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Colonoscopy uses a flexible fiber-optic video endoscope to permit visual examination of the lining of the large

intestine. It¶s indicated for patients with history of constipation or diarrhea, persistent rectal bleeding, and

lower abdominal pain when the results of proctosigmoidoscopy and a barium enema test are negative or

inconclusive.

Purpose

To detect or evaluate inflammatory and ulcerative bowel disease. To locate the origin of lower gastro intestinal bleeding.

To aid in the diagnosis of colonic strictures and benign or malignant

lesions.

To evaluate the colon postoperatively for recurrence of polyps and

malignant lesions.

Patient Procedure

1. Check the patient¶s medical history for allergies, medications, and information pertinent to the current complaint.

2. Tell the patient to maintain a clear liquid diet for 24 to 48 hours before the test and to take nothing by mouth after

midnight the night before.

3. Instruct the patient regarding the appropriate bowel preparation.

4. Inform the patient that he¶ll receive an I.V. line and I.V. sedation before the procedure.

5. Tell the patient that the colonoscope is well lubricated to ease insertion and initially feels cool.

6. Explain that he may feel an urge to defecate when it¶s inserted and advanced.

7. Inform him that air may be introduced through the colonoscope to distend the intestinal walland to facilitate

viewing the lining and advancing the instrument.

Colonoscopy Procedure

1. The patient is assisted onto his left side with knees flexed.

2. Cover the patient with drape.

3. Baseline vital signs are obtained.

4. Vital signs and electrocardiogram are monitored during the procedure.

5. Continuous or periodic pulse oximetry is advisable.

6. The physician palpates the mucosa of the anus and rectum and inserts the lubricated colonoscope through the

patient¶s anus into the sigmoid colon under direct vision.7. A small amount of air is insufflated to locate the bowel lumen and then advance the scope through the rectum.

8. Abdominal palpation or fluoroscopy may be used to help guide the colonoscope through the large intestine.

9. Suction may be used to remove blood and secretions that obscure vision.

10. Biopsy forceps or a cytology brush may be passes through the colonoscope to obtain specimens for histologic or

cytologic examination; an electro-cautery snare may be used to remove polyps.

11. Tissue specimens are immediately placed in a specimen bottle containing 10% formalin and cytology smears in a

Coplin jar containing 95% ethyl alcohol.

12. Specimens are sent to the laboratory immediately.

Nursing Interventions for Colonoscopy

1. The patient is observed closely for signs of bowel perforation.

2. Check the patient¶s vital signs and document them accordingly.3. Watch the patient closely for adverse effects of the sedative.

4. After recovery from the sedation, he may resume his usual diet unless the physician orders otherwise.

5. The patient may pass large amounts of flatus after insufflation.

6. After polyp removal, the stool may contain some blood. Report excessive bleeding immediately.

7. If a polyp is removed, but not retrieved, give enema and strain the stools to retrieve it.



Precautions

1. Although it¶s usually a safe procedure, beware that colonoscopy can cause perforation of the large intestine,

excessive bleeding, and retroperitoneal emphysema.

2. This procedure is contraindicated in pregnant woman near term, the patient who has had a recent acute

myocardial infarction or abdominal surgery, and one with ischemic boweldisease, acute diverticulitis, peritonitis,

fulminant granulomatous colitis, perforated viscus, or fulminant ulcerative colitis. For these cases of for screening

purposes, a virtual colonoscopymay be an option to help visualize polyps early before they become concerns.

Interpretations

Normal Results

Normally, the mucosa of the large intestine beyond the sigmoid colon appears light pink-orange and is marked by

semilunar folds and deep tubular pits.

Blood vessels are visible beneath the intestinal mucosa, which glistens from mucus secretions.

Abnormal Results

Visual examination of the large intestine, coupled with histologic and cytologic test results, may indicate procrititis,

granulomatous or ulcerative colitis, Crohn¶s disease, and malignant or benign lesions. Diverticular disease or the

site of lower gastrointestinal bleeding can be detected through colonoscopy alone.

Interfering Factors

Fixation of the sigmoid colon due to inflammatory bowel disease, surgery, or radiation therapy that may hinder

passage of the colonoscope. Blood from acute colonic hemorrhage that hinders

visualization. Insufficient bowel preparation or barium retained in the intestine from previous diagnostic studies

which makes accurate visual examination impossible.

Complications

Perforation of the large intestine, excessive bleeding and retroperitoneal emphysema.

Barium swallow, also known as esophagography, is the radiographic or fluoroscopic examination of the

pharynx and the fluoroscopic examination of the esophagus after ingestion of thick and thin mixtures of barium

sulfate.

This test, is commonly performed as part of the upper GI series, is indicated for patients with history of dysphagia and

regurgitation. Further testing is usually required for a definitive diagnosis. After the barium is swallowed, it pours over the base of the tongue into the pharynx. A peristaltic wave propels it

through the entire length of the esophagus in about 2 seconds. When the peristaltic wave reaches the base of the

esophagus, the cardiac sphincter opens, allowing the barium to enter the stomach. After passage of the barium, the

cardiac sphincter closes. Normally, it evenly fills and distends the lumen of the pharynx and esophagus, and the

mucosa appears smooth and regular.

Purpose of Barium Swallow

To diagnose hiatal hernia, diverticula, and varices.

To detect strictures, ulcers, tumors, polyps, and motility disorders.

Procedure for Barium Swallow

Patient Preparation

1. Explain to the patient that this test evaluates the function of the pharynx and esophagus.2. Instruct the patient to fast after midnight before the test.

3. If the patient is infant, delay the feeding to ensure complete digestion of the barium.

4. Explain that the test takes approximately 30 minutes.

5. Describe the milkshake consistency and chalky taste of the barium preparation the patient will ingest; although it¶s

flavored, it may be unpleasant to swallow.

6. Tell him he¶ll first receive a thick mixture and then a thin one and that he must drink 12 to 14 oz (355 to 414 ml)

during the examination.



7. Inform him that he¶ll be placed in various positions on a tilting radiograph table and that radiographs will be taken.

8. If gastric reflux is suspected, withhold antacids, histamine-2 (H2) blockers, and proton pumpinhibitors, as ordered.

9. Just before the procedure, instruct the patient to put a hospital gown without snap closures and to remove

jewelry, dentures, hairpins, and other radiopaque objects from the radiograph field.

10. Check the patient history for contraindications to the barium swallow, such as intestinal obstruction and

pregnancy. Radiation may have teratogenic effects.

Implementation

1. The patient is placed in an upright position behind the fluoroscopic screen, and his heart, lungs, and abdomen are

examined.

2. The patient is instructed to take one swallow of the thick barium mixture; pharyngeal action is recorded using

cineradiography.

3. The patient is instructed to take several swallows of the thin barium mixture. Passage of the barium is examined

fluoroscopically; spot films of the esophageal region are taken from lateral angles and from the right and left

posteroanterior angles.

4. To accentuate small strictures or demonstrate dysphagia, the patient may be asked to swallow a ³barium

marshmallow´ (soft white bread soaked in barium) or a barium pill.

5. The patient is then secured to the X-ray table and rotated to trendelenburg position to evaluate esophageal

peristalsis or demonstrate hiatal hernia and gastric reflux.

6. The patient is instructed to take several swallows of barium while the esophagus is examined fluoroscopically;

spot films are taken.

7. After the table is rotated to a horizontal position, the patient takes several swallows of the barium so that the

esophageal junction and peristalsis may be evaluated.

8. Passage of the barium is fluoroscopically observed and the spot films are taken with the patient in the supine and

prone position.

9. During fluoroscopic examination of the esophagus, the stomach and the duodenum are also carefully studied

because neoplasms in these areas may invade the esophagus and cause obstruction.

Nursing Interventions for Barium Swallow

1. Check the additional films and fluoroscopic evaluations haven¶t been ordered before allowing the patient to

resume his usual diet.2. Instruct the patient to drink plenty of fluids, unless contraindicated, to help eliminate the barium.

3. Give cathartic as prescribed.

4. Tell the patient to notify the physician if he fails to expel the barium in 2 to 3 days.

5. Inform the patient that stools will be chalky and light colored for 24 to 72 hours.

Interpretation

Normal Results

The swallowed barium bolus pours over the base of the tongue into the pharynx.

A peristaltic wave reaches the base of the esophagus, the cardiac sphincter opens, allowing the bolus to enter the

stomach. After the passage of the bolus, the cardiac sphincter closes.

The bolus evenly fills and distends the lumen of the pharynx and esophagus, and the mucosa appears smooth

and regular.Abnormal Results

Barium swallow may reveal hiatal hernia, diverticula, and varices.

Strictures, tumors, polyps, ulcers, and motility disorders, such as pharyngeal muscular disorders, esophageal

spasms, and achalasia (cardiospasm) may be detected.

Complications

Barium retained in the intestine may harden, causing obstruction or fecal impaction.

Abdominal distention and absent bowel sounds, which may indicate constipation and may suggest barium

impaction.



Fecal occult blood test is also known as stool occult blood test, hemoccult test, guiaic smear test, gFOBT, or

occult blood test. Fecal occult blood is detected by microscopic analysis or by chemical tests for hemoglobin, such as

the guiaic test. Normally, stools contain small amounts of blood (2-2.5 mL/day); therefore, test for occult blood detect

quantities larger than this. Testing is indicated when clinical symptoms and preliminary blood studies suggest GI

bleeding. Additional tests are required to pinpoint the origin of the bleeding.

Purpose To detect gastro intestinal bleeding.

To aid in the early diagnosis of colorectal cancer.

Procedure

Preparation

1. Explain the patient that this test detects abnormal GI bleeding.

2. Instruct the patient to maintain a high-fiber diet and to refrain from eating red meats, turnips, and horseradish for

48 to 72 hours before the test as well as throughout the collection period.

3. Tell the patient that the test usually requires three fecal specimens but that sometimes only one sample is

needed.

4. Instruct the patient to avoid contaminating the fecal specimen with toilet tissue or urine.

5. Notify the laboratory and physician of drugs the patient is taking that may affect test results; it may be necessary

to restrict them. If the patient must continue using this drugs, note this on the laboratory request.

Implementation

1. Collect three fecal specimens or a random fecal specimen.

2. Obtain specimens from two different areas of each fecal specimen.

Hematest

1. Use a wooden applicator to smear a bit of the fecal specimen on the filter paper supplied with the kit. Or, after

performing a digital rectal examination, wipe the finger you used for the examination on a square of

the filter paper. Place the filter paper with the fecal smear on aglass plate.

2. Remove a reagent tablet from the bottle and immediately replace the cap tightly. Place the tablet in the center of

the fecal smear on the filter paper. Add 1 drop of water to the tablet, and allow it to soak in for 5 to 10 seconds.

Add a second drop, letting it run from the tablet onto the specimen and filter paper.3. After 2 minutes, the filter paper will turn blue if the test result is positive. Don¶t read the color that appears on the

tablet itself or develops on the filter paper after the 2-minute period. Note the results and discard the filter paper.

Remove and discard your gloves and wash your hands thoroughly.

Hematocrit test

1. Open the flap on the side pack and use a wooden applicator to apply a thin smear of the fecal specimen to the

guiaic-impregnated filter paper exposed in a box. Apply a second smear from another part of the specimen to

the filter paper exposed in box B.

2. Let the specimen dry for 3 to 5 minutes. Open the flap at the near of the slide package and place 2 drops of

hematocrit developing solution on the paper over each smear. A positive result yields a blue reaction in 30 to 60

seconds. Record the results and discard the slide package. Remove and discard your gloves and wash your

hands thoroughly.Instant-View Fecal Occult Blood Test

1. Add a fecal sample to the collection tube. Shake it to mix the sample with the extraction buffer, and then dispose

4 drops into the sample well of the cassette.

2. Results will appear on the test region and the control region of the cassette in 5 to 10 minutes, indicating whether

the hemoglobin level is > 0.05 pg/ml of feces.



Nursing Interventions

1. Send the specimen to the laboratory or perform the test immediately, depending on which test is used.

2. Inform the patient that he may resume his usual diet and medications as ordered.

3. Single digital office-based test may not be as accurate as serial home collected test.

Interpretations

Normal Results

Less than 2.5 ml of blood in feces, resulting in a green reaction.

Abnormal Results

GI bleeding, this may result from many disorders, such as varices, a peptic ulcer, carcinoma, ulcerative colitis,

dysentery, hemorrhagic disease.

Interfering Factors

Failure to observe pretest reactions.

Failure to test the specimen immediately or to send it to the laboratory immediately after collection.

Bromides, colchicines, indomethacin, iron preparation, phenylbutazone, rauwolfia derivatives, and steroids

(possible increase from GI blood loss).

Ascorbic acid (false-negative, even with significant bleeding).

Ingestion of 2 to 5 ml of blood (for example, from bleeding gums).

Active bleeding from hemorrhoids (possible false-positive results).

Acute peritonitis is an inflammatory process within the peritoneal cavity most commonly caused by a

bacterial infection. Types of acute peritonitis include primary and secondary. Primary peritonitis, otherwise known as

spontaneous bacterial peritonitis, most commonly occur in patients with cirrhosis and clinically significant ascites.

Secondary peritonitis most commonly occurs as a result of spillage of intestinal, biliary, or urinary tract contents into

the peritoneal space as a result of perforation, suppuration, or ischemic injury. Patients at risk for developing

secondary peritonitis include those with recent abdominal surgery, a perforated ulcer or colon, a ruptured appendix or

viscus, a bowel obstruction, a gangrenous bowel, or ischemic bowel disease.

Signs and Symptoms

Patient assuming a knee-flexed position and complaining of severe localized or generalizedabdominal pain.

Nausea and vomitingPhysical Examination

Vital signs

HR: tachycardia

BP: hypotension

RR: increased and shallow

Temp : elevated

Neurologic

Normal to decreased mentation

Skin

Pale

Flushed Diaphoretic

Cardiovascular

Pulse thready or wear or may be bounding in presence of fever.

Pulmonary

Breath sounds may be diminished secondary to shallow breathing.

Abdominal

Rebound tenderness with guarding



May have referred pain to shoulder

Rigid, distended abdomen

Bowel sounds decrease to absent

Acute Care Management

Nursing Diagnosis: Deficient fluid volume related to intravascular fluid shift to the peritoneal space and inability to

ingest oral fluids.

Outcome Criteria

Central venous pressure 2 TO 6 MM Hg

BP 90 to 120 mm Hg

Mean arterial pressure 70 to 105 mm Hg

Pulmonary artery systolic 15 to 30 mm Hg

Pulmonary artery diastolic 5 to 15 mm Hg

HR 60 to 100 beats/min

Urine output 30 ml/hr

Patient Monitoring

1. Obtain pulmonary artery pressure and central venous pressure and monitor mean arterial pressure hourly or

more frequently if the patient¶s hemodynamic status is unstable.

2. Not the patient¶s response to all therapy.

3. Monitor fluid volume status by measuring urine output hourly and measure nasogastric and other bodily drainage.

4. Determine fluid balance every 8 hours.

5. Continuously monitor ECG fir dysrhythmias resulting from electrolyte disturbances.

Patient Assessment

1. Assess tissue perfusion. Note level of consciousness, skin color and temperature, pulses, and capillary refill.

2. Assess hydration status: note skin turgor on inner thigh or forehead, condition of buccalmembranes, and

development of edema or crackles.

3. Assess the patient¶s abdomen for resolution of rigidity, rebound tenderness, and distention. Auscultate bowel

sounds.

Diagnostic Assessment 1. Review serum sodium and potassium levels, which may become depleted with nasogastric suctioning or fluid

shifts.

2. Review serial WBC count and differentiated to evaluate the course of action.

Patient Management

1. Administer crystalloid or colloid solutions to improve intravascular volume.

2. Replace potassium as ordered; validate adequate urine output before administration.

3. Keep the patient NPO during acute phase and before evaluation by a surgeon.

4. Provide nutritional support as indicated; most patient will benefit from postpyloric delivery of early enteral nutrients

at a minimal hourly rate to prevent v=bacterial translocation and sepsis.

5. Administer antibiotics as prescribed after appropriate cultures obtained.



APPENDICITISIs inflammation of the vermiform appendix caused by an obstruction attributable by infection,

stricture, fecal mass, foreign body or tumor.It can affect by either gender at any age, but is most common in males

ages 10 to 30.It is the most common disease requiring surgery. If left untreated, appendicitis may progress to

abscess, perforation, subsequent peritonitis, and death. Assessment

1. Generalized or localized abdominal pain occurs in the epigastric or periumbilical areas in the upper right

abdomen.

2. Within 2 to 12 hours, the pain localizes in the right lower quadrant and intensity increases.

3. Anorexia, fever, nausea, vomiting, and constipation may also occur.

4. Bowel sounds may be diminished.

5. Tenderness anywhere in the right lower quadrant.

Often localized at McBurney¶s point, just below midpoint of line between umbilicus and iliac crest on the right side.

Guarding and rebound tenderness to right lower quadrant and referred rebound when palpating the left lower

quadrant.

6. Positive Psoas Sign.

Have the patient attempt to raise the right thigh against the pressure of your hand placed over the right knee.

Increased abdominal pain indicates inflammation of the psoas muscle in acute appendicitis.

7. Positive Obturator Sign.

Flex the patient¶s right hip and knee and rotate the leg internally.

Hypogastric pain indicates inflammation of the obturator muscle.

Diagnostic Evaluation

1. WBC count shows moderate leukocytosis (10,000 to 16,000/mm) with shift to the left (increased immature

neutrophils) in WBC differential.

2. Urinalysis rules out urinary disorders.

3. Abdominal X-ray visualizes shadow consistent with fecalith in appendix.

4. Pelvic sonogram rules out ovarian cyst or ectopic pregnancy.

Surgical Interventions

1. Surgical removal is the only effective treatment (simple appendectomy or laparoscopic appendectomy).

2. Preoperatively, maintain patient on bed rest, NPO status, I.V. hydration, possible anti-biotic prophylaxis, and

analgesia, as directed.


1. Monitor frequently for signs and symptoms of worsening condition, indicating perforation, abscess, or peritonitis

(increasing severity of pain, tenderness, rigidity, distention, absent bowel sounds, fever, malaise, and

tachycardia).

2. Notify health care provider immediately if pain suddenly ceases, this indicates perforation, which is a medical

emergency.

3. Assist patient to position of comfort such as semi-fowlers with knees are flexed.

4. Restrict activity that may aggravate pain, such as coughing and ambulation.

5. Apply ice bag to abdomen for comfort.6. Avoid indiscriminate palpation of the abdomen to avoid increasing the patients discomfort.

7. Promptly prepare patient for surgery once diagnosis is established.

8. Explain signs and symptoms of postoperative complications to report-elevated temperature, nausea and vomiting,

or abdominal distention; these may indicate infection.

9. Instruct patient on turning, coughing, or deep breathing, use of incentive spirometer, and ambulation. Discuss

purpose and continued importance of these maneuvers during recovery period.

10. Teach incisional care and avoidance of heavy lifting or driving until advised by the surgeon.



11. Advise avoidance of enemas or harsh laxatives; increased fluids and stool softeners may be used for

postoperative constipation.

Colostomy

Formation of an opening into the colon, brought out onto the abdominal wall as a stoma. The opening can be either

permanent or temporary.Specific Technique

Bowel technique

Discussion

This procedure is usually performed for lesions in the large intestine caused by cancer, diverticulitis, or

obstruction of the large intestine in an area close to the rectum.

Types of colostomy:

1. Temporary colostomy: A temporary colostomy is performed to divert the fecal stream from the distal colon,

which may be obstructed by tumor inflammation, or requires being ³put-to-test´ because of anastomosis or a

pouch procedure. A temporary colostomy may be created in the transverse colon or sigmoidcolon.

2. Permanent colostomy: A permanent colostomy is performed to treat malignancies of the colon. Other

indications may include irrevocable rectal strictures, incontinence of bowel, or inflammatory bowel disease. A

permanent colostomy can be fashioned similar to a temporary colostomy but most often is an end colostomy.

Position

Supine, with arms extended on arm boards.

Incision Site

Dependent on the segment of colon to be used.

Packs/ Drapes

Laparotomy pack

Four folded towels

Transverse Lap sheet

Minor pack

Instrumentation Major Lap tray

Intestinal tray

Closing tray

Internal surgical staples

Supplies/ Equipments

Basin set

Blades

Needle counter

Penrose drain

Internal stapling instruments

Glass rod and tubing with colostomy pouch

Solutions ± saline, water

Sutures

Medications

Dressings

Procedure

1. The abdomen is opened in the usual manner and the segment of colon is mobilized.

2. The colon can be brought out through the main incision, or through an adjacent site from which a disk of skin and

subcutaneous tissue has been excised.



3. The underlying rectus fascia muscle and peritoneal layers are incised to accommodate thecolon. The appropriate

segment is excised between two atraumatic (intestinal) clamps or the internal stapling instrument, which is used

to prepare and create the stoma.

4. In a loop colostomy, a rod or bridge may be placed under the colon to avoid retraction.

5. The abdomen is irrigated with warm saline and closed layers in a routine fashion.

6. A colostomy poucj is applied over the stoma.

Perioperative Nurisng Considerations

1. The colostomy pouch may or may not be applied in surgery.

2. A Vaseline gauze may encircle the stoma with a ³fluff´ type dressing applied.

3. If the institution has an ³Ostomy Nurse´, the application of the colostomy pouch may be delayed until the clinical

specialist can work with the patient and family.

Liver Cirrhosis

is a chronic disease that causes cell destruction and fibrosis(scarring) of hepatic tissue. Fibrosis alters normal liver structure and vasculature, impairing blood and lymph flow and resulting in hepatic

insufficiency and hypertension in the portal vein.

Complications include hyponatremia, water retention, bleeding esophageal varices, coagulopathy, spontaneous

bacterial peritonitis, and hepatic encephalopathy.

Three major forms:

1. Laennec¶s (alcohol induced) Cirrhosis

Fibrosis occurs mainly around central veins and portal areas.

This is the most common form of cirrhosis and results from chronic alcoholism and malnutrition.

2. Postnecrotic (micronodular) Cirrhosis

Consist of broad bands of scar tissue and results from previous acute viral hepatitis or drug-induced massive

hepatic necrosis.

3. Biliary Cirrhosis

Consist of Scarring of bile ducts and lobes of the liver and results from chronic biliary obstruction and infection

(cholangitis), and is much rarer than the preceding forms.

Assessment:

1. Early complaints including fatigue, anorexia, edema of the ankles in the evening, epistaxis, bleeding gums,

and weight loss.

2. In later disease:

Chronic dyspepsia, constipation and diarrhea.

Esophageal varices; dilated cutaneous veins around umbilicus (caput medusa); internal hemorrhoids, ascites,

splenomegaly.

Fatigue, weakness, and wasting caused by anemia and poor nutrition.

Deterioration of mental function.

Estrogen-androgen imbalance causing spider angioma and palmar erythema; menstrual irregularities in

women; testicular and prostatic atrophy, gynecomastia, loss of libido, and impotence in men.

Bleeding tendencies and hemorrhage.

3. Enlarged, nodular liver.

Diagnostic Evaluation:

1. Elevated serum liver enzyme levels, reduced serum albumin.

2. Liver biopsy detects cell destruction and fibrosis of hepatic disease.

3. Liver scan shows abnormal thickening and a liver mass.

4. CT scan determines the size of the liver and its irregular nodular surface.

5. Esophagoscopy determines the presence of esophageal varices.



6. Percutaneous transhepatic cholangiography differentiates extrahepatic from intrahepatic obstructive jaundice.

7. Paracentesis examines ascitic fluid for cell, protein, and bacteria counts.

Pharmacologic Interventions:

1. Provide asymptomatic relief measures such as pain medications and antiemetics.

2. Diuretic therapy, frequently with spironolactone, a potassium-sparing diuretic that inhibits the action of aldosteroe

on the kidneys.

3. I.V albumin to maintain osmotic pressure and reduce ascites.

4. Administration of lactulose or neomycin through a nasogastric tube or retention enema to reduce ammonia levels

during periods of hepatic encephalopathy.

Surgical Intervention:

1. Transjugular intrahepatic portosystemic shunt may be performed in patients whose ascites prove resistant.

This percutaneous procedure creates a shunt from the portal to systemic cisculation to reduce portal pressure

and relieve ascites.

2. Orthotopic liver transplantation may be necessary.

Nursing Interventions:

1. Observe stools and emesis for color, consistency, and amount, and test each one for occult blood.

2. Monitor fluid intake and output and serum electrolyte levels to prevent dehydration and hypokalemia, which may

precipitate hepatic encephalopathy.

3. Maintain some periods of rest with legs elevated to mobilize edema and ascites. Alternate rest periods with

ambulation.

4. Encourage and assist with gradually increasing periods of exercise.

5. Encourage the patient to eat high-calorie, moderate protein meals and supplementary feedings. Suggest small,

frequent feedings.

6. Encourage oral hygiene before meals.

7. Administer or teach self-administration of medications for nausea, vomiting, diarrhea or constipation.

8. Encourage frequent skin care, bathing with soap, and massage with emollient lotions.

9. Keep the patient¶s finger nails short to prevent scratching from pruritus.

10. Keep the patient quiet and limit activity if signs of bleeding are evident.

11. Encourage the patient to eat foods high vitamin C content.12. Use small gauge needles for injections and maintain pressure over injection site until bleeding stops.

13. Protect from sepsis through good handwashing and prompt recognition and management of infection.

14. Pad side rails and provide careful nursing surveillance to ensure the patient¶s safety.

15. Stress the importance of giving up alcohol completely.

16. Involve the person closest to the patient, because recovery usually is not easy and relapses are common.



Hepatic failure can result from acute liver injury, causing acute liver failure (ALF) or fulminant hepatic failure

(FHF), or progressive chronic liver disease such as cirrhosis. An alteration in hepatocyte functioning affects the liver

metabolism, detoxification process, protein synthesis, manufacture of clotting factors, and preservation of

immunocompetence. FHF occurs when severe hepatic injury results in encephalopathy and severe coagulopathy

within 28 days of the onset of symptoms in patients without a history of chronic liver disease. Liver transplant is the

only viable treatment option for patient with FHF. The most commonly identified cause of FHF is drug induced, withacetaminophen the most common culprit, followed by viral hepatitis. Other causes include infection (cytomegalovirus

[CMV], adenovirus), metabolic disorders and severe ischemic insult or shock.

Signs and Symptoms

Manifestation depends on the complications associated with the liver dysfunction.

Patient behavior may range from agitation to frank coma.

Evidence of GI bleeding, renal failure, or respiratory distress may also be present.

The initial manifestation in FHF is commonly bleeding from coagulopathy.

Physical Examination

Vital signs

BP: < 90 mm Hg (with shock)

HR: > 120 beats/min (with shock)

Temperature may be mildly elevated

RR: tachypnea initially progressing to respiratory depression associated with encephalopathy.

Neurologic

Mildly confused to coma

Personality changes

Asterixis

Pulmonary

Crackles

Labored respirations

Gastrointestinal

Hematemesis and melena

Ascites Hepatomegaly may be present

Splenomegaly may be present

Factor hepaticus

Diarrhea

Skin

Jaundice

Ecchymosis and petechiae

Pruritus

Edema

Acute Care Patient Management

Nursing Diagnosis: Deficient fluid volume related to ascites secondary to hypoalbumineia, bleeding secondary todecreased clotting factors or variceal hemorrhage, and diuretic therapy.

Outcome Criteria

BP 90 TO 120 mm Hg

Central venous pressure 2 to 6 mm Hg

Serum albumin 3.5 to 5 mg/dl

Platelet count >50,000/mm3

Urine output 30 ml/hr



Serum sodium 135 to 145 mEq/L

Serum potassium 3.5 to 5 mEq/L

Intake approximates output

Patient Monitoring

1. Obtain pulmonary artery pressure, central venous pressure, and blood pressure until the patient¶s condition is

stable, then hourly.

2. Continuously monitor ECG for lethal dysrhythmias that may result from electrolyte and acid-base imbalances.

3. Monitor fluid volume status. Measure intake and output hourly.

Patient Assessment

1. Assess hydration status. Note skin turgor on inner thigh or forehead, condition of buccal memranes, and

development of edema and crackles.

2. Assess for signs and symptoms of bleeding.

3. Measure abdominal girth once each shift to determine progression of ascites.

4. Assess respiratory status.

Diagnostic Assessment

1. Review serial serum ammonia, albumin, bilirubin, platelet count, PT, PTT and ALT to evaluate hepatic function.

2. Review serial serum electrolytes.

3. Review urine electrolyte, BUN, and creatinine to evaluate renal function.

Patient Management

1. Administer intravenous crystalloids as ordered.

2. Administer potassium as ordered. Validate adequate urine output before potassium administration.

3. Sodium restriction of 0.5 g/day and fluid restriction to 1000 ml/day may be ordered.

4. Vitamin K or fresh frozen plasma (FFP) may be required to promote the clotting process.

5. Institute bleeding precautions. Avoid razor blades and use soft-bristled toothbrushes.

6. Paracentesis may be performed if abdominal distention is severe.

7. Prepare the patient and family for liver transplant, as indicated.

PACREATITIS

Acute pancreatitis is inflammation of the pancreas that occurs suddenly and usually resolves in a few days withtreatment. Acute pancreatitis can be a life-threatening illness with severe complications. Each year, about 210,000people in the United States are admitted to the hospital with acute pancreatitis.

1The most common cause of acute

pancreatitis is the presence of gallstones²small, pebble-like substances made of hardened bile²that causeinflammation in the pancreas as they pass through the common bile duct. Chronic, heavy alcohol use is also acommon cause. Acute pancreatitis can occur within hours or as long as 2 days after consuming alcohol. Other causes of acute pancreatitis include abdominal trauma, medications, infections, tumors, and genetic abnormalities of the pancreas.

Symptoms

Acute pancreatitis usually begins with gradual or sudden pain in the upper abdomen that sometimes extends throughthe back. The pain may be mild at first and feel worse after eating. But the pain is often severe and may becomeconstant and last for several days. A person with acute pancreatitis usually looks and feels very ill and needsimmediate medical attention. Other symptoms may include

y a swollen and tender abdomen

y nausea and vomiting

y fever

y a rapid pulse



Severe acute pancreatitis may cause dehydration and low blood pressure. The heart, lungs, or kidneys can fail. If bleeding occurs in the pancreas, shock and even death may follow.

Diagnosis

While asking about a person¶s medical history and conducting a thorough physical examination, the doctor will order

a blood test to assist in the diagnosis. During acute pancreatitis, the blood contains at least three times the normalamount of amylase and lipase, digestive enzymes formed in the pancreas. Changes may also occur in other bodychemicals such as glucose, calcium, magnesium, sodium, potassium, and bicarbonate. After the person¶s conditionimproves, the levels usually return to normal.

Diagnosing acute pancreatitis is often difficult because of the deep location of the pancreas. The doctor will likelyorder one or more of the following tests:

y Abdominal ultrasound. Sound waves are sent toward the pancreas through a handheld device that atechnician glides over the abdomen. The sound waves bounce off the pancreas, gallbladder, liver, and other organs, and their echoes make electrical impulses that create a picture²called a sonogram²on a videomonitor. If gallstones are causing inflammation, the sound waves will also bounce off them, showing their location.

y Computerized tomography (CT) scan. The CT scan is a noninvasive x ray that produces three-dimensional

pictures of parts of the body. The person lies on a table that slides into a donut-shaped machine. The testmay show gallstones and the extent of damage to the pancreas.

y Endoscopic ultrasound (EUS). After spraying a solution to numb the patient¶s throat, the doctor inserts anendoscope²a thin, flexible, lighted tube²down the throat, through the stomach, and into the small intestine.The doctor turns on an ultrasound attachment to the scope that produces sound waves to create visualimages of the pancreas and bile ducts.

y Magnetic resonance cholangiopancreatography (MRCP). MRCP uses magnetic resonance imaging, anoninvasive test that produces cross-section images of parts of the body. After being lightly sedated, thepatient lies in a cylinder-like tube for the test. The technician injects dye into the patient¶s veins that helpsshow the pancreas, gallbladder, and pancreatic and bile ducts.

Treatment

Treatment for acute pancreatitis requires a few days¶ stay in the hospital for intravenous (IV) fluids, antibiotics, and

medication to relieve pain. The person cannot eat or drink so the pancreas can rest. If vomiting occurs, a tube may beplaced through the nose and into the stomach to remove fluid and air.

Unless complications arise, acute pancreatitis usually resolves in a few days. In severe cases, the person mayrequire nasogastric feeding²a special liquid given in a long, thin tube inserted through the nose and throat and intothe stomach²for several weeks while the pancreas heals.

Before leaving the hospital, the person will be advised not to smoke, drink alcoholic beverages, or eat fatty meals. Insome cases, the cause of the pancreatitis is clear, but in others, more tests are needed after the person is dischargedand the pancreas is healed.

Therapeutic Endoscopic Retrograde Cholangiopancreatography (ERCP) for Acute and Chronic Pancreatitis

ERCP is a specialized technique used to view the pancreas, gallbladder, and bile ducts and treat complications of acute and chronic pancreatitis²gallstones, narrowing or blockage of the pancreatic duct or bile ducts, leaks in thebile ducts, and pseudocysts²accumulations of fluid and tissue debris.

Soon after a person is admitted to the hospital with suspected narrowing of the pancreatic duct or bile ducts, aphysician with specialized training performs ERCP.

After lightly sedating the patient and giving medication to numb the throat, the doctor inserts an endoscope²a long,flexible, lighted tube with a camera²through the mouth, throat, and stomach into the small intestine. The endoscopeis connected to a computer and screen. The doctor guides the endoscope and injects a special dye into the



pancreatic or bile ducts that helps the pancreas, gallbladder, and bile ducts appear on the screen while x rays aretaken.

The following procedures can be performed using ERCP:

Sphincterotomy. Using a small wire on the endoscope, the doctor finds the muscle that surrounds the pancreatic ductor bile ducts and makes a tiny cut to enlarge the duct opening. When a pseudocyst is present, the duct is drained.

Gallstone removal. The endoscope is used to remove pancreatic or bile duct stones with a tiny basket. Gallstoneremoval is sometimes performed along with a sphincterotomy.

Stent placement. Using the endoscope, the doctor places a tiny piece of plastic or metal that looks like a straw in anarrowed pancreatic or bile duct to keep it open.

Balloon dilatation. Some endoscopes have a small balloon that the doctor uses to dilate, or stretch, a narrowedpancreatic or bile duct. A temporary stent may be placed for a few months to keep the duct open.

People who undergo therapeutic ERCP are at slight risk for complications, including severe pancreatitis, infection,bowel perforation, or bleeding. Complications of ERCP are more common in people with acute or recurrentpancreatitis. A patient who experiences fever, trouble swallowing, or increased throat, chest, or abdominal pain after

the procedure should notify a doctor immediately.

Complications

Gallstones that cause acute pancreatitis require surgical removal of the stones and the gallbladder. If the pancreatitisis mild, gallbladder removal²called cholecystectomy²may proceed while the person is in the hospital. If thepancreatitis is severe, gallstones may be removed using therapeutic endoscopic retrogradecholangiopancreatography (ERCP)²a specialized technique used to view the pancreas, gallbladder, and bile ductsand treat complications of acute and chronic pancreatitis. Cholecystectomy is delayed for a month or more to allowfor full recovery. For more information, see the Gallstones fact sheet from the National Institute of Diabetes andDigestive and Kidney Diseases (NIDDK).

If an infection develops, ERCP or surgery may be needed to drain the infected area, also called an abscess.Exploratory surgery may also be necessary to find the source of any bleeding, to rule out conditions that resemblepancreatitis, or to remove severely damaged pancreatic tissue.

Pseudocysts²accumulations of fluid and tissue debris²that may develop in the pancreas can be drained usingERCP or EUS. If pseudocysts are left untreated, enzymes and toxins can enter the bloodstream and affect the heart,lungs, kidneys, or other organs.

Acute pancreatitis sometimes causes kidney failure. People with kidney failure need blood-cleansing treatmentscalled dialysis or a kidney transplant.

In rare cases, acute pancreatitis can cause breathing problems. Hypoxia, a condition that occurs when body cells andtissues do not get enough oxygen, can develop. Doctors treat hypoxia by giving oxygen to the patient. Some peoplestill experience lung failure²even with oxygen²and require a respirator for a while to help them breathe.

CHRONIC PREATITIS

Chronic pancreatitis is inflammation of the pancreas that does not heal or improve²it gets worse over time and leadsto permanent damage. Chronic pancreatitis, like acute pancreatitis, occurs when digestive enzymes attack thepancreas and nearby tissues, causing episodes of pain. Chronic pancreatitis often develops in people who arebetween the ages of 30 and 40.

The most common cause of chronic pancreatitis is many years of heavy alcohol use. The chronic form of pancreatitiscan be triggered by one acute attack that damages the pancreatic duct. The damaged duct causes the pancreas tobecome inflamed. Scar tissue develops and the pancreas is slowly destroyed.



Other causes of chronic pancreatitis are

y hereditary disorders of the pancreas

y cystic fibrosis²the most common inherited disorder leading to chronic pancreatitis

y hypercalcemia²high levels of calcium in the blood

y hyperlipidemia or hypertriglyceridemia²high levels of blood fats

y some medicinesy certain autoimmune conditions

y unknown causes

Hereditary pancreatitis can present in a person younger than age 30, but it might not be diagnosed for several years.Episodes of abdominal pain and diarrhea lasting several days come and go over time and can progress to chronicpancreatitis. A diagnosis of hereditary pancreatitis is likely if the person has two or more family members withpancreatitis in more than one generation.

Sy mptoms

Most people with chronic pancreatitis experience upper abdominal pain, although some people have no pain at all.The pain may spread to the back, feel worse when eating or drinking, and become constant and disabling. In some

cases, abdominal pain goes away as the condition worsens, most likely because the pancreas is no longer makingdigestive enzymes. Other symptoms include

y nausea

y vomiting

y weight loss

y diarrhea

y oily stools

People with chronic pancreatitis often lose weight, even when their appetite and eating habits are normal. The weightloss occurs because the body does not secrete enough pancreatic enzymes to digest food, so nutrients are notabsorbed normally. Poor digestion leads to malnutrition due to excretion of fat in the stool.

Di agnos

i s

Chronic pancreatitis is often confused with acute pancreatitis because the symptoms are similar. As with acutepancreatitis, the doctor will conduct a thorough medical history and physical examination. Blood tests may help thedoctor know if the pancreas is still making enough digestive enzymes, but sometimes these enzymes appear normaleven though the person has chronic pancreatitis.

In more advanced stages of pancreatitis, when malabsorption and diabetes can occur, the doctor may order blood,urine, and stool tests to help diagnose chronic pancreatitis and monitor its progression.

After ordering x rays of the abdomen, the doctor will conduct one or more of the tests used to diagnose acutepancreatitis²abdominal ultrasound, CT scan, EUS, and MRCP.

Treatment

Treatment for chronic pancreatitis may require hospitalization for pain management, IV hydration, and nutritionalsupport. Nasogastric feedings may be necessary for several weeks if the person continues to lose weight.

When a normal diet is resumed, the doctor may prescribe synthetic pancreatic enzymes if the pancreas does notsecrete enough of its own. The enzymes should be taken with every meal to help the person digest food and regainsome weight. The next step is to plan a nutritious diet that is low in fat and includes small, frequent meals. A dietitiancan assist in developing a meal plan. Drinking plenty of fluids and limiting caffeinated beverages is also important.



People with chronic pancreatitis are strongly advised not to smoke or consume alcoholic beverages, even if thepancreatitis is mild or in the early stages.

C ompl ic at i ons

People with chronic pancreatitis who continue to consume large amounts of alcohol may develop sudden bouts of

severe abdominal pain.

As with acute pancreatitis, ERCP is used to identify and treat complications associated with chronic pancreatitis suchas gallstones, pseudocysts, and narrowing or obstruction of the ducts. Chronic pancreatitis also can lead tocalcification of the pancreas, which means the pancreatic tissue hardens from deposits of insoluble calcium salts.Surgery may be necessary to remove part of the pancreas.

In cases involving persistent pain, surgery or other procedures are sometimes recommended to block the nerves inthe abdominal area that cause pain.

When pancreatic tissue is destroyed in chronic pancreatitis and the insulin-producing cells of the pancreas, calledbeta cells, have been damaged, diabetes may develop. People with a family history of diabetes are more likely todevelop the disease. If diabetes occurs, insulin or other medicines are needed to keep blood glucose at normallevels. A health care provider works with the patient to develop a regimen of medication, diet, and frequent blood

glucose monitoring.

Lung Cancer

Also called bronchogenic cancer .

It is a malignant tumor of the lung arising within the bronchial wall or epithelium.

Bronchogenic cancer is classified according to cell type: epidermoid (squamous cell ± most common),

adenocarcinoma, small cell (oat cell) carcinoma, and large cell (undifferentiated) carcinoma.

The lung is also a common site of metastasis from cancer elsewhere in the body through venous circulation or

lymphatic spread.

The primary predisposing factor in lung cancer is cigarette smoking.

Lung cancer risk is also high in people occupationally exposed to asbestos, arsenic, chromium, nickel, iron,

radioactive substances, isopropyl oil, coal tar products, and petroleum oil mists. Complications include superior vena cava syndrome, hypercalcemia (from bone metastasis), syndrome of

inappropriate antidiuretic hormone (SIADH), pleural effusion, pneumonia, brain metastasis, and spinal cord

compression.

ASSESSMENT

New or changing cough, dyspnea, wheezing, excessive sputum production, hemoptysis,chest pain (aching,

poorly localized), malaise, fever, weight loss, fatigue, or anorexia.

Decreased breath sounds, wheezing, and possible pleural friction rub (with pleural effusion) on examination.

DIAGNOSTIC EVALUATION

Chest X-ray may be suspicious for mass; CT or position emission tomography scan will be better visualize tumor.

Sputum and pleural fluid samples for cytologic examination may show malignant cells.

Fiberoptic bronchoscopy determines the location and extent of the tumor and may be used to obtain a biopsy

specimen.

Lymph node biopsy and mediastinoscopy may be ordered to establish lymphatic spread and help plan treatment.

Pulmonary function test, which may be combined with a split-function perfusion scan, determines if the patient will

have adequate pulmonary reserve to withstand surgical procedure.

PHARMACOLOGIC INTERVENTIONS

Expectorants and antimicrobial agents to relieve dyspnea and infection.

Analgesics given regularly to maintain pain at tolerable level. Titrate dosages to achieve pain control.



Chemotherapy using cisplatin in combination with a variety of other agents and immunotherapy treatments may

be indicated.

SURGICAL INTERVENTIONS

Resection of tumor, lobe, or lung.

THERAPEUTIC INTERVENTIONS

Oxygen through nasal cannula based on level of dyspnea.

Enteral or total parenteral nutrition for malnourished patient who is unable or unwilling to eat.

Removal of the pleural fluid (by thoracentesis or tube thoracostomy) and instillation of sclerosing agent to

obliterate pleural space and fluid recurrence.

Radiation therapy in combination with other methods.

NURSING INTERVENTIONS

1. Elevate the head of the bed to ease the work of breathing and to prevent fluid collection in upper body (from

superior vena cava syndrome).

2. Teach breathing retraining exercises to increase diaphragmatic excursion and reduce work of breathing.

3. Augment the patient¶s ability to cough effectively by splinting the patient¶s chest manually.

4. Instruct the patient to inspire fully and cough two to three times in one breath.

5. Provide humidifier or vaporizer to provide moisture to loosen secretions.

6. Teach relaxation techniques to reduce anxiety associated with dyspnea. Allow the severely dyspneic patient to

sleep in reclining chair.

7. Encourage the patient to conserve energy by decreasing activities.

8. Ensure adequate protein intake such as milk, eggs, oral nutritional supplements; and chicken, fowl, and fish if

other treatments are not tolerated ± to promote healing and prevent edema.

9. Advise the patient to eat small amounts of high-calorie and high-protein foods frequently, rather than three daily

meals.

10. Suggest eating the major meal in the morning if rapid satiety is the problem.

11. Change the diet consistency to soft or liquid if patient has esophagitis from radiation therapy.

12. Consider alternative pain control methods, such as biofeedback and relaxation methods, to increase the patient¶s

sense of control.

13. Teach the patient to use prescribed medications as needed for pain without being overly concerned aboutaddiction.

THORACENTESIS

Also known as pleural fluidaspiration, the thoracic wall is punctured to obtain a specimen of pleural fluid for analysis

or to relieve pulmonary compression and resultant respiratory distress. Locating the fluid beforethoracentesis reduces

the risk of puncturing the lung, liver, or spleen.

The pleural cavity should contain less than 20 ml of serous fluid. Pleural effusionresults from the abnormal formation

or reabsorption ofpleural fluid. Certain characteristics classify pleural fluid as either a transudate or exudates.

Pupose

To provide pleural fluid specimens to determine the cause and nature of pleural effusion.

To provide symptomatic relief with large pleural effusion.

Procedure

Preparation

1. Check the patient¶s history for bleeding disorders or anticoagulant therapy.

2. Explain that a chest X-ray or ultrasound study may precede the test.

3. Explain the procedure to the patient.

4. Instruct the patient no to cough, breathe deeply, or move during the test to minimize the risk of lung injury.

5. Record the patient¶s baseline vital signs.



6. Shave the area around the needle insertion site, if necessary, and position the patientproperly.

Implementation

1. Position the patient to widen the intercostals spaces and allow easier access to the pleural cavity.

2. If the patient can¶t sit up, position him on his unaffected side with the arm on the affected side elevated.

3. After the patient is in proper position, prepare and drape the site.

4. Inject a local anesthetic into the subcutaneous tissue; the thoracenthesis needle is then inserted.

5. When the needle reaches the pocket of fluid, it¶s attached to a 50-ml syringe or a vacuum bottle and the fluid is

removed.

6. During aspiration, the patient is monitors for signs of respiratory distress and hypotension.

7. Pleural fluid characteristics and total volume are noted.

8. After the needle is withdrawn, apply pressure until hemostasis is obtained and a small dressing is applied.

9. Place specimens in proper containers, labeled appropriately, and send to the laboratory immediately.

10. Pleural fluid for pH determination must be collected anaerobically, heparinized, kept on ice, and analyzed

promptly.


1. Elevate the head of the bed to facilitate breathing.

2. Obtain a chest X-ray.

3. Tell the patient to immediately report difficulty of breathing.

4. Immediately report signs and symptoms of pneumothorax, tension pneumothorax, andpleural

fluid reaccumulation.

5. Monitor the patient for reexpansion pulmonary edema (RPE), a rare but serious complication

of thoracentesis. Thoracentesis hould be halted If the patient has sudden chest tightness or coughing.

6. Monitor vital signs, pulse oximetry, and breathe sounds.

7. Observe the puncture site and dressings.

8. Watch for subcutaneous emphysema.

9. Monitor pleural pressure.

Interpretation

Normal Results

Negative pressure in the pleural cavity with less than 50 ml serous fluid.Abnormal Results

Bloody fluid suggests possible hemothorax, malignancy, and traumatic tap.

Milky fluid suggests chylothorax.

Fluid with pus suggests empyema.

Transudative effusion suggests heart failure, hepatic cirrhosis, or renal disease.

Exudative effusion, suggests lymphatic drainage abstraction, infections, pulmonary infarctions, and neoplasma.

Positive cultures suggest infection.

Predominating lymphocytes suggest tuberculosis or fungal or viral effusions.

Pleural fluid glucose levels that are 30 to 40 mg/dl lower than blood glucose levels may indicate cancer, bacterial

infection, or metastasis.

Increased amylase suggests pleural effusions associated with pancreatitis.Interfering Factors

Failure to use sterile technique.

Antimicrobial therapy before fluid aspiration for culture (possible decrease in numbers of bacteria, making it

difficult to isolate the infecting organism).

Precautions

Thoracentesis is contraindicated in the patient who has a history of bleeding disorders oranticoagulant therapy.

The strict sterile technique.



Complications

Laceration of intercostals vessels

Pneumothorax

Mediastinal shift

Reexpansion pulmonary edema (RPE)

Bleeding and infection

COPD is a disease state characterized by airflow limitation that is not fully reversible. This newest definition COPD,

provided by the Global Initiative for Chrnonic Obstructive Lung Disease (GOLD), is a broad description that better

explains this disorder and its signs and symptoms (GOLD, World Health Organization [WHO] & National Heart, Lung

and Blood Institute [NHLBI], 2004). Although previous definitions have include emphysema and chronic bronchitis

under the umbrella classification of COPD, this was often confusing because most patient with COPD present with

over lapping signs and symptoms of these two distinct disease processes.

COPD may include diseases that cause airflow obstruction (e.g., Emphysema, chronic bronchitis) or any combination

of these disorders. Other diseases as cystic fibrosis, bronchiectasis, and asthma that were previously classified as

types of chronic obstructive lung disease are now classified as chronic pulmonary disorders. However, asthma is now

considered as a separate disorder and is classified as an abnormal airway condition characterized primarily by

reversible inflammation. COPD can co-exist with asthma. Both of these diseases have the same major symptoms;

however, symptoms are generally more variable in asthma than in COPD.

Currently, COPD is the fourth leading cause of mortality and the 12th

leading cause of disability. However, by the year

2020 it is estimated that COPD will be the third leading cause of death and the firth leading cause of disability (Sin,

McAlister, Man. Et al., 2003). People with COPDcommonly become symptomatic during the middle adult years, and

the incidence of the disease increases with age.

The Upper Airway and Trachea

When you breathe in, air enters your body through your nose or mouth. From there, it travels down your throat

through the larynx (or voicebox) and into the trachea (or windpipe) before entering your lungs. All these structures act

to funnel fresh air down from the outside world into your body. The upper airway is important because it must always

stay open for you to be able to breathe. It also helps to moisten and warm the air before it reaches your lungs.

The Lungs

Structure

The lungs are paired, cone-shaped organs which take up most of the space in our chests, along with the heart. Their

role is to take oxygen into the body, which we need for our cells to live and function properly, and to help us get rid of

carbon dioxide, which is a waste product. We each have two lungs, a left lung and a right lung. These are divided up

into µlobes¶, or big sections of tissue separated by µfissures¶ or dividers. The right lung has three lobes but the left lung

has only two, because the heart takes up some of the space in the left side of our chest. The lungs can also be

divided up into even smaller portions, called µbronchopulmonary segments¶.

These are pyramidal-shaped areas which are also separated from each other by membranes. There are about 10 of

them in each lung. Each segment receives its own blood supply and air supply.

How they work

Air enters your lungs through a system of pipes called the bronchi. These pipes start from the bottom of the trachea

as the left and right bronchi and branch many times throughout the lungs, until they eventually form little thin-walled

air sacs or bubbles, known as the alveoli. The alveoli are where the important work of gas exchange takes place

between the air and your blood. Covering each alveolus is a whole network of little blood vessel called capillaries,

which are very small branches of the pulmonary arteries. It is important that the air in the alveoli and the blood in the

capillaries are very close together, so that oxygen and carbon dioxide can move (or diffuse) between them. So, when

you breathe in, air comes down the trachea and through the bronchi into the alveoli. This fresh air has lots of oxygen



in it, and some of this oxygen will travel across the walls of the alveoli into your bloodstream. Traveling in the opposite

direction is carbon dioxide, which crosses from the blood in the capillaries into the air in the alveoli and is then

breathed out. In this way, you bring in to your body the oxygen that you need to live, and get rid of the waste product

carbon dioxide.

Blood Supply

The lungs are very vascular organs, meaning they receive a very large blood supply. This is because the pulmonary

arteries, which supply the lungs, come directly from the right side of your heart. They carry blood which is low in

oxygen and high in carbon dioxide into your lungs so that the carbon dioxide can be blown off, and more oxygen can

be absorbed into the bloodstream. The newly oxygen-rich blood then travels back through the paired pulmonary veins

into the left side of your heart. From there, it is pumped all around your body to supply oxygen to cells and organs.

The Work of Breathing

The Pleurae

The lungs are covered by smooth membranes that we call pleurae. The pleurae have two layers, a µvisceral¶ layer

which sticks closely to the outside surface of your lungs, and a µparietal¶ layer which lines the inside of your chest wall

(ribcage). The pleurae are important because they help you breathe in and out smoothly, without any friction. They

also make sure that when your ribcage expands on breathing in, your lungs expand as well to fill the extra space.

The Diaphragm and Intercostal Muscles

When you breathe in (inspiration), your muscles need to work to fill your lungs with air. The diaphragm, a large,

sheet-like muscle which stretches across your chest under the ribcage, does much of this work. At rest, it is shaped

like a dome curving up into your chest. When you breathe in, the diaphragm contracts and flattens out, expanding the

space in your chest and drawing air into your lungs. Other muscles, including the muscles between your ribs (the

intercostal muscles) also help by moving your ribcage in and out. Breathing out (expiration) does not normally require

your muscles to work. This is because your lungs are very elastic, and when your muscles relax at the end of

inspiration your lungs simply recoil back into their resting position, pushing the air out as they go.

The Respiratory System and Ageing

The normal process of ageing is associated with a number of changes in both the structure and function of

the respiratory system. These include:

Enlargement of the alveoli. The air spaces get bigger and lose their elasticity, meaning that there is less area for

gases to be exchanged across. This change is sometimes referred to as µsenile emphysema¶.

The compliance (or springiness) of the chest wall decreases, so that it takes more effort to breathe in and out.

The strength of the respiratory muscles (the diaphragm and intercostal muscles) decreases. This change is

closely connected to the general health of the person.

All of these changes mean that an older person might have more difficulty coping with increased stress on

their respiratory system, such as with an infection like pneumonia, than a younger person would.

Risk factors for COPD include environmental exposures and host factors. The most important risk factor for COPD is

cigarette smoking. Other risk factors are pipe, cigar, and other types of tobacco smoking. In addition, passive

smoking contributes to respiratory symptoms and COPD. Smoking depresses the activity of scavenger cells and

affects the respiratory tract¶s ciliary cleansing mechanism, which keeps breathing passages free of inhaled irritants,bacteria, and other foreign matter. When smoking damages this cleansing mechanism, airflow is obstructed and air

becomes trapped behind the obstruction. The alveoli greatly distend, diminished lung capacity. Smoking also irritates

the goblet cells and mucus glands, causing an increased accumulation of mucus, which in turn produces more

irritation, infection, and damage to the lung. In addition, carbon monoxide (a by product of smoking) combines with

hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen

efficiently.



A host risk factor for COPD is a deficiency of alpha antitrypsin, an enzyme inhibitor that protects the lung parenchyma

from injury. This deficiency predisposes young people to rapid development of lobular emphysema, even if they do

not smoke. Genetically susceptible people are sensitive to environmental factors (eg. Smoking, air pollution,

infectious agents, allergens) and eventually developed chronic obstructive symptoms. Carriers of this genetic defect

must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease.

PATHOPHYSIOLOG Y

In COPD, the airflow limitation is both progressive and associated with an abnormal inflammatory response of the

lungs to noxious particles or gases. The inflammatory response occurs throughout the airways, parenchyma, and

pulmonary vasculature. Because of the chronic inflammation and the body¶s attempts to repair it, narrowing occurs in

the small peripheral airways. Over time, this injury-and-repair process causes scar tissue formation and narrowing of

the airway lumen. Airflow obstruction may also be caused by parenchymal destruction, as is seen with emphysema, a

disease of the alveoli or gas exchange units.

In addition to inflammation, processes related to imbalances of proteinases and antiproteinases in the lung may be

responsible for airflow limitation. When activated by chronic inflammation, proteiness and other substances may be

released, damaging the parenchyma of the lung. The parenchymal changes may occur as a consequence of

inflammation or environmental or genetic factors (eg. Alpha1-antitrypsin deficiency).

Early in the course of COPD, the inflammatory response causes pulmonary vasculature changes that are

characterized by thickening of the vessel wall. These changes may result from exposure to cigarette smoke, use of

tobacco products, and the release of inflammatory medicators.

CHRONIC BRONCHITIS

Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in

clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. In the

airways of the lung, the hallmark of chronic bronchitris is an increased number (hyperplasia) and increased size

(hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the

airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration

of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the

walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia

(an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the

airway wall). The consequence of these changes is a limitation of airflow.Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred

to as ³blue bloaters´ because of the bluish color of the skin and lips (cyanosis) seen in them. The hypoxia and fluid

retention leads to them being called ³Blue Bloaters.´

ACUTE BRONCHITIS

PHYSICAL MANIFESTATIONS

One of the most common symptoms of COPD is shortness of breath (dyspnea). People withCOPD commonly

describe this as: ³My breathing requires effort´, ³I feel out of breath´, or ³I can not get enough air in´. People

with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over

the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as

housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly

present. Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness,and tiredness. People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens,

cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon

dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is

cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected

lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.

There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases.

Some people have COPD and have none of these signs. Common signs are:



tachypnea, a rapid breathing rate

wheezing sounds or crackles in the lungs heard through a stethoscope

breathing out taking a longer time than breathing in

enlargement of the chest, particularly the front-to-back distance (hyperinflation)

active use of muscles in the neck to help with breathing

breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).

Emphysema is a chronic obstructive pulmonary disease (COPD, as it is otherwise known, formerly termed a

chronic obstructive lung disease). It is often caused by exposure to toxic chemicals, including long-term exposure to

tobacco smoke. Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung

tissue caused by destruction of structures feeding the alveoli, owing to the action of alpha 1 antitrypsin deficiency.

This causes the small airways to collapse during forced exhalation, as alveolar collapsibility has decreased. As a

result, airflow is impeded and air becomes trapped in the lungs, in the same way as other obstructive lung diseases.

Symptoms include shortness of breath on exertion, and an expanded chest. However, the constriction of air

passages isn¶t always immediately deadly, and treatment is available.

PHYSICAL MANIFESTATIONS

Signs of emphysema include pursed-lipped breathing, central cyanosis and finger clubbing. The chest has hyper

resonant percussion notes, particularly just above the liver, and a difficult to palpate apex beat, both due to

hyperinflation. There may be decreased breath sounds and audible expiratory wheeze. In advanced disease, there

are signs of fluid overload such as pitting peripheral edema. The face has a ruddy complexion if there is a secondary

polycythemia. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist.

DIAGNOSTIC EVALUATION

1. PFTs demonstrative airflow obstruction ± reduced forced vital capacity (FVC), FEV1, FEV1 to FVC ration;

increased residual volume to total lung capacity (TLC) ratio, possibly increased TLC.

2. ABG levels- decreased PaO2, pH, and increased CO2.

3. Chest X-ray ± in late stages, hyperinflation, flattened diaphragm, increased rettrosternal space, decreased

vascular markings, possible bullae.

4. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema.

TREATMENT The goals of COPD treatment are 1) to prevent further deterioration in lung function, 2) to alleviate symptoms, 3) to

improve performance of daily activities and quality of life. The treatment strategies include 1) quitting cigarette

smoking, 2) taking medications to dilate airways (bronchodilators) and decrease airway inflammation, 3) vaccinating

against flu influenza and pneumonia and 4) regular oxygen supplementation and 5) pulmonary rehabilitation.

Quitting cigarette smoking

The most important treatment for COPD is quitting cigarette smoking. Patients who continue to smoke have a more

rapid deterioration in lung function when compared to others who quit. Aging itself can cause a very slow decline in

lung function. In susceptible individuals, cigarette smoking can result in a much more dramatic loss of lung function. It

is important to note that when one stops smoking the decline in lung function eventually reverts to that of a non-

smoker.

Nicotine in cigarettes is addictive, and, therefore, cessation of smoking can cause symptoms of nicotine withdrawalincluding anxiety, irritability, anger, depression, fatigue, difficulty concentrating or sleeping, and intense craving for

cigarettes. Patients likely to develop withdrawal symptoms typically smoke more than 20 cigarettes a day, need to

smoke shortly after waking up in the morning, and have difficulty refraining from smoking in non-smoking areas.

However, some 25% of smokers can stop smoking without developing these symptoms. Even in those smokers who

develop symptoms of withdrawal, the symptoms will decrease after several weeks of abstinence.



Bronchodilators

Treating airway obstruction in COPD with bronchodilators is similar but not identical to treating bronchospasm in

asthma. Bronchodilators are medications that relax the muscles surrounding the small airways thereby opening the

airways. Bronchodilators can be inhaled, taken orally or administered intravenously. Inhaled bronchodilators are

popular because they go directly to the airways where they work. As compared with bronchodilators given orally, less

medication reaches the rest of the body, and, therefore, there are fewer side effects.

Metered dose inhalers (MDIs) are used to deliver bronchodilators. An MDI is a pressurized canister containing a

medication that is released when the canister is compressed. A standard amount of medication is released with each

compression of the MDI. To maximize the delivery of the medications to the airways, the patient has to learn to

coordinate inhalation with each compression. Incorrect use of the MDI can lead to deposition of much of the

medication on the tongue and the back of the throat instead of on the airways.

To decrease the deposition of medications on the throat and increase the amount reaching the airways, spacers can

be helpful. Spacers are tube-like chambers attached to the outlet of the MDI canister. Spacer devices can hold the

released medications long enough for patients to inhale them slowly and deeply into the lungs. Proper use of spacer

devices can greatly increase the proportion of medication reaching the airways.

Oxygen Therapy

Other treatments Pulmonary rehabilitation has become a cornerstone in the management of moderate to severe COPD.

Pulmonary rehabilitation is a program of education regarding lung function and dysfunction, proper breathing

techniques (diaphragmatic breathing, pursed lip breathing), and proper use of respiratory equipment and

medications. An essential ingredient in this program is the use of increasing physical exercise to overcome the

reduced physical capacity that usually has developed over time. In addition, occupational and physical therapy

are used to teach optimal and efficient body mechanics.

Lung vol ume red uc t i on surger y (LVRS) has received much fanfare in the lay press. LVRS is a surgical procedure

used to treat some patients with COPD. The premise behind this surgery is that the over-inflated, poorly-

functioning upper parts of the lung compress and impair function of the better-functioning lung elsewhere. Thus, if

the over-inflated portions of lung are removed surgically, the compressed lung may expand and function better. In

addition, the diaphragm and the chest cavity achieve more optimal positioning following the surgery, and thisimproves breathing further. The best criteria for choosing patients for LVRS are still uncertain. A national study

was completed in 2003. Patients primarily with emphysema at the top of their lungs, whose exercise tolerance

was low even after pulmonary rehabilitation, seemed to do the best with this procedure. On average, lung function

and exercise capacity among surviving surgical patients improved significantly following LVRS, but after two

years returned to about the same levels as before the procedure. Patients with forced expiratory volume in FEVI

of less than 20% of predicted and either diffuse disease on the CAT scan or lower than 20% diffusing capacity or

elevated carbon dioxide levels had higher mortality. The role of LVRS is at present is very limited.

PHARMACOLOGIC INTERVENTIONS

Beta-agonists

Beta-2 agonists have the bronchodilating effects of adrenaline without many of its unwanted side effects.

Beta-2 agonists can be administered by MDI inhalers or orally. They are called ³agonists´ because theyactivate the beta-2 receptor on the muscles surrounding the airways. Activation of beta-2 receptors relaxes

the muscles surrounding the airways and opens the airways. Dilating airways helps to relieve the symptoms

of dyspnea (shortness of breath). Beta-2 agonists have been shown to relieve dyspnea in many COPD

patients, even among those without demonstrable reversibility in airway obstruction. The action of beta-2

agonists starts within minutes after inhalation and lasts for about 4 hours. Because of their quick onset of

action, beta-2 agonists are especially helpful for patients who are acutely short of breath. Because of their

short duration of action, these medications should be used for symptoms as they develop rather than as



maintenance. Evidence suggests that when these drugs are used routinely, their effectiveness is diminished.

These are referred to as rescue inhalers. Examples of beta-2 agonists include albuterol (Ventolin, Proventil),

metaproterenol (Alupent), pirbuterol (Maxair), terbutaline (Brethaire), and isoetharine (Bronkosol).

Levalbuterol (Xopenex) is a recently approved Beta-2 agonist.

In contrast, Beta-2 agonists with a slower onset of action but a longer period of activity, such as salmeterol

xinafoate (Serevent) and formoterol fumarate (Foradil) may be used routinely as maintenance medications.

These drugs last twelve hours and should be taken twice daily and no more. Along with some of these

inhalers to be mentioned, these are often referred to as maintenance inhalers.

Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast heart rate, and low blood

potassium.

Anti-cholinergic Agents

Acetylcholine is a chemical released by nerves that attaches to receptors on the muscles surrounding the

airway causing the muscles to contract and the airways to narrow. Anti-cholinergic drugs such as ipratropium

bromide (Atrovent) dilate airways by blocking the receptors for acetylcholine on the muscles of the airways

and preventing them from narrowing. Ipratropium bromide (Atrovent) usually is administered via a MDI. In

patients with COPD, ipratropium has been shown to alleviate dyspnea, improve exercise tolerance and

improve FEV1. Ipratropium has a slower onset of action but longer duration of action than the shorter-acting

beta-2 agonists. Ipratropium usually is well tolerated with minimal side effects even when used in higher

doses. Tiotropium (SPIRIVA) is a long acting and more powerful version of Ipratropium and has been shown

to be more effective.

In comparing ipratropium with beta-2 agonists in the treatment of patients with COPD, studies suggest that

ipratropium may be more effective in dilating airways and improving symptoms with fewer side effects.

Ipratropium is especially suitable for use by elderly patients who may have difficulty with fast heart rate and

tremor from the beta-2 agonists. In patients who respond poorly to either beta-2 agonists or ipratropium alone,

a combination of the two drugs sometimes results in a better response than to either drug alone without

additional side effects.

Methylxanthines

Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl, Theo-24) and aminophylline are examples of

methylxanthines. Methylxanthines are administered orally or intravenously. Long acting theophyllinepreparations can be given orally once or twice a day. Theophylline, like a beta agonist, relaxes the muscles

surrounding the airways but also prevents mast cells around the airways from releasing bronchoconstricting

chemicals such as histamine. Theophylline also can act as a mild diuretic and increase urination.

Theophylline also may increase the force of contraction of the heart and lower pressure in the pulmonary

arteries. Thus, theophylline can help patients with COPD who have heart failure and pulmonary hypertension.

Patients who have difficulty using inhaled bronchodilators but no difficulty taking oral medications find

theophylline particularly useful.

The disadvantage of methylxanthines is their side effects. Dosage and blood levels of theophylline or

aminophylline have to be closely monitored. Excessively high levels in the blood can lead to nausea, vomiting,

heart rhythm problems, and even seizures. In patients with heart failure or cirrhosis, dosages of

methylxanthines are lowered to avoid high blood levels. Interactions with other medications, such ascimetidine (Tagamet), calcium channel blockers (Procardia), quinolones (Cipro), and allopurinol (Zyloprim)

also can alter blood levels of methylxanthines.

Corticosteroids

When airway inflammation (which causes swelling) contributes to airflow obstruction, anti-inflammatory

medications (more specifically, corticosteroids) may be beneficial. Examples of corticosteroids include

Prednisone and Prednisolone. Twenty to thirty percent of patients with COPD show improvement in lung

function when given corticosteroids by mouth. Unfortunately, high doses of oral corticosteroids over prolonged

periods can have serious side effects, including osteoporosis, bone fractures, diabetes mellitus, high blood



pressure, thinning of the skin and easy bruising, insomnia, emotional changes, and weight gain. Therefore,

many doctors use oral corticosteroids as the treatment of last resort. When oral corticosteroids are used, they

are prescribed at the lowest possible doses for the shortest period of time to minimize side effects. When it is

necessary to use long term oral steroids, medications are often prescribed to help reduce the development of

the above side effects.

Corticosteroids also can be inhaled. Inhaled corticosteroids have many fewer side effects than long term oral

corticosteroids. Examples of inhaled corticosteroids include beclomethasone dipropionate (Beclovent,

Beconase, Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), fluticasone (Flovent), budesonide

(Pulmicort), mometasone furoate (Asmanex) and flunisolide (Aerobid). Inhaled corticosteroids have been

useful in treating patients with asthma, but in patients with COPD, it is not clear whether inhaled corticosteroid

have the same benefit as oral corticosteroids. Nevertheless, doctors are less concerned about using inhaled

corticosteroids because of their safety. The side effects of inhaled corticosteroids include hoarseness, loss of

voice, and oral yeast infections. A spacing device placed between the mouth and the MDI can improve

medication delivery and reduce the side effects on the mouth and throat. Rinsing out the mouth after use of a

steroid inhaler also can decrease these side effects.

Treatment of Alpha-1 antitrypsin deficiency

Emphysema can develop at a very young age in some patients with severe alpha-1 antitrypsin deficiency

(AAT). Replacement of the missing or inactive AAT by injection can help prevent progression of the

associated emphysema. This therapy is of no benefit in other types of COPD.

COMPLICATIONS

1. Respiratory failure

2. Pneumonia, overwhelming respiratory infection

3. Right-sided heart failure, dysrhythmias

4. Depression

5. Skeletal muscle dysfunction

NURSING INTERVENTIONS

Monitoring

1. Monitor for adverse effects of bronchodilators ± tremulousness, tachycardia, cardiac arrhythmias, central nervous

system stimulation, hypertension.2. Monitor condition after administration of aerosol bronchodilators to assess for improved aeration, reduced

adventitious sounds, reduced dyspnea.

3. Monitor serum theophylline level, as ordered, to ensure therapeutic level and prevent toxicity.

4. Monitor oxygen saturation at rest and with activity.

Supportive Care

1. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually reduces pulmonary

irritation, sputum production, and cough. Keep the patient¶s room as dust-free as possible.

2. Use postural drainage positions to help clear secretions responsible for airway obstructions.

3. Teach controlled coughing.

4. Encourage high level of fluid intake ( 8 to 10 glasses; 2 to 2.5 liters daily) within level of cardiac reserve.

5. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Add moisture (humidifier,vaporizer) to indoor air.

6. Avoid dairy products if these increases sputum production.

7. Encourage the patient to assume comfortable position to decrease dyspnea.

8. Instruct and supervise patient¶s breathing retraining exercises.

9. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and depth of respiration and

improve respiratory muscle coordination.

10. Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.

11. Maintain the patient¶s nutritional status.



12. Reemphasize the importance of graded exercise and physical conditioning programs.

13. Encourage use of portable oxygen system for ambulation for patients with hypoxemia and marked disability.

14. Train the patient in energy conservation technique.

15. Assess the patient for reactive-behaviors such as anger, depression and acceptance.

Education and health maintenance

1. Review with the patient the objectives of treatment and nursing management.

2. Advise the patient to avoid respiratory irritants. Suggest that high efficiency particulate air filter may have some

benefit.

3. Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial obstruction and

sputum obstruction.

4. Warn patient to avoid persons with respiratory infections, and to avoid crowds and areas with poor ventilation.

5. Teach the patient how to recognize and report evidence of respiratory infection promptly such as chest pain,

changes in character of sputum (amount, color and consistency), increasing difficulty in raising sputum,

increasing coughing and wheezing, increasing of shortness of breath.

Asthma is a chronic, reversible, obstructive airway disease, characterized by wheezing. It is caused by a spasm of

the bronchial tubes, or the swelling of the bronchial mucosa, after exposure to various stimuli.

Asthma is the most common chronic disease in childhood. Most children experience their firstsymptoms by 5 years of

age.

ETIOLOG Y:

Asthma commonly results from hyperresponsiveness of the trachea and bronchi to irritants. Allergy influences both

the persistence and the severity of asthma, and atopy or the genetic predisposition for the development of an IgE-

mediated response to common airborne allergens is the most predisposing factor for the development of asthma.

CLASSIFICATION:

1. Extrinsic Asthma ± called Atopic/allergic asthma. An ³allergen´ or an ³antigen´ is a foreign particle which enters

the body. Our immune system over-reacts to these often harmless items, forming ³antibodies´ which are normally

used to attack viruses or bacteria. Mast cells release these antibodies as well as other chemicals to defend the body.

Common irritants:

Cockroach particles Cat hair and saliva

Dog hair and saliva

House dust mites

Mold or yeast spores

Metabisulfite, used as a preservative in many beverages and some foods

Pollen

2. Intrinsic asthma ± called non-allergic asthma, is not allergy-related, in fact it is caused by anything except an

allergy. It may be caused by inhalation of chemicals such as cigarette smoke or cleaning agents, taking aspirin, a

chest infection, stress, laughter, exercise, cold air, food preservatives or a myriad of other factors.

Smoke

Exercise Gas, wood, coal, and kerosene heating units

Natural gas, propane, or kerosene used as cooking fuel

Fumes

Smog

Viral respiratory infections

Wood smoke

Weather changes



ANATOMY AND PHYSIOLOG Y:

The upper respiratory tract consists of the nose, sinuses, pharynx, larynx, trachea, and epiglottis.

The lower respiratory tract consist of the bronchi, bronchioles and the lungs.

The major function of the respiratory system is to deliver oxygen to arterialblood and remove carbon dioxide from

venous blood, a process known as gas exchange.

T he normal gas exchange depends on three process:

Ventilation ± is movement of gases from the atmosphere into and out of the lungs. This is accomplished through

the mechanical acts of inspiration and expiration.

Diffusion ± is a movement of inhaled gases in the alveoli and across the alveolar capillary membrane

Perfusion ± is movement of oxygenated blood from the lungs to the tissues.

C ontrol of gas exchange ± involves neural and chemical process

The neural system, composed of three parts located in the pons, medulla and spinal cord, coordinates respiratory

rhythm and regulates the depth of respirations

The chemical processes perform several vital functions such as:

regulating alveolar ventilation by maintaining normal blood gas tension

guarding against hypercapnia (excessive CO2 in the blood) as well as hypoxia (reduced tissue oxygenation

caused by decreased arterial oxygen [PaO2]. An increase in arterial CO2(PaCO2) stimulates ventilation;

conversely, a decrease in PaCO2 inhibits ventilation.

helping to maintain respirations (through peripheral chemoreceptors) when hypoxia occurs.

The normal functions of respiration O2 and CO2 tension and chemoreceptors are similar in children and adults.

however, children respond differently than adults to respiratory disturbances; major areas of difference include:

Poor tolerance of nasal congestion, especially in infants who are obligatory nose breathers up to 4 months of age

Increased susceptibility to ear infection due to shorter, broader, and more horizontally positioned eustachian

tubes.

Increased severity or respiratory symptoms due to smaller airway diameters

A total body response to respiratory infection, with such symptoms as fever, vomiting and diarrhea.

SIGNSAND SYMPTOMS:

1. Non Productive to Productive Cough 2. Dyspnea

3. Wheezing on expiration

4. Cyanosis

5. Mild apprehension and restlessness

6. Tachycardia and palpitation

7. Diaphoresis

PATHOPHYSIOLOG Y:

CLINICALMANIFESTATIONS:

1. Increased respiratory rate

2. Wheezing (intensifies as attack progresses)

3. Cough (productive)4. Use of accessory muscles

5. Distant breath sounds

6. Fatigue

7. Moist skin

8. Anxiety and apprehension

9. Dyspnea

Steps of Clinical and Diagnostic as per National Asthma Education and Prevention Program

M i ld Intermi ttent Asthma



Symptoms ? 2 times per week

Brief exacerbations

Nighttime symptoms ? 2 times a month

Asymptomatic and normal PEF (peak expiratory flow) between exacerbations

PEF or FEV, (forced expiratory volume in 1 second) ? 80% of predicted value

PEF variability < 20%

M i ld Persi stent Asthma

Symptoms > 2 times/week, but less than once a day

Exacerbations may affect activity

Nighttimes symptoms > 2 times a month

PEF/FEV ? 80% of predicted value

PEF variability 20%-30%

M oderate Persi stent Asthma

Daily Symptoms

Daily use of inhaled short-acting ?2 - agonists

Exacerbations affect activity

Exacerbations ? 2 times a week

Exacerbations may last days

Nighttime symptoms > once a week

PEF/FEV > 60%-<80% of predicted value

PEF variability > 30%

S evere Persi stent Asthma

Continual symptoms

Frequent exacerbations

Frequent nighttime symptoms

Limited physical activity

PEF or FEV ? 60% of predicted value

PEF variability > 30 %

LABORATORY AND DIAGNOSTIC FINDINGS: Spirometry will detect:

a. Decreased for expiratory volume (FEV)

b. Decreased peak expiratory flow rate (PEFR)

c. Diminished forced vital capacity (FVC)

d. Diminished inspiratory capacity (IC)

NURSINGMANAGEMENT:

1. Assess respiratory status by closely evaluating breathing patterns and monitoring vital signs

2. Administer prescribed medications, such as bronchodilators, anti-inflammatories, and antibiotics

3. Promote adequate oxygenation and a normal breathing pattern

4. Explain the possible use of hyposensitization therapy

5. Help the child cope with poor self-esteem by encouraging him to ventilate feelings and concerns. Listen actively asthe child speaks, focus on the child¶s strengths, and help him to identify the positive and negative aspects of his

situation.

6. Discuss the need for periodic PFTs to evaluate and guide therapy and to monitor the course of the illness.

7. Provide child and family teaching. Assist the child and family to name signs and symptoms of an acute attack and

appropriate treatment measures

8. Refer the family to appropriate community agencies for assistance.

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