Chronic Inflammatory Bowel Disease

Chronic Inflammatory Bowel Disease

Ulcerative Colitis chronic inflammatory disease of the rectum and colon may lead to ulcerations and cause bleeding causes: unknown, possibly related to infectious

process, stress, food allergies occurs in adolescents, young adults (20-40 y.o)

S/SX: profuse watery diarrhea (20 stools / day) containing

blood, mucus and pus cramping pain at R lower quadrant, flatulence w/

eating electrolyte loss may lead to metabolic acidosis

Diagnostic test : x-ray, sigmoidoscopy, colonoscopy, occult blood in the stool, fecalysis – pus, mucus

Ulcerative Colitis

Regional Enteritis (Crohn’s disease)non-specific inflammation of the small bowel, usually the terminal ileum,chac. by cobble stone-like ulcerations along the mucosa, with thickening of intestinal wall and formation of scar tissue

S/SX : severe abdominal pain, cramps (RLQ) mild diarrhea (semi-formed stool) WBC, fever, anorexia, malaise, wt. loss may lead to fistula formation or intestinal obstruction long history of diarrhea dehydration a mass can be felt in the area of the appendix and cecum

Complications: perforation, polyps, fistula, strictures

Chronic Inflammatory Bowel Disease

Chronic Inflammatory Bowel Disease

Management: place on NPO during acute stage, IV fluids, TPN Diet:

protein, calorie, bland, low residue diet avoid whole grain, nuts, raw fruits except banana, excess milk, raw vegetables, tough meats, fried or highly seasoned meats avoid gas-producing or irritating foods and milk products small, frequent feedings Vit. supplements (A,D,E,K) avoid too hot, too cold foods

fluid intake (3L/day) promote bed rest ( intestinal motility), quiet, comfortable stress-free environment antibiotics for infection anticholinergics, antidiarrheals - gastric motility and cramping keep perianal skin clean and dry, proper hygiene

Management of Chronic Inflammatory Bowel Disease

Diverticulum

Diverticulosis / DiverticulitisDiverticulum – outpouching or formation of sacs in the musculature of the intestineDiverticulosis – the condition of being afflicted with diverticulumDiverticulitis – inflammation of the diverticulum

most common in the sigmoid colon

Risk factors : diet low in fiber and high in refined and processed foods

age (over 40 yrs.) chronic constipation

S/Sx: crampy pain in left lower quadrant of the abdomen constipation, alternating with diarrhea fever WBC

Diagnostic Test – barium enema

Management :

acute episodes : NPO, antibiotics, IV fluids, low fiber, low residue diet

ongoing care : high fiber, high-roughage diet, laxatives, anti-spasmodics

surgery : bowel resection with or without temporary colostomy

keep pt. on NPO until pain subsides then liquid diet keep on bed rest to intestinal motility observe for complications of perforation or

peritonitis

Diverticulosis / Diverticulitis

Diverticulosis / Diverticulitis

Measures to control divertoculosis:1.High fiber diet – fruits, raw vegetables, whole wheat, cereals2.Take stool softeners – metamucil3. stress in lifestyle

.4daily fluid intake5.Avoid activities that intraabdominal pressure6.Avoid nuts, fruits and vegetables w/ seeds to prevent seeds from lodging in the intestinal pouches and causing infection

Hernia a protrusion of an organ or structure from its normal cavity through a congenital or acquired defect or opening a hernia may contain peritoneal fat, a loop of intestine, a section of a bladder or a portion of the stomach

Reducible hernia if the protruding structure or organ can be returned by manipulation back to its own cavity

Irreducible hernia or incarcerated hernia when the protruding structure is stuck and cannot be returned

Strangulated hernia when the blood supply to the structure w/in the hernia becomes occluded necrosis and gangrene if intestines are involved lead to intestinal obstruction

Causes and Risk Factors1. Defect in the integrity of the muscular wall

A. CongenitalB. Weak muscle strength

- obese & malnourished patientsC. Injury or trauma D. Aging - muscle tissue infiltrated with

fatty & connective tissue

2. Increase Intra-abdominal PressureA. ObesityB. Frequent heavy liftingC. Frequent straining

- urinary flow obstruction- constipation

D. Chronic “coughers” - asthmatic patients

- chronic bronchitis

A. ObesityB. Frequent heavy liftingC. Frequent straining

- urinary flow obstruction- constipation

D. Chronic “coughers”- asthmatic patients- chronic bronchitis

Types of HerniaIndirect inguinal hernia

when a loop of the intestine passes through the abdominal ring to the inguinal canalcaused by in intraabdominal pressure w/c forces the intestines to be pushed into a congenital defect failure of the processus vaginalis to close during fetal development

Direct inguinal herniaone that passes through the posterior inguinal wall in an area of muscular weaknesscaused by intraabdominal pressure against a weak posterior inguinal wallmore common in men, more difficult to repair

Femoral hernia the loop of intestine passes through the femoral ring and down the femoral canal due to congenital weakness of femoral ring muscleappears as a round bulge below the inguinal ligamentmore common in women, high incidence of strangulated hernia

Types of Hernia

Umbilical herniawhen a loop of intestine passes through the umbilical ringcaused by failure of the umbilicus to close at birth or by a defect in the umbilical scar, which opens in adult life when there is intraabdominal pressure such as in pregnancy, intestinal obstruction, chronic cough

Incisional hernia one that occurs through an old surgical incisioncaused by the failure of the resected and approximated muscles and fascial tissues to heal properly because of wound infections, drains or poor physical condition intraabdominal pressure push the organ or tissue through the weakened scar

Incisional Hernia

Clinical Manifestations lump, bulge, or mass in the groin, around the umbilicus or

protruding from an old surgical incision swelling that appears after coughing, straining, lifting or other

vigorous exertion palpation of the hernia will reveal soft and nodular or smooth

edges the swelling may disappear when the person lies down and

reappear on standing or coughing strangulated hernia – may cause severe pain and symptoms of

intestinal obstruction such as nausea, vomiting and distention

Medical Management Surgery – Herniorrhaphy – the herniating tissues are returned to

the abdominal cavity and the defect in the fascia or muscle is closed with sutures

Strangulated hernia resection of the area of gangrene and do anastomosis

Hernia

HerniaNsg. Management:Post-operative nursing care

give food or fluids as tolerated monitor post-op urinary elimination apply ice bags if scrotal edema occurs

Patient teaching: report any early signs of wound infection (redness,

discomfort) that may weaken the surgical repair any post-operative echymosis will disappear in a few

days sexual functioning is not affected by surgery restrict driving for 2 weeks avoid heavy lifting, pulling or pushing for 6 weeks

Hemorrhoids/ Anal FissureHemorrhoids : dilated veins under the mucous membranes in the anal area, may either be internal or externalAnal fissure : linear ulceration on the margin of the anus

Predisposing factors : straining at stool – constipation pregnancy portal hypertension congestive heart failure

Complications: − bleeding - strangulation− thrombosis - infection

S/Sx : pain and pruritus around the anus abdominal distention - urinary retention blood in stool

GRADE I - bleeding on defecation, - no prolapse

GRADE II – there’s prolapse but reduce spontaneously

GRADE III – with prolapse and reduced manually

GRADE IV – cannot be reduced, incarcerated

Management

ointment / suppositories to shrink hemorrhagewarm sitz bathsurgery – hemorrhoidectomy : excision of dilated veins fissurectomy : excision of fissureprovide analgesics for pain relief, ice packs or warm compressgive low-residue, soft diet as tolerated for 1st week post-op then include vegetable and fruitsforce fluids 2,500-3,000 ml / daywatch out for symptoms of anal stricture ( pain with BM, difficulty passing stool) and report to physician

Health Teachings

B. Drink 6-8 glasses of water per dayC. Regular exercise

walking, swimming

1. EASING CONSTIPATION

A. Eat more high fiber foodcerealsvegetablesfresh fruits, prune juice

D. May take over the counter fiber

supplement- fibrosine- metamucil

2. DEVELOP GOOD BOWEL HABITS

A. Sit on the toilet only as long as necessary

A. Avoid straining – prevent irritation that leads to swelling

C. Use the toilet at a fixed time – like when you wake up

3. AVOID FOODS WHICH COULD CAUSE LOCAL IRRITATION

A. Spicy foodB. Alcohol

4. TRY TO AVOID LIFTING HEAVY WEIGHTS

Intestinal Obstruction90% of bowel obstructions occur in the small bowel, esp. in the ileum, - narrowest segmenthas a high mortality rate if not diagnosed and treated w/in 24 hrs.

Etiology and Risk factors:A. Mechanical Factors 1. Adhesions

most common cause may form after abdominal surgery fibrous bands of scar tissue can become looped over a

portion of the bowel the presence of multiple adhesions increases the risk of

obstruction

Etiology and Risk factors (cont.)

2. Hernia an incarcerated hernia may or may not cause obstruction,

depending on the size of the hernial ring a strangulated hernia is always obstructed bec. the bowel

cannot function when its blood supply is cut off3. Volvulus

twisting of the bowel 180o twist can cause obstruction and ischemia infarction of the

bowel4. Intussusception

is a telescoping of the bowel (slipping of a section of bowel into an adjacent section)

often associated w/ a tumor of the large bowel5. Cancer

chief cause of obstruction in the large bowel

Etiology and Risk factors (cont.)B. Neurogenic Factor Paralytic Ileus – lack of peristaltic activity

- prevents forward flow of intestinal contents- commonly occurs after abdominal surgery

C. Vascular Factors - when the blood supply to any part of the body is interrupted, the part ceases to function 1. Complete occlusion ( Mesenteric infarction) Mesenteric thrombosis

- usual cause is an embolus- causes intense abdominal pain –-- due to ischemia bowel

necrosis and gangrene and sepsis

- other s/sx: fever, WBC, signs of shock- surgical intervention must be done immediately

2. Partial occlusion (Abdominal angina)- usually results from atherosclerosis of the mesenteric arteries- pain develop 15-30 mins after eating - need for O2- manifestation arise when interruption in blood flow/supply is

sufficient to compromise bowel function

Pathophysiology

Normally 7-8 liters of electrolyte-rich fluids is secreted by the bowel, and most of the fluid is reabsorbed bowel obstruction this fluid is partially retained w/in the bowel and partially eliminated by vomiting severe in circulating blood volume

hypotension, hypovolemic

shock, renal blood flow (oliguria), cerebral blood flow

(LOC)Fluids and air collect proximal to the site of obstruction distentionDistension causes a temporary in peristalsis as the bowel attempts to force the material through the obstructed areaAfter a few hours --- the bowel becomes flaccidGreater pressure w/in the bowel reduces its absorptive ability, fluid retention in the bowel

Pathophysiology (cont.)

The bowel wall becomes permeable to bacteria and bowel organisms enter the peritoneal cavity peritonitis and infection

pressure in the bowel wall, slows arterial blood flow and blood supply necrosis, sepsis, perforation and peritonitis

Bacterial proliferation in the strangulated or necrotic bowel

release of endotoxins into the peritoneal cavity & systemic circulation

Septic Shock and Death

Clinical Manifestations

4 Cardinal Signs of Complete Small Bowel Obstruction1.Abdominal pain2.Vomiting3.Absolute constipation4.Distention

Severe distention may raise the diaphragm inhibit respiration Hypoxia and Dyspnea

At first, vomitus is semidigested food and chyme, later becomes watery and contains bile. Finally, the client vomits dark fecal material

Signs of dehydration and hypovolemic shock Electrolyte imbalances (Na, K, Cl) and metabolic acidosis Signs of peritonitis – rigid abdomen, fever, bowel sounds

Interventions

Surgery – to relieve the obstruction, remove the ischemic bowel and establish patency

type of surgery depends on the type of obstruction and location- bowel resection, colostomy, ileostomy

Nursing Interventions: replace fluids and electrolytes (IV w/ NaCl, K, NaHCO3) an NGT is inserted and attached to suction to relieve the

vomiting and distention (GI decompression) Assess and measure emesis and drainage from NGT

(document color, odor, consistency and volume)

Interventions (cont.)

monitor VS closely and WOF signs of shock monitor UO < 30 ml/hr. hypovolemia inform MD if distention occurs during post-op period report signs of paralytic ileus post-op semi-fowler’s position, deep breathing, coughing, turn to

sides administer antibiotics as ordered emotional care comfort measures (oral care)

Cancer of the Colon 70% of cases occur in the rectosigmoid area

Risk Factors: Age > 50, family history of cancer history of ulcerative colitis, polyps Diet - fat, food additives, low-fiber chronic constipation

S/Sx: constipation, blood in stool vague-dull pain anorexia, wt. loss, weakness, anemia signs of obstruction hemorrhage, perforation

Dx:rectal exam (palpable tumor) - sigmoidoscopy, colonoscopy - barium enema - stool exam for occult blood

Management : surgery : colon resection, colectomy, colostomy : abdomino-perineal resection (removal of anus and rectum) with a permanent colostomy Radiation therapy Chemotherapy

Duke’s Classification of Colorectal Cancer

Stage A: confined to bowel mucosa- 5 year survival

rate

Stage B: invading muscle wall

Stage C: lymph node involvement

Stage D: metastases

Surgeries for Colorectal CancerRight Hemicolectomy

Resection or removal of ascending colon and hepatic flexure Ileum is anastomosed (connected) to the transverse colon

Left Hemicolectomy Resection of splenic flexure, descending colon and sigmoid colon Transverse colon is anastomosed to the rectum

Anterior Rectosigmoid Resection Resection of part of descending colon, the sigmoid colon, and

upper rectum Descending colon anastomosed to remaining rectum

Abdominoperineal Resection Resection of sigmoid colon and rectum Proximal end of descending colon is brought out through the

abdominal wall to form a permanent colostomy

Obstruction or perforation of the colon usually requires a temporary colostomy, followed later by closure of the colostomy

Nursing Care of Patient Experiencing Bowel Surgery

Pre-operative Care1.Preventing infection

a. give low-residue diet several days before surgeryb. give clear liquids on day prior to surgeryc. give prescribed antibioticsd. give prescribed enema and laxatives

2. Teachinga. describe deep-breathing and coughing exercisesb. explain use of siderails to facilitate turning in bed w/o

exerting pull on abdomen

Nursing Care of Patient Experiencing Bowel Surgery

Post-operative care1.Promoting oxygenation

a. encourage turning and deep breathing exercisesb. encourage pt to be active

2.Maintaining fluid and electrolyte balancea. maintain patency of NGT tube & record amount of drainage

accuratelyb. maintain prescribed flow of IV fluidsc. monitor for signs of fluid deficit (dry skin & mucous

membranes, decreased skin turgor)

Post-operative Care (cont.)

3. Promoting eliminationa. monitor for signs of returning peristalsis (passage of flatus,

bowel sounds)b. encourage ambulationc. monitor character of initial stool

4. Promoting comforta. give good oral hygiene until oral fluids are taken freelyb. give analgesics on a fairly regular basis during the 1st 48 hrs to

prevent severe pain5. Teaching

a. drink at least 2000 ml of fluid daily to avoid constipationb. avoid use of laxatives without medical approval—stool

softeners or metamucil may be used c. drink prune juice or fruit juices dailyd. avoid heavy lifting for at least 6 weeks after surgery

Colostomy Care:

a. skin care- use of effective skin barriers or wafers to prevent skin irritation; cleanse with mild soap and water using cotton cloth

b. odor control- avoid foods known to cause odor; dairy products, fish, eggs, and cabbage; use of pulverized charcoal, sodium bicarbonate, deodorant tablet

c. control of gas-avoid carbonated beverages and gas forming foods

d. diet- avoid overeating; chew food thoroughly; prevent diarrhea or constipation

e. colostomy irrigation- to stimulate peristalsis; to establish a regular pattern of evacuation

Functions of the Liver1. Carbohydrate, protein, fat metabolisma.Carbohydrate metabolism

1) glycogen formation (glycogenesis) and storage glycogen – the form of glucose that can be stored by the body –

when there is excess glucose intake

b. Protein Metabolism1) Convert protein to glucose – when there is carbohydrate intake

(protein catabolism)2) Protein synthesis- produce the following plasma proteins:

albumin – responsible for maintaining colloid oncotic pressure Alpha & beta globulins (immunoglobulins) clotting factors I, II, V, VII, IX, X C – reactive protein and enzymes Transferrin

3) formation of needed amino acids (transamination)

2) glucose formation – where there is glucose intake glycogen is broken down to glucose (glycogenolysis) new glucose is formed from amino acids, lactic acids and glycerol

(gluconegenesis)

c. Fat metabolism1) Oxidation of fatty acids for energy2) Ketone formation – by-product of fat metabolism 3) synthesis of cholesterol and phospholipids4) formation of triglycerides from dietary lipids, and excessive

dietary carbohydrates & proteins (lipogenesis)5) formation of lipoproteins

2. Production of Bile Salts Bile – water, cholesterol, phospholipids, bile salts, bile pigment (bilirubin) protein & electrolytes, metabolites of drugs that need to be excreted Bile Salts – necessary for breakdown & absorption of fats, cholesterol and fat–soluble vitaminsliver secretes 700 ml. of bile daily

Functions of the Liver(cont.)

Functions of the Liver(cont.)3. Bilirubin Metabolism

Hemoglobin

Globin Heme

Iron Protoporphyrin

indirect or converted by liver enzymeunconjugated bilirubin glucoronyl transferase(fat-soluble, cannot be excreted by the kidneys) direct or conjugated

bilirubin (water soluble)

secreted in the bile to the

duodenumreabsorbed by the liver

bilirubin metabolized to urobilinogen

excreted into the urine (by bacterial action)

excreted into the feces as stercobilin

Functions of the Liver(cont.)4. Detoxification of endogenous and exogenous substances

1. Ammonia – a major toxic product produced by bacteria in the GIT and also produced by the liver from deamination or removal of amino group (NH2) from amino acids - ammonia is detoxified by conversion to urea – which is

excreted by the kidneys2. steroid hormones – (estrogen, progesterone, testosterone,

cortisone, aldosterone) - are in activated by the liver when there is increased

production3. Drugs

are detoxified by the liver barbiturates, sedatives are inactivated by the liver prevent toxicity of drugs

5. Storage of Minerals and Vitamins Vit. A, D, B12, E, K Iron in the form of ferritin is stored to resupply iron for hemoglobin

formation copper

6. Reservoir of blood when venous blood volume increase and cannot be handled by the

right side of the heart – excess blood can accumulate in the liver

7. Remove bacteria, damaged RBC, other foreign substances from the blood by phagocytosis -Kupffer cells (macrophages that stay in the liver)

Functions of the Liver(cont.)

Gallbladder is a saclike organ that lies on the inferior surface of the liver primary function is to store and concentrate bile between meals bile flows from the liver through the hepatic duct cystic duct gallbladder mucosa of the gallbladder wall readily

absorbs water and electrolytes, leaving a high concentration of bile salts, bilirubin and cholesterol (90 ml. of bile)

within 30mins. after eating presence of fat molecules in the duodenum stimulate release of hormone cholecystokinin stimulate contraction of the gallbladder and the Sphincter of Oddi relaxes forcing bile into the duodenum

Diagnostic Tests1. UTZ of the liver

to identify hepatic tumor, hematoma, abscesses identify the cause of jaundice preparation of the pt.: NPO 8-12 hours before the procedure

2. CT Scan of the Abdomen place pt. on NPO 8-12 hours before the procedure if contrast medium is to be used – assess allergies to iodine

3. Biopsy of the Liver to determine the cause of liver disease a needle is inserted through the chest or abdomen into the liver

and a small piece of tissue is removed for study Vit. K IV may be given for several days before procedure to

prevent bleeding instruct client to hold his breath and remain still and do not move

to prevent the needle to slip and tear the liver covering

Diagnostic Tests (cont.)3. Liver Biopsy (cont.)

NPO 6 hours before procedure, a sedative is given 30mins. before procedure

CT scan or UTZ guided needle biopsy 8th or 9th intercostal space - usual area of biopsy

After procedure: monitor PR, BP, RR q 30 mins. then hourly for 24 hours.

monitor for bleeding in the biopsy site advise pt. to lie on the R side with small pillow or blanket under

the costal margin place pt. on CBR for 24 hours after the test

4. Paracentesis or peritoneal tap to remove peritoneal fluid for lab. test or to drain large volumes of

ascitic fluid when there is resp. distress, cardiac dysfunction, severe abdominal discomfort

maintain sterile technique have the pt. void before procedure to prevent puncture of bladder obtain consent monitor v.s. urine output, monitor for bleeding

Liver Abscess may result from a variety of organisms including E. coli,

staphylococcus, streptococcus, Pseudomonas, Proteus, and Klebsiella, Entamoeba histolytica (Amoebiasis)

may also occur in pts. with decreased immune function such as in leukemia, neutropenia

Pathophysiology abscesses can occur as either singular large abscess or multiple

small abscesses the organisms originate in various areas of the body & reach

the liver through the biliary tract, vascular or lymphatic system the organisms may also be introduced by penetrating injuries to

the liver lead to liver tissue destruction and abscess (pus) formation

disrupt hepatic function If untreated, they continue to in size and can perforate into

the peritoneal cavity (peritonitis) or pleural cavity

Liver Abscess (cont.)S/sx: – caused by the infectious process

fever , temp 38.8 – 410c , chills cough, difficulty breathing diaphoresis right upper abdominal quadrant pain and tenderness anorexia, nausea, vomiting, wt. loss signs of peritonitis - board-like abdomen, distention of abdomen altered hepatic function: hepatomegaly, jaundice & pruritus,

splenomegaly, abdominal distention, ascites Amoebiasis – bloody, mucoid diarrhea, abdominal pain, rectal

tenesmus, dehydration, hypotension

Diagnostic Tests leukocytosis, ESR – due to infection serum alkaline phosphatase, SGOT, SGPT bilirubin (hyperbilirubinemia) UTZ, CT scan

Liver Abscess (cont.)Medical Mgt.

supportive measure – F & E replacement and control of temp. elevation

surgical drainage of abscess and antibiotics Metronidazole (Flagyl), Chloroquine, Emetine for amoebic

abscesses Nursing Mgt.

provide adequate fluids and nutrition provide comfort measures for fever, pruritus - coal sponge baths - prevention of dry skin - use of soft linens - provide cool environment frequent oral hygiene pt. education

complete dose of medications (several weeks to months) to prevent recurrence

monitor for signs of recurrence or worsening hepatic function cirrhosis

proper hygiene, drink clean water and avoid uncooked foods

Liver TumorsPrimary Hepatic Carcinoma

may arise w/in the liver cell (hepatocellular) or the bile duct cell (cholangiocellular)

chronic liver disease from Hepatitis B or cirrhosis may predispose individuals to primary liver cancer

Metastatic Tumor of the Liver more common than primary tumor cancer cells may come from the GIT, lungs, breasts, kidneys and

melanomas of the skinPathophysiology

Cancer cells compress the surrounding normal liver cells and may spread by invading the portal veins

cause hemorrhage by extension into the vascular tissue of the liver

cause necrosis – by depriving normal hepatic tissue of adequate circulation

Tend to grow rapidly and metastasize to the lungs, spleen, kidney, pancreas, adrenal glands

Liver Tumors (cont.)S/Sx:

depends on the extent of tumor growth, hepatocellular damage, and liver failure

enlarge R upper quadrant masses, hepatomegaly, epigastric fullness, pain or discomfort

wt. loss, abnormal liver function tests, weakness ascites, hepatic failure, jaundice, fever

Diagnostic tests: blood studies - ESR, Hgb, RBC (anemia),

hyperbilirubinemia alkaline phosphatase, AST, ALT, blood glucose, hypoalbuminemia

Alpha – fetoprotein (AFP) – a special blood test used to help diagnose primary liver cancer (500 ng/ml – 50mg/ml)

CT scan, UTZ liver biopsy

Liver Tumors (cont.)Medical Management1. Supportive measures – if the tumor is far advanced at the time of diagnosis

Control of pain & other discomforts Paracentesis – to decrease ascites Low sodium diet Restrict protein intake – to ammonium production

2. Surgery – removal of solitary tumors- Liver transplant

3. Chemotherapy Done to decrease or slow down tumor growth Ex. 5- FU (5- flurouracil), Doxorubicin, mitomycin

4. Radiation therapy May occasionally be used to control pain Does not contribute to survival

Liver Tumors (cont.)Nursing Management

Help pt. cope with anxiety & fear, provide emotional support Provide care when liver failure progresses – fluid volume excess,

pain, pruritus, alteration in LOC & thought processCare of pt. having hepatic resection/surgery Pre – operative careAdminister Vit. K and other vitamins, fluid therapy & blood transfusionBowel preparationPost operative careClose monitoring (VS, UO, I&0, ABG, electrolytes, CBC)WOF for signs of hypovolemia, shock, sepsis and cardio/pulmo complications Administer glucose, albumin, blood replacement Restrict protein – to ammonia

Maintain chest tube drainage to water–sealed bottle Promote turning, coughing, splinting, proper positioning (Fowler’s position) Adequate pain control Frequent mouth care, pt. on NPO, with NGT to suction Encourage ambulation (4th post day) Feeding started (5th post–op day) – maintain adequate intake , protein

Jaundice there is excess bilirubin in the blood leading to distribution of

bilirubin to the skin, mucous membranes and other body fluids and tissues, giving them yellowish discoloration

occurs when bilirubin level is > 2.5 mg/dl Bilirubin in the skin causes pruritus (itching)

Causes: intrahepatic cholestasis (stasis of bile w/in the liver) due to drug interactions extrahepatic abstruction – obstruction of hepatic, gallbladder or

common bile duct, gallbladder stones, pancreatisis, cancer of pancreas

hepatocellular damage – interference w/ the uptake, conjugation and excretion of bilirubin into bile

Hepatitis acute inflammatory disease of the liver caused by a virus (most

common), bacteria or toxic or chemical injuryTypes:1. Toxic Hepatitis

injury to the liver cells caused by alcohol, drugs, industrial chemical and toxins

Ex. Industrial toxins – Carbon tetrachloride, chlorinated tetracarbons cleaning agents, solvents to remove paint

Drugs – acetaminophen (paracetamol) – large doses1. Tetracycline2. Rifampicin, Isoniazid (INH)3. Phenytoin4. Chemotherapy drugs

Toxic Hepatitis (cont.)

Pathophysiology:Damage to the liver - fatty infiltrations altered liver function

- necrosis - stasis of bile (cholestasis) can lead to- inflammation liver failureS/Sx :

anorexia nausea, vomiting, lethargy, weakness jaundice (icterus), hepatomegaly, liver tenderness AST, ALT – the higher the enzyme levels, the more severe

the cellular damage to the liver bilirubin in blood and urine low albumin, prolonged PT

Toxic Hepatitis (cont.)

Medical Mgt.: identify the toxic agent and remove or eliminate it insert NGT and do gastric lavage and cleansing of the bowel supportive medical care of the symptoms present

Nsg. Mgt.: promote comfort, maintain fluid & electrolyte balance promote well- balanced diet promote rest pt. teaching

- proper use of chemicals at home- avoid exposure to chemical in the work environment- proper use of drugs, follow doctor’s advice

Viral Hepatitis4 types: Hepatitis A, Hepatitis B, non-A, non-B hepatitis, Delta hepatitis

Viral Hepatitis(cont.)

Viral Hepatitis(cont.)

Virus invades portal tracts (blood vessels going to the liver) and lobules of liver, causing inflammation and destruction of parenchymal cells

hyperplasia of Kupffer cells (phagocytes)

damage cells are gradually phagocytized

and cell regeneration occurs

S/Sx: Pre-icteric (before yellowish discoloration appears) – last for 1 week

flu like symptoms (malaise, fever, chills) dull pain and tenderness in RUQ of abdomen, liver enlargement nausea and vomiting dyspepsia, anorexia headache weakness wt. loss

Viral Hepatitis(cont.)Icteric (2-3 weeks) – starts with jaundice

jaundice (yellow sclera & skin esp. palms and soles of the feet clay colored stools, dark – amber urine, urine bilirubin and

urobilinogen Pruritus Fatigue, anorexia, abdominal tenderness, weakness Abnormal liver function test ( AST, ALT, bilirubin), alkaline

phosphatasePost icteric (2-4 months) – begins with disappearance of jaundice

resolving jaundice gradual return of appetite & energy

Medical Mgt.: (no specific medical treatment)- rest, symptomatic support - F/E replacement -antihistamine for pruritus- interventions to prevent transmission – Vit. K replacement- antiemetic for vomiting

Viral Hepatitis(cont.)Nsg. Interventions:prevent transmission of infectionhandwashing, good personal hygieneHep. A - use disposable eating utensils/dishes or separate themHep. B – Hep. B immune globulin, Hep. B vaccine to exposed personsuniversal precautionsaseptic techniqueCBR, calm, restful environmentavoid administering drugs toxic to the liverproper skin care (pruritus), comfort measuresencourage well-balanced diet, adequate nutrients /calories fluid intake, avoid fatty foodsInstruct pt. to avoid sexual activity, avoid alcohol intake, not to share personal items, not to donate blood

Liver Cirrhosis a chronic, degenerative disease of the liver causing

inflammation destruction, fibrotic regeneration and hepatic insufficiency loss of liver function

2x common in men than women, 40-60 years old.Predisposing/ Precipitating factors:

malnutrition effects of alcohol abuse chronic impairment of bile excretion – biliary obstruction in the

liver and common bile duct (gallbladder stones) necrosis from hepatotoxins or viral hepatitis chronic congestion heart failure

Pathophysiology: liver cell damage result in inflammation & hepatomegaly attempts at regeneration eventually result to fibrosis and a

small nodular liver hepatic function is slowly impaired obstruction of venous channels blocks hepatic blood flow and

cause portal hypertension

Liver Cirrhosis (cont.)S/Sx - early:

anorexia, nausea, indigestion aching or heaviness in right upper quadrant weakness & fatigue

Late signs: abnormal liver function tests: bilirubin, AST, ALT, alkaline phos.

intermittent jaundice, pruritus edema, ascites, prominent abdominal wall veins, albumin bleeding tendencies, prolonged prothrombin time, plt. ct. anemia: folic acid deficiency, RBC production, RBC

destruction in spleen frequent infection, WBC

Nsg. Interventions:1. Reduce metabolic demands on the liver

provide bed rest eliminate ingestion of toxic substances to the liver: sedatives

opiates, alcohol, acetaminophen activities

Liver Cirrhosis (cont.)2. Provide adequate nutrition & hydration

Low – protein, high-carbohydrate, high calorie, sodium- restricted diet

multiple vitamin therapy restrict fluids & sodium if there is edema or ascites provide mouth care before meals monitor I/O, daily wt.

3. Prevent infection encourage good personal hygiene reverse isolation assess for signs of urinary/esp. infection encourage deep breathing/position changes

4. Protect pt. from bleeding monitor urine, stool, gums, skin for signs of bleeding/ bruising avoid injections, apply pressure to venipuncture sites for at least 5

mins. Monitor prothrombin time, bleeding time Teach pt. to use soft toothbrush, avoid constipation Prevent scratching from pruniturs, proper skin care Administer Vit. K as ordered

Complications of Liver Cirrhosis1. Ascites

abnormal intraperitoneal accumulation of watery fluid containing small amounts of protein

due to: colloid asmotic pressure from albumin prod. by liver capillary hydrostatic pressure from portal hypertension Na and H2O retention

S/sx: abdominal enlargement, wt. fatigue abdominal discomfort, respiratory difficulty

Med. Mgt. (depending on severity of ascites)Na+ & fluid restriction (500-1000 ml/day)diuretic therapy (aldactone/ spirinolactone)salt-poor albumin transfusion to restore plasma volumeplacement of LeVeen Shunt (catheter to remove fluid from peritoneum to vena cava)Paracentesis – used for diagnosis or when fluid volume compromise comfort & breathing

Complications of Liver Cirrhosis (cont.)Nursing Interventions to ascites & increase/promote comfort

maintain on bed rest fluid & Na restriction monitor I/O, daily wt. measure abd. girth every shift maintain on high-Fowlers for max. respiration support abdomen with pillows administer diuretics, salt-poor albumin IV as ordered

- monitor for signs of CHF, pulmonary edema, dehydration,

electrolyte imbalance, hypersensitivity reactionAssist with Paracentesis

have the client void before the procedure high –fowlers position during the procedure monitor pt. for hypovolemia & electrolyte imbalance observe puncture wound for leakage & signs of infection

Complications of Liver Cirrhosis (cont.)

2. Hepatic Encephalopathy cerebral dysfunction assoc. with severe liver disease inability of the liver to metabolize substances that can be toxic

to the brain such as ammonia, which is produced by the breakdown of protein in the intestinal tract

S/Sx: Asterixis- flapping hand tremors ---early signLOC – lethargy progressing to coma mental status, confusion, disorientationdullness, slurred speechbehavioral changes, lack of interest in grooming/ appearance twitching, muscular incoordination, tremorsFetor hepaticuselevated serum ammonia level

Complications of Liver Cirrhosis (cont.)Interventions:a. ) ammonia production

dietary protein to 20-40 g/day, maintain adequate calories ammonia formation in the intestine – give laxative, enema as

ordered and Neomycin - bacterial ammonia productionb.) Protect pt. from injury

side rails up turning to side assess mental status, LOC proper positioning (semi-Fowler’s) prevent aspiration

c.) Prevent further episodes of encephalopathy low protein diet prescribed medications avoid constipation ( to ammonia production by bacteria in

the GIT) early signs of encephalopathy (restlessness, slurred speech,

dec. attention span)

Complications of Liver Cirrhosis (cont.)3. Esophageal Varices

distention of the smaller blood vessels of the esophagus as a result of portal hypertension – due to obstruction of venous circulation w/in the damaged liver

the portal venous pressure causes blood to be forced into these vessels – become tortous and fragile

blood vessel become prone to injury by mechanical trauma from ingestion of coarse food and acid pepsin erosion which may result in bleeding

bleeding may also occur as a result of coughing, vomiting, sneezing, straining at stool or any physical exertion that abdominal venous pressure

S/Sx: upper GI bleeding

- blood in vomitus (hematemesis)- melena

massive hemorrhage signs/symptoms of hypovolemic shock

Complications of Liver Cirrhosis (cont.)

Medical Management: find the source of bleeding – esophagoscopy, angiography control bleeding – gastric lavage, administration of antacid

via NGT surgery – ligation and shunts insertion of Sengstaken–Blakemore tube with gastric

and esophageal balloon that are inflated to stop bleeding

has a nasogastric suction tube to remove blood in the stomach

the balloon is deflated periodically to prevent ulceration to the gastric mucosa

if the balloon ruptures or the tube dislodged – deflate the balloon and remove immediately

CholelithiasisCholelithiasis – stone formation in the gallbladderCholecystitis – inflammation of the gallbladder that can be acute or chronic and is usually precipitated by gallstones, can also be caused by bacterial infectionCholedocholithiasis – stones in the common bile ductGallstones – composed primarily of cholesterol, bile salts, calcium, bilirubin and proteins

Etiology/causes: (4x more common in women)1.Metabolic factors – serum cholesterol level in situations like obesity, pregnancy, diabetes, hypothyroidism

75% of gallstones are cholesterol stones 25% of gallstones are bilirubin stones – consists of bilirubin

pigment stones – occurs in persons with hemolytic disease2. Biliary stasis – leading to stagnation of bile in the gall bladder leads to excessive absorption of water w/c allows the salts to precipitate and form mixed stones

Cholesterol Stones

PIGMENT STONES

3. Inflammation of the biliary tract cause the bile constituents to become altered and the

inflamed gallbladder mucosa absorbs more of the bile acids results to formation of cholesterol stones

Stones may lodge anywhere in the biliary tract cause obstruction lead to jaundice and poor absorption of fats

may cause pressure, subsequent necrosis and infection of the walls of the biliary tract

may stimulate spasm and pain a stone can block the entrance of pancreatic fluid and bile into

the duodenum cause pancreatitis

Cholelithiasis (cont.)

Predisposing Factors: 5 F’s1. Female2. Fat (obese)3. Fair complexion4. Forty (age 40 and above)5. Fertile (multipara)

Cholelithiasis (cont.)Pathophysiology Clinical ManifestationsStasis of bile

Stone formationObstruction of bile flow total and conjugated serum bilirubin

urinary bilirubin, urine urobilinogenImpairment of fat - jaundice, pruritus, dark amber urineabsorption bec. of impaired Vit. K absorption – prolonged PTbile in the intestine - bleeding tendencies

intolerance to fatty foods - indigestion - nausea - eructation (bleching) -

vomitingclay–colored stools

Smooth muscle contractions biliary colic – RUQ painin the gallbladder & bile duct - severe pain- radiate to back & R shoulder

Acute or chronic – chills, fever, elevated WBC, N/VInflammation of the gallbladderAcute Cholecystitis May lead to perforation & peritonitis

Impacted stone

Acute Cholecystitis- swollen- edematous- vascular

Cholelithiasis (cont.)Dx: Abdominal Ultrasound, HBT UTZ

Management:1.low – fat diet2.weight reduction3.dissolution therapy (chenodeoxycholic acid) - dissolves stones

Surgery: Cholecystectomy (removal of gall bladder and cystic duct)

removal of stones in common bile duct - placement of T- tube to maintain duct patency during healing

Cholelithiasis (cont.)Nsg. Interventions:provide pain relief – analgesics, anti-spasmodic drugsGive antibiotics as orderedPost op-care – place pt. in semi-fowler’s positionEncourage coughing, deep breathing, turning to prevent atelectasisChange dressing as needed (bile is very irritation to the skin)Care for the T – tube – avoid tension and obstruction of tubingmeasure amt. of drainage ( 200-1000 ml/day for 1st several days)Clamp as ordered in 3-4 days, before meals to allow bile to drain into duodenum, assess toleranceUsually removed 10-12 days post-opAdvance from clear liquids to low-fat diet as tolerated

Laparoscopic Cholecystectomy

Pancreas produce 2,000 ml. of secretions daily, composed of:a) electrolyte solution w/ a high concentration of bicarbonateb) digestive enzymes – secreted by the acinar cells in the

pancreas

Pancreatic enzymes1.Trypsinogen – converted by enterokinase to trypsin – breakdown polypeptides into peptides and amino acids2.Amylase – hydrolyzes starch (carbohydrates) into maltose, lactose and sucrose3.Lipase – catalyzes splitting of fats into glycerol and fatty acids

The release or secretion of pancreatic enzymes are stimulated by hormones released from the duodenum: a). secretin b). cystokinin – pancreozymin (CCK – PZ)

- these hormones are stimulated by the presence of food in the intestine

Acute PancreatitisPancreatitis – a serious inflammatory disorder of the pancreas that can be acute or chronicAcute Pancreatitis

can occur as a single episode or as recurrent attacks the pancreas returns to normal after successful treatment

except for alcohol- induced pancreatitisCauses:

alcoholism biliary tract disease – gallstones in the biliary tract that cause

obstruction of the pancreatic duct Post-operative abdominal or non-abdominal surgery blunt abdominal trauma infections esp. viral Drugs (antihypertensives, diuretics, antibiotics,

immunosupresstants, oral contraceptives Intestinal disease such as duodenal ulcers, regional enteritis Unknown

Acute Pancreatitis (cont.)

Pathophysiology:

reflux of bile, obstruction of pancreatic duct, ischemia, anorexia, trauma, endotoxins and exotoxins from bacteria or microorganisms

stimulate activation of proteolytic enzymes Ex. Trypsinogen trypsin inside the pancreas

Auto digestion

- trypsin and other proteolytic enzymes digest pancreatic and other surrounding tissues and cell membranes

edema, interstitial hemorrhage,

parenchymal cell necrosis in the pancreas

Acute Pancreatitis (cont.)Summary of major Pathologic events that occur in Acute

Pancreatitis

Altered glucose Stress responseMetabolism cardiac (hyperglycemia) contractility

Release of Acute Pancreatitis release of Insulin kinin Vasodilation

(activated by trypsin) Obstruction of edema, distention of Shock

bile flow capsule, obstruction of pancreatic flow Exudate of blood

and protein into Hypovolemia

Altered bilirubin peritoneal spacemetabolism

Pain Peritonitis gastrointestinal Fever

function

Acute Pancreatitis (cont.)Complications of Acute Pancreatitis

hypotension, shock Anemia due to blood loss Atelectasis, pleural effusion, ARDS, respiratory failure Peptic ulcers, gastritis Hemorrhage, pancreatic abscess, ascites Hyperglycemia

S/Sx: severe abdominal pain (epigastric or LUQ)

- more intense when pt. is lying supine nausea, vomiting, low grade fever abdominal distension and rigidity & tenderness, bowel

sounds Signs of dehydration (poor skin turgor, dry mouth, tachycardia Jaundice – obstruction of common bile duct Purplish discoloration of the flank area (Grey Turner’s sign) or

the periumbilical area (Cullen’s sign) – due to hemorrhagic necrosis of pancreas

Acute Pancreatitis (cont.)Diagnostic test:

serum enzyme levelsa.) serum amylase greater than 300 units – indicate acute pancreatitisb.) serum lipase greater than 1.5 units

WBC, Anemia ( Hgb, RBC), bilirubin abdominal x-ray, UTZ

Medical Management•place pt. on NPO – to decrease stimulation of pancreatic secretion to rest the pancreas•insertion of NGT – to decompress the bowel and relieve abdominal distention and allow to drain•fluid and electrolyte replacement•pain relief (analgesics, anti-inflammatory drugs)•Drugs (antibiotic, somatostatin - pancreatic secretion)•Monitor blood glucose levels (insulin may be given)

Acute Pancreatitis (cont.)Nursing Interventions1. Maintain fluid & electrolyte balance – I& O, V.S, daily wt.

Hemodynamic measurements measure urine output accurately, foley catheter care monitor for signs of shock maintain correct IVF infusion rates

2. Promote nutrition- NPO, provide oral care- gradual diet from clear liquids – low fat, bland diet, small frequent

feedings- monitor for nausea, vomiting, pain- TPN

3. Controlling discomfort pain relievers every 3-4 hrs. position on side-lying, Knee-chest position., or sitting position to

decrease pain relaxation techniques, deep breathing exercises, guided

imaginary

Acute Pancreatitis (cont.)4. providing self-care

prevent skin breakdown, pressure sores provide adequate rest periods assist or perform self-care for the patient during the acute

stage5. Patient teaching

prevent future attacks by avoiding alcohol, maintaining a nutritious diet, low-fat, bland diet, avoid caffeine

small frequent feedings regular follow-up