressive hydration
• Management of metabolic complications
• Minimization of pancreatic stimulation
SURGICAL THERAPY
✔Acute pancreatitis related to Gallstone:
ERCP together with endoscopic sphincterotomy followed by
laparoscopic cholecystectomy to reduce potential for
recurrence

✔Severe acute pancreatitis:

Drainage of necrotic fluid collections
NUTRITIONAL MANAGEMENT

▪ Initially the patient to kept on NPO to decrease the gastric

acid secretions
▪ Enteral feeding: Nasojejunal feeding tube
▪ IV lipids : Blood triglyceride levels are monitored
▪ When food is allowed, small, frequent feedings are given.
▪ Carbohydrate rich diet should be given
▪ Needs to abstain from alcohol
▪ Supplemental fat-soluble vitamins may be given
CHRONIC PANCREATITIS

• Chronic pancreatitis (CP) is characterized by prolonged

pancreatic inflammation and fibrosis leading eventually to
destruction of pancreatic parenchyma and loss of exocrine
and endocrine function.
ETIOLOGY
✔Alcohol abuse
✔Obstruction caused by cholelithiasis
✔Tumor
✔Pseudocyst
✔Trauma
✔Systemic disease (Systemic lupus erythematosus)
✔Auto immune pancreatitis
✔Cystic fibrosis
CLINICAL MANIFESTATION
Abdominal pain :
• Episode of acute pain and it remains almost constant
• Pain may be locate in the same area as acute pancreatitis
• Describe as heavy, gnawing feeling or sometimes burning and camplike
Others include:
• Malabsorption with weight loss constipation, mild jaundice with dark urine,
steatorrhea and diabetes mellitus
• Steatorrhea may be voluminous, foul smelling fatty stools
• Urine and stool may be frothy
• Some abdominal tenderness may be present
COMPLICATIONS

▪ Pseudocyst formation
▪ Bile duct or duodenal obstruction
▪ Pancreatic ascites
▪ Pleural effusion
▪ Splenic vein thrombosis
▪ Pseudoaneurysm
▪ Pancreatic cancer
SURGICAL MANGEMENT
Pancreatojejunostomy
Side-to-side anastomosis of the
pancreatic duct to the jejunum,
allows drainage of the
pancreatic secretions into the
jejunum.
SURGICAL MANGEMENT
Whipple resection (pancreaticoduodenectomy )
Removal of the head of the pancreas, the first part of the small
intestine (duodenum), the gallbladder and the bile duct.
SURGICAL MANGEMENT

Other surgical procedures:

• Revision of the sphincter of the ampulla of Vater
• Internal drainage of a pancreatic cyst into the stomach
• Insertion of a stent and wide resection or removal of the
pancreas.
SURGICAL MANAGEMENT
Autotransplantation
• Implantation of the pancreatic islet cells
• Moving the pancreas to another location within the abdomen with revised
vascular and enteric anastomosis
Gallbladder disease : The obstruction is treated by surgery to explore the
common duct and remove the stones; the gallbladder is removed at the same
time.
Drainage : common bile duct and the pancreatic duct
A T-tube usually is placed in the common bile duct, requiring drainage system to
collect the bile
NURSING MANAGEMENT
• Health History.
• Assess for
• History of gallbladder disease
• History of other GI diseases (e.g., peptic ulcer disease, IBD)
• History of alcohol use: amount and duration
• Medications in use: prescription, over the counter, and herbal
preparation
NURSING MANAGEMENT
• Diminished or absent bowel sounds on auscultation
• Fever : > 102° F
• Signs of third spacing: falling urinary output, decreased skin
turgor, dry or sticky mucous membranes, increased
abdominal girth
NURSING DIAGNOSIS
• Acute pain related to inflammation, edema, distension of
pancreatic capsule and activation of pancreatic enzyme
• Ineffective breathing pattern related to severe pain, pulmonary
infiltrates , pleural effusion, atelectasis and elevated diaphragm
• Risk for deficient fluid volume related to vomiting, hyperglycemia,
and increased capillary permeability secondary to acute
pancreatitis
• Imbalanced nutrition less than body requirement related to
vomiting, NPO status and malabsorption secondary to pancreatitis
• Impaired skin integrity related to poor nutritional status, bed rest,
multiple drains, and surgical wound
CHOLECYSTITIS
Is the acute or chronic inflammation of the gallbladder. It
normally happens because a gallstone gets stuck at the
opening of the gallbladder. It can lead to fever, pain, nausea,
and severe complications.
Classification

• Calculous cholecystitis. In calculous cholecystitis, a

gallbladder stone obstructs bile outflow.
• Acalculous cholecystitis. Acalculous cholecystitis describes
acute inflammation in the absence of obstruction by
gallstones.
Pathophysiology
• Obstruction. Calculous cholecystitis occurs when a
gallbladder stone obstructs the bile outflow.
• Chemical reaction. Bile remaining in the gallbladder initiates a
chemical reaction; autolysis and edema occur.
• Compression. Blood vessels in the gallbladder compressed,
compromising its vascular supply.
Statistics and Incidences

• Although not all occurrences of cholecystitis are related

cholelithiasis, more than 90% of patients with acute
cholecystitis have gallstones.
• The acute form is most common during middle age.
• The chronic form usually occurs among elderly patients.
Causes

• Gallbladder stone. Cholecystitis is usually associated with gallstone

impacted in the cystic duct.
• Bacteria. Bacteria plays a minor role in cholecystitis; however,
secondary infection of bile occurs in approximately 50% of cases.
• Alterations in fluids and electrolytes. Acalculous cholecystitis is
speculated to be caused by alterations in fluids and electrolytes.
• Bile stasis. Bile stasis or the lack of gallbladder contraction also play
a role in the development of cholecystitis.
Causes
• Tumor. A tumor may prevent bile from draining out of gallbladder properly,
causing bile buildup that can lead to cholecystitis.
• Infection. AIDS and certain viral infections can trigger gallbladder
inflammation.
• Blood vessel problems. A very severe illness can damage blood vessels
and decrease blood flow to the gallbladder, leading to cholecystitis.
Clinical Manifestations
• Pain. Right upper quadrant pain occurs with cholecystitis.
• Leukocytosis. An increase in the WBC occurs because of the body’s
attempt to ward off pathogens.
• Fever. Fever occurs in response to the infection inside the body.
• Palpable gallbladder. The gallbladder becomes edematous as infection
progresses.
• Sepsis. Infection reaches the bloodstream and the body undergoes
sepsis.
Clinical Manifestations
• Murphy sign: A Murphy sign is a “catch” in the breath elicited by gently
pressing on the right upper quadrant and asking the patient to take a
deep breath. Patient will have pain during inhalation.
• Boas sign: Boas' or Boas sign is hyperesthesia (increased or altered
sensitivity) below the right scapula can be a symptom in acute
cholecystitis (inflammation of the gallbladder). Originally this sign
referred to point tenderness in the region to the right of the 9th to 11th
thoracic vertebrae.
• Mirrizi syndrome: defined as common hepatic duct obstruction caused
by extrinsic compression from an impacted stone in the cystic duct or
infundibulum of the gallbladder . Patients with Mirizzi syndrome can
present with jaundice, fever, and right upper quadrant pain.
Clinical Manifestations
• Charcot's cholangitis triad: is the combination of jaundice; fever, usually
with rigors; and right upper quadrant abdominal pain. It occurs as a
result of ascending cholangitis (an infection of the bile duct in the liver).
• Courvoisier's law (or courvoisier syndrome, or courvoisier's sign or
courvoisier-terrier's sign): states that in the presence of a palpable
enlarged gallbladder which is non-tender and accompanied with mild
painless jaundice, the cause is unlikely to be gallstones.
• Reynolds pentad: collection of signs and symptoms suggesting the
diagnosis obstructive ascending cholangitis, a serious infection of the
biliary system. It is a combination of Charcot's triad (right upper quadrant
pain, jaundice, and fever) with shock (low blood pressure, tachycardia)
and an altered mental status.
Complications
• Empyema. An empyema of the bladder develops if the
gallbladder becomes filled with purulent fluid.
• Gangrene. Gangrene develops because the tissues do not
receive enough oxygen and nourishment at all.
• Cholangitis. The infection progresses as it reaches the bile
duct.
Assessment and Diagnostic
• Biliary ultrasound: Reveals calculi, with gallbladder and/or bile duct
distension (frequently the initial diagnostic procedure).
• Oral cholecystography (OCG): Preferred method of visualizing general
appearance and function of gallbladder, including presence of filling
defects, structural defects, and/or stone in ducts/biliary tree. Can be done IV
(IVC) when nausea/vomiting prevent oral intake, when the gallbladder
cannot be visualized during OCG, or when symptoms persist following
cholecystectomy. IVC may also be done preoperatively to assess structure
and function of ducts, detect remaining stones after lithotripsy or
cholecystectomy, and/or to detect surgical complications. Dye can also be
injected via T-tube drain postoperatively.
Assessment and Diagnostic
• Endoscopic retrograde cholangiopancreatography (ERCP): Visualizes biliary
tree by cannulation of the common bile duct through the duodenum.
• Percutaneous transhepatic cholangiography (PTC): Fluoroscopic imaging
distinguishes between gallbladder disease and cancer of the pancreas
(when jaundice is present); supports the diagnosis of obstructive jaundice
and reveals calculi in ducts.
• Cholecystography (for chronic cholecystitis): Reveals stones in the biliary
system. Note: Contraindicated in acute cholecystitis because patient is too ill
to take the dye by mouth.
Assessment and Diagnostic
• Nonnuclear CT scan: May reveal gallbladder cysts, dilation of bile ducts, and
distinguish between obstructive/nonobstructive jaundice.
• Hepatobiliary (HIDA, PIPIDA) scan: May be done to confirm diagnosis of
cholecystitis, especially when barium studies are contraindicated. Scan may
be combined with cholecystokinin injection to demonstrate abnormal
gallbladder ejection.
• Abdominal x-ray films (multipositional): Radiopaque (calcified) gallstones
present in 10%–15% of cases; calcification of the wall or enlargement of the
gallbladder.
• Chest x-ray: Rule out respiratory causes of referred pain.
Assessment and Diagnostic
• CBC: Moderate leukocytosis (acute).
• Serum bilirubin and amylase: Elevated.
• Serum liver enzymes—AST; ALT; ALP; LDH: Slight elevation; alkaline
phosphatase and 5-nucleotidase are markedly elevated in biliary
obstruction.
• Prothrombin levels: Reduced when obstruction to the flow of bile into the
intestine decreases absorption of vitamin K.
• Ultrasonography. Ultrasound is the preferred initial imaging test for the
diagnosis of acute cholecystitis; scintigraphy is the preferred alternative.
• CT scan. CT scan is a secondary imaging test that can identify extra-biliary
disorders and acute complications of cholecystitis.
Assessment and Diagnostic
• MRI. Magnetic resonance imaging is also a possible secondary choice for
confirming a diagnosis of acute cholecystitis.
• Oral cholecystography. Preferred method of visualizing general appearance
and function of the gallbladder.
• Cholecystogram. Cholecystography reveals stones in the biliary system.
• Abdominal xray. Radiopaque or calcified gallstones present in 10% to 15% of
cases.
Medical Management
Management may involve controlling the signs and symptoms and the
inflammation of the gallbladder.
• Fasting. The patient may not be allowed to drink or eat at first in order to
take the stress off the inflamed gallbladder; IV fluids are prescribed to
provide temporary food for the cells.
• Supportive medical care. This may include restoration pf
hemodynamic stability and antibiotic coverage for gram-negative enteric
flora.
• Gallbladder stimulation. Daily stimulation of gallbladder contraction
with IV cholecystokinin may help prevent the formation of gallbladder
sludge in patients receiving TPN.
Pharmacologic Therapy
Antibiotic therapy. Levofloxacin and Metronidazole for prophylactic
antibiotic coverage against the most common organisms.
Promethazine or Prochlorperazine may control nausea and prevent fluid
and electrolyte disorders.
Oxycodone or Acetaminophen may control inflammatory signs and
symptoms and reduce pain.
Surgical Management
Cholecystectomy.
Cholecystectomy is most
commonly performed by using a
laparoscope and removing the
gallbladder.
Endoscopic retrograde
cholangiopancreatography
(ERCP). ERCP visualizes the biliary
tree by cannulation of the
common bile duct through the
duodenum.
Nursing Management

• Integumentary system. Assess skin and mucous membranes.

• Circulatory system. Assess peripheral pulses and capillary refill.
• Bleeding. Assess for unusual bleeding: oozing from injection sites, epistaxis,
bleeding gums, petechiae, ecchymosis, hematemesis, or melena.
• Gastrointestinal system. Assess for abdominal distension, frequent belching,
guarding, and reluctance to move.
Nursing Diagnosis

• Acute pain related to the inflammatory process.

• Risk for imbalanced nutrition related to self-imposed dietary restrictions
and pain.
Immunologic Disorders
Systemic Lupus Erythematosus

• is an autoimmune disease of the body's connective tissues.

• Autoimmune means that the immune system attacks the
tissues of the body.
• attacks parts of the cell nucleus.
• between the ages of 15 and 40, although it can show up at
any age.
Pathophysiology
• A healthy immune system produces proteins called antibodies and
specific cells called lymphocytes that help fight and destroy viruses,
bacteria, and other foreign substances that invade the body.
• In lupus, the immune system produces antibodies against the body's
healthy cells and tissues.
• These antibodies, contribute to the inflammation of various parts of the
body and can cause damage to organs and tissues.
• Lupus can affect -joints, skin, kidneys, heart, lungs, blood vessels, and
brain.
Causes
• The exact causes is not known.
• Inherited genes, viruses, ultraviolet light, and drugs may all play some role.
• Genetic factors increase the tendency of developing autoimmune diseases
• female hormones play an important role in the expression of SLE.
• a key enzyme's failure to dispose of dying cells may contribute the
development of SLE.
• a genetic mutation
• Drug-induced lupus. ( hydralazine, beta- blokers, isoniazid) .
Diagnostic test
• Complete history
• Physical examination
• Blood tests
Typical symptoms include: fever, fatigue,
weight loss, arthritis, pleurisy and pericarditis.
Systemic Lupus Erythematosus

Drug – induced SLE

is caused by certain medications
like hydralazine, procainamide,
isoniazid, chlorpromazine, and
some antiseizure medications
Clinical Manifestations
• Skin manifestations – usually acute
cutaneous lesion consisting of
butterfly-shaped rash across the
bridge of the nose and the cheeks.
• Cardiac – commonly pericarditis
• Atherosclerosis
• Renal – kidney failure
• CNS – changes in behavior and
cognition, depression and
psychosis
Medical Management
Corticosteroids
✔single most important medication
Anti-malarial drugs
✔For cutaneous, musculoskeletal and
mild systemic features of SLE
NSAIDs
✔For minor clinical manifestations
Nursing Responsibilities

• Reduce fatigue
• Promote skin integrity
• Enhance body image
Patient education – to understand the need for routine periodic
screenings, medication, early recognition of complications
Acute Glomerulonephritis

• Acute glomerulonephritis is an immune – mediated

inflammatory disease of the capillary loops in the renal
glomeruli. The antigen – antibody complex deposition within
the glomeruli results in glomerular injury which is manifested as
hematuria, oliguria, edema and hypertension.
Etiology
✔Presumed cause – antigen – antibody reaction secondary to an infection
in the body.
✔Initial infection:
Usually either an upper respiratory infection or a skin infection, usually one to
3 weeks before the onset of symptoms
Most frequent causative agent – nephritogenic strains of group - A beta –
hemolytic streptococcus (type 12), acute post – streptococcal
glomerulonephritis (APSGN) is the most common.
Clinical manifestations
• Urinary symptoms:
Decreased urine output
bloody or brown – colored urine.
• Oedema:
Present in most patients Usually mild.
Often manifested by Periorbital oedema in the morning
May appear only as rapid weight gain.
May be generalized and influenced by posture.
Clinical manifestations
• Hypertension:
Present in over 50 per cent of patients.
Usually mild.
Rise in blood pressure may be sudden.
Usually appears during the first four to five days of the illness.
• Malaise
• Mild headache
Clinical manifestations
Gastrointestinal disturbances, especially anorexia and vomiting,
often with abdominal and long pain.
Pallor
Irritability
Lethargy
Dysuria
Fever
Diagnosis

• History of illness and physical examination help in clinical diagnosis.

The confirmation of diagnosis is done by the following:
• Urine examination:
It shows increased specific gravity, smoke dirty brown colour urine with
reduced total amount in 24 hrs. Mild to moderate or severe albuminuria is
detected. Microscopic examination reveals presence of red cells, WBCs, pus
cells, epithelial cells and granular cast. Proteinuria (3+ to 4+)
Diagnosis
• Blood examination:
Blood examination demonstrates increased level of urea, creatine, ESR, ASO
titer and anti – DNAase ‘B’. There is decreased level of Hb%, serum
complement and albumin in blood. Hyponatremia and hyperkalemia may
occur in persistent oliguria.
• Throat swab culture:
• Throat swab culture may show presence of beta – hemolyticus
streptococcus in some children.
• Chest X-ray:
It may show pulmonary congestion
Complications
• Hypertensive encephalopathy
• Congestive heart failure
Cardiac failure may occur due to persistent hypertension, hypervolemia
and peripheral vasoconstriction.
• Uremia
Acidosis
• Anemia
• Renal failure
Management
• AGN with impaired renal function as severe oliguria and
azotemia needs hospitalization for special attention. Mild
oliguria patients with normal blood pressure can be managed
at home with OPD – based treatment.
• Treatment is essentially symptomatic
• Monitoring:
The patient should be monitored closely for the presence of
hematuria, decreased urinary output, and signs of volume
overload like edema, hypertension and congestive heart failure.
Management
• Daily record the general condition, edema, consciousness level,
weight, heart rate, respiratory rate, blood pressure, fluid intake
and urinary output.
The kidney function tests must be monitored at regular intervals.
• Bed rest:
It is rarely indicated except during the acute phase when
complications of acute renal failure may be present.
Protect the child from fatigue and contact with other respiratory
infections.
Management

• Position:
In congestive heart failure or hypertension, make the patient lie in
a propped up position and provide oxygen.
• Diet:
Diet should be arranged with restriction of protein, salt and fluid
intake, till oliguria and increased blood urea level persist.
Carbohydrate containing food to be allowed freely.
Management

The diet of the patient need not be restricted routinely.

Fluid intake should be allowed in a calculated amount (i.e., total
amount of previous day urine output in 24 hrs plus insensible losses
to be allowed to drink on that day).
Daily weight recording is important to assess the increase and
decrease of edema.
Management

Diuretics are of limited value when severe renal failure is not

severe, diuretic therapy (usually furosemide
{lasix} is helpful if significant edema and fluid overload are
present.
Rarely, children with AGN develop ARF with oliguria that
significantly alters the fluid and electrolyte balance.
Fluid restriction is needed in case of acute renal failure when urine
output is diminished.
Management

• Hypertension:
Acute hypertension must be anticipated and identified early.
Blood pressure measurements are taken every 4 to 6 hrs.
Significant but not severe hypertension is controlled with loop
diuretics.
Other antihypertensive drugs, such as calcium channel blockers,
beta blockers, or angiotensin – converting enzyme inhibitors, may
be needed in severe cases.
Management
• Dialysis:
May be required in patient with severe and prolonged oliguria or
anuria, and renal failure.
• Penicillin:
Administered of antibiotic (preferably Penicillin) is needed for 7 to
10 days to eradicate streptococci in the throat or skin.
Anti hypertensive (nifedipine, atenolol) and diuretics are used to
control hypertension and its consequences.
Management
Magnesium sulphate may be prescribed in the encephalopathy
to reduce cerebral edema.
Sedatives (diazepam) may be required in restless patients.
Management of complication like CCF, hypertensive
encephalopathy, etc should be done promptly to prevent life
threatening outcome. Dopamine infusion, steroid therapy and
respiratory support may require for some patients.
Nursing diagnosis
• Impaired urinary elimination related to glomerular dysfunction.
• Infection related to group A beta- hemolytic streptococcus pharyngitis, upper
respiratory infection.
• Fluid volume excess related to altered renal function (or) diminished glomerular
filtration increased Na+ retention.
• Activity intolerance related to edema.
• Altered skin integrity related to edema
• Altered nutritional, less than body requirement, related to albuminuria and GI
disturbances.
• Fear and anxiety related to disease processes.
• High risk for seizure activity related to hypertensive encephalopathy.
• Knowledge deficit regarding care of the child with renal disease and continuation
of care at home.
Diabetes Mellitus Type 1
Often referred to as type 1 diabetes, is a chronic autoimmune
disorder that affects the body’s ability to produce insulin. Unlike
type 2 diabetes, which is linked to insulin resistance, type 1
diabetes occurs when the immune system mistakenly attacks
and destroys the insulin-producing beta cells in the pancreas.
This results in an absolute deficiency of insulin, leading to high
levels of glucose in the bloodstream.
Clinical Manifestations
Clinical Manifestations
• Hyperglycemia
• Glycosuria
• Polydipsia
• Polyuria
• Polyphagia
• Weight loss
• Nonspecific malaise
• Diabetic ketoacidosis (DKA). DKA is characterized by drowsiness, dry skin,
flushed cheeks, and cherry-red lips, acetone breath with a fruity smell, and
Kussmaul breathing.
Assessment and Diagnostic
• Fingerstick glucose test
• Urine dipstick test
• Fasting blood sugar (FBS) (FBS result of 200 mg/dl or higher)
• Lipid profile
• Glycated hemoglobin
• Microalbuminuria
Medical Management
• Insulin therapy
• Diet
• Activity
• Continuous glucose monitoring
Nursing Assessment
• History
Weight loss or weight Gain, evidence of polyuria, polydipsia, dehydration,
and fatigue.
• Physical exam
Measure the height and weight and examine the skin for evidence of
dryness or slowly healing sores; note signs of hyperglycemia, record vital
signs, and collect a urine specimen; perform a blood glucose level
determination using a bedside glucose monitor.
Nursing diagnoses
• Imbalanced nutrition: less than body requirements related to insufficient
caloric intake to meet growth and development needs and the inability of
the body to use nutrients.
• Risk for impaired skin integrity related to slow healing process and
decreased circulation.
• Risk for infection related to elevated glucose levels.
• Deficient knowledge related to complications of hypoglycemia and
hyperglycemia.
• Deficient knowledge related to appropriate exercise and activity.
Rheumatoid Arthritis

• Rheumatoid arthritis is
autoimmune disorder in
which Immune system
identifies the synovial
membrane as "foreign" and
begins attacking
Rheumatoid Arthritis

• Females > males 3:1

• but people of any age can be
affected
• Peak age 45-65 but onset early
from age 20-45yrs
• About 75% of these are women.
• The disease strikes women three
times more
• often than men
Risk factors
• Idiopathic
• Positive family history
• Inherited tissue type major histocompatibility complex (MHC) antigen
• Smoking
• Bacterial and Fungal Infection
• Herpes simplex virus infections
• Epstein-Barr virus (EBV)
• Vitamin D deficiency
 Sign and Symptoms
• The joints of the hands are often
the very first joints affected by
rheumatoid arthritis. These joints
are swollen red and tender
when squeezed.
• Swelling due to synovitis
 Sign and Symptoms
• Joint pain. One of the classic signs, joints that are painful are not easily moved.
• Swelling. Limitation in function occurs as a result of swollen joints.
• Warmth. There is warmth in the affected joint and upon palpation, the joints are
spongy or boggy.
• Erythema. Redness of the affected area is a sign of inflammation.
• Lack of function. Because of the pain, mobilizing the affected area has limitations.
• Deformities. Deformities of the hands and feet may be caused by misalignment
resulting in swelling.
• Rheumatoid nodules. Rheumatoid nodules may be noted in patients with more
advanced RA, and they are nontender and movable in the subcutaneous tissue.
Diagnosis
• X rays
• MRI
• Ultrasounds
• Blood test
Rheumatoid Factor (RF)
RF is a specific antibody in the blood.
A negative RF does not rule out RA. The arthritis is then called seronegative,
most common during the first year of illness and converting to seropositive status
over time.
Diagnosis
Anti-citrullinated Protein Antibodies (ACPAs)
Like RF, this testing is only positive in a proportion of all RA cases.
Unlike RF, this test is rarely found positive if RA is NOT present, giving it a specificity
of about 95%.
• Other blood tests performed when RA is suspected:
Erythrocyte Sedimentation Rate (ESR)
The rate at which red blood cells precipitate in a 1 hour period.
C-Reactive Protein
A protein found in the blood in response to inflammation.
Medical Management
Early Rheumatoid Arthritis
• NSAIDs. COX-2 medications block the enzyme involved in inflammation
while leaving intact the enzyme involved in protecting the stomach lining.
• Methotrexate. Methotrexate is currently the standard treatment of RA
because of its success in preventing both joint destruction and long-term
disability.
• Analgesics. Additional analgesia may be prescribed for periods of
extreme pain.
Medical Management
Moderate, Erosive Rheumatoid Arthritis
Cyclosporine. Neoral, an immunosuppressant is added to enhance the
disease modifying effect of methotrexate.

Persistent, Erosive Rheumatoid Arthritis

Corticosteroids. Systemic corticosteroids are used when the patient has
unremitting inflammation and pain or needs a “bridging” medication while
waiting for slower DMARDs to begin taking effect.
Medical Management
Advanced, Unremitting Rheumatoid Arthritis
Immunosuppressants. Immunosuppressive agents are prescribed because of
their ability to affect the production of antibodies at the cellular level.
Antidepressants. For most patients with RA, depression and sleep deprivation
may require the short-term use of low-dose antidepressants such as
amitriptyline, paroxetine, or sertraline, to reestablish an adequate sleep
pattern and to manage chronic pain.
Surgical Management
• Reconstructive surgery. Reconstructive surgery is indicated when pain
cannot be relieved by conservative measures and the threat of loss of
independence is eminent.
• Synovectomy. Synovectomy is the excision of the synovial membrane.
• Tenorrhaphy. Tenorrhaphy is the suturing of a tendon.
• Arthrodesis. Arthrodesis is the surgical fusion of the joint.
• Arthroplasty. Arthroplasty is the surgical repair and replacement of the
joint.
Nursing assessment
• History and physical exam. The history and physical examination address
manifestations such as bilateral and symmetric stiffness, tenderness,
swelling, and temperature changes in the joints.

• Extra-articular changes. The patient is also assessed for extra-articular

changes and these include weight loss, sensory changes, lymph node
enlargement, and fatigue.
Nursing Diagnosis
• Acute and chronic pain related to inflammation and
increased disease activity, tissue damage, fatigue, or lowered
tolerance level.
• Fatigue related to increased disease activity, pain,
inadequate sleep/rest, deconditioning, inadequate nutrition,
and emotional stress/depression
• Impaired physical mobility related to decreased range of
motion, muscle weakness, pain on movement, limited
endurance, lack or improper use of ambulatory devices.
Nursing Diagnosis
• Self-care deficit related to contractures, fatigue, or loss of
motion.
• Disturbed body image related to physical and psychological
changes and dependency imposed by chronic illness.
• Ineffective coping related to actual or perceived lifestyle or
role changes.