Bedside Clinic on Bronchitis, Cholelithiasis

7/30/2019 Bedside Clinic on Bronchitis, Cholelithiasis

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Cindy Claire L. Alcantara

N40; Group 4

BEDSIDE CLINIC

Chronic Bronchitis, Hepatomegaly withCholelithiasis

I. INTRODUCTION

A. Chronic Bronchitis

Bronchitis is a term that describes inflammation of

the bronchial tubes (bronchi and the smaller branches

termed bronchioles) that results in excessive secretions ofmucus into the tubes, leading to tissue swelling that can

narrow or close off bronchial tubes. There are two major

types of bronchitis, acute and chronic. Many investigators

conclude that recurrent incidences of acute bronchitis are

the first steps that can lead to developing chronic

bronchitis.

Acute bronchitis is bronchitis that is short-lived;

the bronchitis lasts about two weeks and usually people

recover with no permanent damage to the bronchial tree.

Viruses such as influenza, respiratory syncytial virus

(RSV), and rhinoviruses cause the majority (about 90%) of

cases of acute bronchitis, while the remainder are caused

by bacteria (for example, Mycoplasma, Pneumococcus) or

short-term exposure to chemical irritants (for example,

tobacco smoke, gastric reflux contents, inhaled solvents).

Symptoms of acute bronchitis may include:

a cough,

mild wheezing,

fever,

chills and malaise, and

shortness of breath especially with exertion.

Some people may cough up phlegm. Chronic bronchitis

differs from acute bronchitis in several ways described

below (for example, pathology, progression of disease,

major causes, treatments, and outcomes).

Chronic bronchitis is defined as a cough that occurs

every day with sputum production that lasts for at least 3

months, two years in a row. This definition was developed

to help select uniform patient populations for researchpurposes, for example, to study medication therapies for

treatment of chronic bronchitis.

Many of the bronchi develop chronic inflammation with

swelling and excess mucus production. The inflammation

causes a change in the lining cells of the airways to
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varying degrees. Many cells that line the airway lose the

function of their cilia (hair-like appendages that are

capable of beating rapidly), and eventually the ciliated

cells are lost. Cilia perform the function of moving

particles and fluid (usually mucus) over the lining surface

in such structures as the trachea, bronchial tubes, and

nasal cavities to keep these hollow structures clear of

particles and fluids. These ciliated cells that help in

clearance of secretions are often replaced by so-called

goblet cells. This group of cells secretes mucus into the

airway. The warm moist environment of the airway along with

the nutrients in the mucus is an excellent medium for

growing bacteria. The mucus often becomes infected and

discolored from the bacterial overgrowth and the body's

inflammatory response to it. The inflammation, swelling,

and mucus frequently and significantly inhibit the airflow

to and from the lung alveoli by narrowing and partially

obstructing the bronchi and bronchioles.

The muscles that surround the some of the airways can

be stimulated by this airway irritation. This muscular

spasm also known as bronchospasm can result in further

airway narrowing. With long standing inflammation, as can

be seen in chronic bronchitis, this muscular spasm and

inflammation results in a fixed, nonreversible narrowing of

the airway and the condition is termed chronic obstructive

pulmonary disease (COPD). Chronic coughing develops as the

body attempts to open and clear the bronchial airways of

particles and mucus or as an overreaction to ongoinginflammation. Chronic bronchitis can be a progressive

disease; symptoms (listed below) increase over time. Some

NIH investigators consider chronic bronchitis a type of

COPD.

COPD also includes the entities of emphysema, chronic

bronchitis, and chronic asthma. These conditions are not

always separable and patients often have components of

each. In the case of chronic bronchitis, the fixed airway

obstruction, airway inflammation and retained secretions

can result in a mismatch of blood flow and airflow in thelungs. This can impair oxygenation of the blood as well as

removal of the waste product, carbon dioxide.

Although people of any age can develop chronic

bronchitis, the majority of people diagnosed with the

disease are 45 years of age or older.

There can be many causes of chronic bronchitis, but

the main cause is cigarette smoke. Statistics from the US

Centers for Disease Control and Prevention (CDC) suggest

that about 49% of smokers develop chronic bronchitis and24% develop emphysema/COPD. Some researchers suggest that

about 90% of cases of chronic bronchitis are directly or

indirectly caused by exposure to tobacco smoke.

Many other inhaled irritants (for example, smog,

industrial pollutants, and solvents) can also result in

chronic bronchitis.
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Viral and bacterial infections that result in acute

bronchitis may lead to chronic bronchitis if people have

repeated bouts with infectious agents.

Also, underlying disease processes (for example,

asthma, cystic fibrosis, immunodeficiency, congestive heart

failure, familial genetic predisposition to bronchitis, and

congenital or acquired dilation of the bronchioles, known

as bronchiectasis) may cause chronic bronchitis to develop,

but these are infrequent causes compared to cigarette

smoking.

The major risk factor for individuals to develop

chronic bronchitis is tobacco smoking and second-hand

tobacco smoke exposure. However, there are others, such as

repeated exposure to pollutants (especially airborne

materials such as ammonia, sulfur dioxide, chlorine,

bromine, hydrogen sulfide), dust, repeated bouts of acute

bronchitis or pneumonia, and gastric reflux (by inhalation

of gastric contents).

The major symptoms of chronic bronchitis are as follows:

Cough and sputum production are the most common

symptoms; they usually last for at least 3 months and

occur daily. The intensity of coughing and the amount

and frequency of sputum production vary from patient to

patient. Sputum may be clear, yellowish, greenish, or

occasionally, blood-tinged. Since cigarette smoke is themost common cause for chronic bronchitis, it should not

be surprising that the most common presentation is so

called smoker's cough. This is characterized by a cough

that tends to be worse upon arising and is often

productive of discolored mucus in the early part of the

day. As the day progresses, less mucus is produced.

Dyspnea (shortness of breath) gradually increases with

the severity of the disease. Usually, people with

chronic bronchitis get short of breath with activity and

begin coughing; dyspnea at rest usually signals that

COPD or emphysema has developed. Wheezing (a coarse whistling sound produced when airways

are partially obstructed) often occurs.

In addition, symptoms of fatigue, sore throat, muscle

aches, nasal congestion, and headaches can accompany the

major symptoms. Severe coughing may cause chest pain;

cyanosis (bluish/grayish skin coloration) may develop in

people with advanced COPD. Fever may indicate a secondary

viral or bacterial lung infection. When symptoms worsen or

become more frequent, this is often referred to as an

exacerbation of chronic bronchitis. These exacerbationsoften require antibiotics, and may need steroid medication

and an increase in respiratory inhaled medications.

B. Hepatomegaly
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Hepatomegaly is enlargement of the liver. The liver

edge is normally palpable in children and thin adults and

some patients may have a palpable right lobe of the liver.

It is smooth, uniform, non-tender and descends to meet the

palpating fingers on inspiration. The best way to assess

size is by percussion - a normal sized liver can appear

enlarged if displaced downwards by lung disorders. An

enlarged liver expands down and across towards the left

iliac fossa. To avoid missing a really big liver, always

begin liver palpation in the LIF and work back towards the

right upper quadrant.

Associated symptoms may be few or rather vague, eg loss of

appetite, weight loss and lethargy.

There may be symptoms relating to liver dysfunction, eg

jaundice, bruising, gynaecomastia, spider naevi, ascites;

or related to the underlying cause, eg xanthelasma suggests

autoimmune liver disease.

Measure the hepatomegaly by percussing the upper and lower

borders (will rule out causes such as emphysema which can

push the liver down giving a false impression of

hepatomegaly).

On palpation:

Smooth hepatomegaly suggests: hepatitis, chronic heart

failure, sarcoid, early alcoholic cirrhosis, tricuspid

incompetence with a pulsatile liver.

Craggy hepatomegaly suggests: primary hepatoma or secondarytumours.

C. Cholelithiasis

Cholelithiasis is the medical term for gallstone

disease. Gallstones are concretions that form in the

biliary tract, usually in the gallbladder.

Gallstones develop insidiously, and they may remain

asymptomatic for decades. Migration of a a gallstone into

the opening of the cystic duct may block the outflow ofbile during gallbladder contraction. The resulting increase

in gallbladder wall tension produces a characteristic type

of pain (biliary colic). Cystic duct obstruction, if it

persists for more than a few hours, may lead to acute

gallbladder inflammation (acute cholecystitis).

Choledocholithiasis refers to the presence of one or

more gallstones in the common bile duct. Usually, this

occurs when a gallstone passes from the gallbladder into

the common bile duct.

A gallstone in the common bile duct may impact

distally in the ampulla of Vater, the point where the

common bile duct and pancreatic duct join before opening

into the duodenum. Obstruction of bile flow by a stone at

this critical point may lead to abdominal pain and

jaundice. Stagnant bile above an obstructing bile duct
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the trachea, which branches off into one of two bronchi.

Each bronchus enters a lung. There are two lungs, one on

each side of the breastbone and protected by the ribs. Each

lung is made up of lobes, or sections. There are three

lobes in the right lung and two lobes in the left one. The

lungs are cone shaped and made of elastic, spongy tissue.

Within the lungs, the bronchi branch out into minute

pathways that go through the lung tissue. The pathways are

called bronchioles, and they end at microscopic air sacs

called alveoli. The alveoli are surrounded by capillaries

and provide oxygen for the blood in these vessels. The

oxygenated blood is then pumped by the heart throughout the

body. The alveoli also take in carbon dioxide, which is

then exhaled from the body.

Inhaling is due to contractions of the diaphragm and of

muscles between the ribs. Exhaling results from relaxation

of those muscles. Each lung is surrounded by a two-layered

membrane, or the pleura, that under normal circumstanceshas a very, very small amount of fluid between the layers.

The fluid allows the membranes to easily slide over each

other during breathing.

B. Hepatobiliary System

The liver is the second largest organ of the

body, weighing 1200 to 1500 grams, or 4-5% of body

weight. It is located in the right upper abdominal

quadrant, or the right hypochondriac and epigastricregions, behind the lower ribs. The falciform ligament

divides the liver anatomically into two unequal lobes:

right and left. Two additional smaller lobes, the quadrate

and caudate lobes are more visible in cross section.

Physiologically though, the division is equal, following the

fossa for gall bladder and inferior vena cava. There is no

evidence for difference in functions among the four anatomical

lobes.

The gall bladder is a saccular organ located posterior

to the liver that functions to store bile. It has a

mean capacity of 30-50 mL. Mucosal folds, calledthe spiral valves of Heister, maintain patency of the

cystic duct to allow passage of bile. Presence of fats in

the duodenum stimulates the gall bladder to contract.


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III. Pathophysiology

A. Chronic Bronchitis

B. Hepatomegaly

CHRONIC BRONCHITIS


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IV. NURSING PROFILE

A. Patients Profile


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Patient X, a 63 year old woman, weighing 84

kilograms, a Roman catholic by birth was admitted by

two of her daughters, to Manuel J. Santos Hospital

last October 8, 2012, Monday due to difficulty of

breathing and jaundice with icteric sclera. As her

daughter narrated, Patient X had suffered from on and

off fever,and cough for about two weeks prior to

admission but was said to have been underestimated by

Patient X as common flu. Unexpectedly, on the said day

of admission at about 10 oclock in the morning,

Patient X had experienced difficulty of breathing and

was cyanotic. Patients jaundice and yellowish

discoloration of the her eyes had worsened Patient Xs

familys worries that had made them decide to submit

Patient X to the hospital for appropriate medical

management. Thus, her daughters rushed Patient X from

their home in Purok 3, Emelia Compound, Barangay Holy

Redeemer, Butuan City to Manuel J. Santos Hospital.

It was exactly 10:45 am when they arrived in the

Emergency Room of the said hospital. Patient X was

then seen by her attending physician, Dr. Virginia

Lim-Yu. She was then administered with Oxygen and was

was subjected to several tests, namely Chest X-ray,

Serum Potassium, Calcium, Sodium, Creatinine, Urea

Nitrogen, ALT (SGPT), and Complete Blood Count. The

tests had revealed that patient had atherosclerotic,

clear lung fields but with non-dilated bronchial tree,

which is suggestive of bronchitis. Patient Xs pasthistory revealed that she had failed to continue

taking her maintenance drug for her bronchitis for

about seven years already, of which she had forgot

already the drug name.

Furthermore, Patient was then submitted for an

Ultrasound on the next day which in turn revealed that

she had hepatomegaly and cholelithiasis. She also had

undergone serologic test for typhoid fever, of which

the result was negative. She too was additionally

indicated for a CT Scan to rule malignancy andinvolvement of the mass in her liver, and

unfortunately, she and her family refused to submit to

such diagnostic test because of financial reasons.

Patient X has been admitted to be monitored and

treated in the Annex Station at Room 327 Bed C. Her

condition had shown persistent problem with

oxygenation and breathing. She also experienced

constant pain on her abdomen, particularly on her

epigastric region which occur more frequently at

night. She has been treated with very potentantibiotics IVTT and orally, and it showed that after

several days of therapy, onset and severity of pain

has reduced and became infrequent and rare. Moreover,

her attending Physician had noticed that her abdominal

girt had reduced, and bloating was no longer noted.

Patient X with her condition was supposedly for

surgery, particularly cholecystectomy, however Dr.


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Lim-Yu did not consider such as a good option

considering patients age and heart condition, and

that any surgery performed would bring extreme danger

to her.

Last October 16, 2012, I had been able to take

part of her care. Wherein upon assessment, Patient X

was lethargic, with fast shallow breathing, elevated

BP of 160/90 mm Hg and was quite cyanotic with hooked

IVF, D50.9NaCl 1 liter, regulated at KVO rate at right

metacarpal vein. She had an O2 inhalation at 3 liters

per minute via nasal cannula. She too had a Foley bag

catheter attached to drain to a urobag. In our care,

Patient Rob had been given with Domperidone (Dompenyl)

orally, GIT protector and a anti-flatulent drug to

prevent and lessen risks of duodenal ulcer, which can

occur because of inflammatory process of the gall

bladder and liver, Tramadol + Paracetamol (Algesia)

orally, for pain and inflammation in the GIT, and

Ipratropium + Salbutamol (Duavent) via nebulisation

for bronchospasm, vital signs monitoring was done

every 4 hours.

I was able to witness her condition for 7 days,

and during the course of our care, and I noticed

Patients X gradual improvements. At first, she was

lethargic and dependent with her significant others

for her needs. She too, could not tolerate breathing

without oxygen inhalation. She was very sedentary andwas lying down her bed without trying to sit up at

times and her temperature fluctuates from time to

time. But days after, as her condition improved, she

was now able to sit up on bed at times and during

times of eating and drinking oral medications and her

febrile episodes were no longer present. She was tried

to be weaned of her supplemental O2 inhalation on

October 17, 18 and 19, 2012 and her O2 saturation was

observed. Immediately after removal, her O2 inhalation

was within the normal range however, an hour or two

after, her O2 saturation had went down to 82% to 91%only even with aid of deep breathing and sitting up,

thus, her O2 inhalation was continued. The nurses

notes on the weekends, October 20 and 21, 2012

revealed that her O2 inhalation was tried to be weaned

on the Sunday and was indicated for a 24-hour

observation to decide patients tolerance and ability

for discharge. However, her O2 inhalation was again

administered back because her O2 saturation had been

persistently low. On October, 23, 2012, her O2

inhalation was again removed for observation, and this

time, it showed that Patient X could now tolerateindependent breathing with good O2 saturation.

Fortunately, her attending physician and her family

agreed to discharge Patient X for home care.

Thus, on October 24, 2012, Patient X was finally

discharged at about 4 in the afternoon with prescribed

home medications and low salt, low fat diet. She was


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advised to come back for a follow up check up with Dr.

Lim-Yu on November 11, 2012, at her clinic. A diet

list of Low Salt, Low fat diet was explained and

provided to her. Each home medications indications

and schedules were also explained and that she too

understood the side effects of the drugs.

V. Laboratory Tests and Interpretation

10/8/12 - Chest X-ray

Interpretation: Atherosclerotic Aorta

- Blood Chemistry

Uric Acid = 6.1 mg/dl (2.7-7.3) INCREASED

Creatinine = 0.78 mg/dl (0.7-1.3) NORMAL

ALT (SGPT) 24.0 u/L (


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a. 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 agonists because they activate

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.

b. 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 maintenancemedications. 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.

c. Side effects of beta-2 agonists include anxiety, tremor,

palpitations or fast heart rate, and low blood

potassium.

Anti-cholinergic Agents

a. Acetylcholine is a chemical released by nerves thatattaches 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 + Albuterol sulfate (Duavent) dilate airways by

blocking the receptors for acetylcholine on the muscles

of the airways and preventing them from narrowing.

Ipratropium bromide + Albuterol sulfate (Duavent)

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 ofaction 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.

b. In comparing ipratropium with beta-2 agonists in the

treatment of patients with COPD, studies suggest that


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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

a. Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl,

Theo-24) and aminophylline are examples of

methylxanthines. Methylxanthines are administered orally

or intravenously. Long acting theophylline preparations

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.

b. The disadvantage of methylxanthines is their sideeffects. 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 as cimetidine

(Tagamet), calcium channel blockers (Procardia),

quinolones (Cipro), and allopurinol (Zyloprim) also can

alter blood levels of methylxanthines.

Corticosteroids

a. 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, bonefractures, 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
http://nursingcrib.com/nursing-notes-reviewer/medical-surgical-nursing/pulmonary-hypertension/http://nursingcrib.com/nursing-notes-reviewer/medical-surgical-nursing/pulmonary-hypertension/http://nursingcrib.com/drug-guides/corticosteroids/http://nursingcrib.com/nursing-notes-reviewer/medical-surgical-nursing/pulmonary-hypertension/http://nursingcrib.com/nursing-notes-reviewer/medical-surgical-nursing/pulmonary-hypertension/http://nursingcrib.com/drug-guides/corticosteroids/


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it is necessary to use long term oral steroids,

medications are often prescribed to help reduce the

development of the above side effects.

b. 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, andoral 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.

Lists of Patients Drugs:

DRUG NAME CLASSIFICATION

Captopril ( Capomed) 25 mg

1 tab SL every 6 hours forBP 160/100

ACE Inhibitor

Telmisartan (Pritor) 40

mg/tab OD

Angiotensin receptor blocker

Isosorbide Mononitrate

(Imdur) 60 mg tab OD

Vasodilator

ASA (Aspilet) 80 mg 1 tab

OD

Analgesic, Antipyretic,

NSAID

Erdosteine (Zertin) 300 mg

1 cap BID

Mucolytic

Paracetamol (Tempra Forte)

1 tab every 4 hours forfever

NSAID, Antipyretic

Tramadol + Paracetamol

(Algesia) 1 tab TID

Analgesic, Antipyretic

Ipratropium + Salbutamol

(Duavent) 1 UDV every 6

hours

Anti-cholinergic

Domperidone (Dompenyl) 1

tab TID

Anti-flatulent, GIT

Protector

Omeprazole (Omepron) 20 mg

1 cap BID

Proton Pump Inhibitor

VII. Nursing Management

Monitoring


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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

patients 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 patients 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 patients 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 weatherand 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),


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increasing difficulty in raising sputum, increasing

coughing and wheezing, increasing of shortness of breath.

REFERENCES:

Brunner and Suddarths. Medical and Surgical Nursing

Udan, Josie Quiambao. Medical Surgical Nursing

Lippincott. Manuals of Nursing Practice

Mosby. Medical Surgical Nursing

Shaker SB, Dirksen A, Bach KS, Mortensen J (June 2007).

Bach PB, Brown C, Gelfand SE, McCrory DC (2001). "Managementof acute

exacerbations of chronic obstructive pulmonary disease: asummary and appraisal of published evidence".Ann.Intern. Med.134 (7): 60020.

Documents

Bedside Clinic on Bronchitis, Cholelithiasis