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INTRODUCTION

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. While acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

Respiratory failure may be classified as hypoxemic or hypercapnic. Hypoxemic respiratory failure (type I) is characterized by a PaO2 of less than 60 mm Hg with a normal or low PaCO2. This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failures are cardiogenic or non cardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 of more than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (e.g., asthma, chronic obstructive pulmonary disease [COPD]). (www.emedicine.com, retrieved on July 25, 2007)

Significance of the Study

In another source, type I failure exists when PaO2 is <50 mm Hg with the patient at rest and breathing room air. And PaCO2 >50 mm Hg or pH <7.35 is significant for acute respiratory academia, more reflective of type II. Some patients may manifest respiratory failure of types I and II simultaneously. (Baird, 2005: 201).

Prevalence / Statistics

Acute respiratory failure remains a major cause of morbidity and mortality in both pediatric and adult populations. The annual incidence in the United States may be as high as 150,000 cases, with mortality rates generally ranging between 50% and 70%.

This study aims to present more information about Acute Respiratory Failure, its causes, effects, Pathophysiology, nursing intervention and underlying treatments that are applicable to this case. It also helps to promote prevention and awareness from the learning of its causes and predisposing factors.

ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM

Narrative form

The respiratory system’s major function is gas exchange, in which air enters the body on inhalation (inspiration); travels throughout the respiratory passages, exchanging oxygen for carbon dioxide at the tissue level; and expels carbon dioxide on exhalation (expiration).

The upper airway composed of the nose, mouth, pharynx, and larynx allows airflow into the lungs. This area is responsible for warming, humidifying, and filtering the air, thereby protecting the lower airway form foreign matter.

The lower airway consists of the trachea, mainstem bronchi, secondary bronchi, bronchioles, and terminal bronchioles. These structures are anatomic dead spaces and function only as passageways for moving air into and out of the lungs. Distal to each terminal bronchiole is the acinus, which consists of respiratory bronchioles, alveolar ducts, and alveolar sacs. The bronchioles and ducts function as conduits, and the alveoli are the chief units of gas exchange. These final subdivisions of the bronchial tree make up the lobules.

In addition to warming, humidifying, and filtering inspired air, the lower airway protects the lungs with several defense mechanisms. Clearance mechanisms include the cough reflex and mucociliary system. The mucociliary system produces mucus, trapping foreign particles. Foreign matter is then swept to the upper airway for expectoration by specialized fingerlike projections called cilia. A breadown in the epithelium of the lungs or the mucociliary system can cause the defense mechanisms to malfunction, and pollutants and irritants then enter and inflame the lungs. The lower airway also provides immunologic protection and initiates pulmonary injury responses.

The external component of respiration (ventilation or breathing) delivers inspired air to the lower respiratory tract and alveoli. Contraction and relaxation of the respiratory muscles moves air into and out of the lungs.

Normal expiration is passive; the respiratory muscles cease to contract, and the elastic recoil of the lungs and the chest wall causes them to contract again. These actions raise the pressure within the lungs to above atmospheric pressure, moving air from the lungs to the atmosphere.

An adult lung contains an estimated 300 million alveoli; each alveolus is supplied by many capillaries. To reach the capillary lumen, oxygen must cross the alveolar capillary membrane.

The pulmonary alveoli promote gas exchange by diffusion – the passage of gas molecules through respiratory membranes. In diffusion, oxygen passes to the blood, and carbon dioxide, a by-product of cellular metabolism, passes out of the blood and is channeled away.

Circulating blood delivers oxygen to the cells of the body for metabolism and transports metabolic wastes and carbon dioxide from the tissues back to the lungs. When oxygenated arterial blood reaches tissue capillaries, the oxygen diffuses from the blood into the cells because of an oxygen tension gradient. The amount of oxygen available to cells depends on the concentration of hemoglobin (the principal carrier of oxygen) in the blood, the regional blood flow, the arterial oxygen content, and cardiac output.

Because circulation is continuous, carbon dioxide doesn’t usually accumulate in tissues. Carbon dioxide produced during cellular respiration diffuses from tissues to regional capillaries and is transported by the systemic venous circulation. When carbon dioxide reaches the alveolar capillaries, diffuses into the alveoli, where the arterial pressure of carbon dioxide (PaC02) is lower. Carbon dioxide is removed from the alveoli during exhalation.

For effective gas exchange, ventilation and perfusion at the alveolar level must match closely.

The ratio of ventilation to perfusion is called the V/Q ratio. A V/Q mismatch can result from ventilation-perfusion dysfunction or altered lung mechanics.

The amount of air carrying oxygen that reaches the lungs depends on lung volume and capacity, compliance, and resistance to airflow. Changes in compliance can occur in either the lung or the chest wall. Destruction of the lung’s elastic fibers, which occurs in acute respiratory distress syndrome, decreases lung compliance. The lungs become stiff. Making breathing difficult, the alveolar capillary membrane may also be affected, causing hypoxia. Chest wall compliance is affected by disorders causing thoracic deformity, muscle spasm, and abdominal distention.

Respiration is also controlled neurologically by the lateral medulla oblongata of the brain stem. Impulses travel down the phrenic nerves to the diaphragm and then down the intercostals verves to the intercostals muscles between the ribs. The rate and depth of respiration are controlled similarly.

Apneustic ad pneumotaxic centers in the pons of the midbrain influence the pattern of breathing. Stimulation of the lower pontine apneustic center (by trauma, tumor, or stroke) produces forceful inspiratory gasps alternating with weak expiration. This pattern doesn’t occur if the vagi are intact. The apneustic center continually excites the medullary inspiratory center and thus facilitates inspiration. Signals fro the pneumotaxic center and afferent impulses form the vagus nerve inhibit the apneustic center and “turn off” inspiration.

In addition, chemoreceptor’s respond to the pH of arterial blood, PaC02, and the partial pressure of arterial oxygen (Pa02). Central chemoreceptor responds indirectly to arterial blood by sensing changes in the pH of the cerebrospinal fluid (CSF). PaC02 also helps regulate ventilation by impacting the pH of CSF. If PaC02 is high, the respiratory rate increases; if PaC02 is low, the respiratory rate decreases. Information from peripheral chemoreceptor in the carotid and aortic bodies also responds to decreased Pa02 and pH. Either of these changes results in increased respiratory drive within minutes.


PATHOPHYSIOLOGY OF ACUTE RESPIRATORY FAILURE

Narrative Form

Acute Respiratory Failure (ARF) may develop in COPD patients from any condition that increases the work of breathing and decreases the respiratory drive. These conditions may result from respiratory tract infections (such as bronchitis or pneumonia), bronchospasm or accumulated secretions secondary to cough suppression. Other common causes are related to ventilatory failure, in which the brain fails to direct respiration, and gas exchange failure, in which respiratory structures fail to function properly.

Other causes of ARF include central nervous system (CNS) depression due to head trauma or injudicious use of sedatives, opioids, tranquilizers, or oxygen and cardiovascular disorders such as myocardial infarction, heart failure, or pulmonary emboli. ARF also results from airway irritants, such as smoke and fumes, endocrine or metabolic disorders, myxedema or metabolic acidosis, and thoracic abnormalities, such as chest trauma, pneumothorax, and thoracic or abdominal surgery.

In my case, ARF developed from Pneumonia. Pneumonia is the inflammation or infection of the lungs that involves the small air sacs (alveoli) and bronchioles or excess of fluid in the lungs resulting from an inflammatory process which results in gas exchanged problems. The inflammation process is triggered by many infectious organisms and by inhalation of irritating agents. Infectious pneumonias are categorized and as community-acquired or hospital-acquired (nosocomial), depending on where the client was exposed to the infectious agent. This distinction is important because nosocomial pneumonias are more likely to be resistant to antibiotics than are CAPs.

Pneumonia may be caused by bacteria, viruses, mycoplasma, rikettsias, or fungi. The causative organism gains entry by aspiration of oropharyngeal or gastric contents, inhalation of respiratory droplets, from others who are infected, by way of the blood stream, or directly with surgery or trauma.

Patients who develop bacterial pneumonia usually are immunosuppressed or compromised by chronic disease, or have had a recent viral illness. The most common type of bacterial pneumonia is pneumococcal pneumonia, in which the Streptococcus pneumonia organism reaches the lungs via the respiratory passageways and result in the collapse of alveoli. The inflammatory response that this generates causes protein-rich fluid to migrate into the alveolar spaces and provides culture media for the organism to proliferate and spread.

The inflammatory exudates progresses through four stages. The first one is stage of congestion, is characterized by local inflammation, edema in the alveoli, bacteria laden fluid fills alveoli which the edema may thicken alveolar walls. The second stage is red hepatization, occurs 2-3 days after initial infection. It is characterized by polymorphonuclear neutrophils (PMNs) rushes to area; capillary vasodilation, fluid in the alveoli made up of fibrin deposits, RBCs, PMNs, leukocytes, epithelial cells; lung tissues appear dry, granular and dark reddish-brown resembling the liver and consolidation occurs. The third stage is gray hepatization, lasts 2 days or more after red hepatization. It is characterized by macrophages replace PMN’s and ingest debris, alveolar exudates contains fibrin which is needed for repair of the alveolar wall, alveoli is relatively bloodless due to the fibrin and lungs appear dense and friable. The secretion and mucosal edema occlude the bronchi and result to decreased alveolar mucosal tension that would result to hypoventilation. A decreased of oxygen results to decreased venous blood, that would decreased pulmonary circulation. There would be ventilation and perfusion mismatch in order of the lungs to compensate. This would result to mixing of oxygenated and deoxygenated blood, and eventually results to hypoxia, and respiratory failure, then to respiratory arrest. This will cause death of the patient. When there is a consolidation after the third stage achieved, it will either lead to resolution stage or the infection will continue until there will be necrosis of pulmonary tissues and overwhelming sepsis. If the patient reaches resolution stage, the exudate and fibrin are removed and the fibrin becomes a dense scar.

The mechanical disturbances in respiration are further complicated by disruptions in the normal exchange of gases (oxygen and carbon dioxide) across the alveolar-capillary membrane. Gases trapped in the alveoli reduce ventilator efficiency. The disruptions in ventilation cause arterial oxygen tension (PaO2) to fall (hypoxemia), even though the patient is working harder to inspire sufficient oxygen. As obstruction worsens, PaO2 continues to fall, initially, arterial carbon dioxide tension (PaCO2) is low (hypocapnia) owing to the hyperventilating alveoli, which are able to compensate for the hypoventilated alveoli. As the severity of the episode increases, it becomes impossible for the remaining functioning alveoli to compensate. These alveoli begin to hypoventilate and PaCO2 begins to rise (Hypercapnea). Respiratory acidosis reheated to increase PaCO2 occurs. The body responds to hypercapnia with cerebral depression, hypotension, circulatory failure, and increased heart rate and cardiac output. Metabolic acidosis also exists as a result of the increases energy expenditure needed to breathe and the subsequent decrease in oxygen available for tissue metabolism. If the impairment in ventilation and gas exchange continues, respiratory failure may result.

Hypoxemia and hypercapnia characterized of respiratory failure. They stimulate strong compensatory responses by all body systems, including the kidney, respiratory system, cardiovascular system, and CNS. In response to hypoxemia, for example, the sympathetic nervous system triggers vasoconstriction, increases peripheral resistance, and increases the heart rate. The blood supply also going to the brain is diminished resulting into hypoxic ischemic encephalopathy, coma and then death. The renal system also affected because of the decreased blood supply, resulting to damage of the glomerular base membrane and eventually leads to renal failure. Untreated V/Q imbalances can lead to right-to-left shunting in which blood passes from the heart’s right side to its left without being oxygenated.

When hypoxemia and hypercapnia occur, the patient may show evidence of restlessness, confusion, loss of concentration, irritability, tremulousness, diminished tendon reflexes, papilledema and coma.

Tachycardia, with increased cardiac output and mildly elevated blood pressure secondary to adrenal release of catecholamine, occurs early in response to low PaO2. With myocardial hypoxia, arrhythmias may develop. Pulmonary hypertension, secondary to pulmonary capillary vasoconstriction, may cause increased pressures on right side of the heart, distended jugular veins, an enlarged liver, and peripheral edema. The constant strain and workload of the heart affects the right ventricle to dilate and hypertrophy. Eventually, the right side of the heart weakens and is unable to accommodate venous blood returning to the heart. As the result, pressure in the systemic venous circulation increases, causing cor pulmonale, or right-sided heart failure. It will then lead to cardiopulamonary collapse and death.

Diagram

Risk Factors:

• Gender (male)
• Age (40 years and above)
• Smoking
• Alcoholism
• Malnutrition
• Air pollution
• Immunosuppression
• Prolonged immobility (coma)
• Impaired gag/cough reflex
• Presence of NGT or ETT
• Abdominal and thoracic surgery
• Chronic illnesses and debilitation
• Contact with people with such Infections (PTB; Pneumonia)
• Upper Respiratory Infection (PTB; Pneumonia)



Nursing Care Plans

Problem No. 1: Difficulty of breathing (July 29, 2007)

Assessment

Objective:

 Shortness of breath

 RR of 37 bpm (N = 16-20 bpm)

 HR of 140

 Blood Pressure of 90/30

 Increase PH 7.49 (N= 7.35-.7.45) (July 28. 2007)

 Decrease PaCO2 174 (N=35-45)

 Increase PaO2 101 (N=80-100)

 H2CO3 13.4 (N=22-26)

 O2 Sat 88% (N=92-100)

 Coma

 Crackles

 02 via nasal 3Lpm

 Use of accessory muscles



Nursing Diagnosis

Ineffective breathing pattern related to altered O2 supply secondary alveolar edema.

Rationale: As interstitial edema increase pressure in the interstitial space rises fluid leaks into alveoli; Plasma protein accumulating in the interstitial space lower the osmotic gradient between the capillary and interstitial compartment and because of this gases o12 and CO2 are unable to pass through and blood will not be oxygenated (Lemon: 2004; 1170)

Planning

After 30 minutes of nursing intervention the patient will be able to manifest effective breathing pattern as evidence by RR of 20 bpm.

Nursing Intervention

Independent

 Assess Respiratory. Both rapid shallow breathing patterns and hypoventilation affect gas exchange. (Gulanick: 91)

 Monitor Vital signs. With initial hypoxia and hypercania blood pressure heart rate and respiratory rate all rise (Ibid)

 Use pulse oximetry to monitor O2 saturation and pulse rate continuously. Pulse oximetry is a useful tool to detect changes in oxygenation. (ibid)

 Position with proper body alignment for optimal respiratory excursion. This promotes lung expansion and improves air exchange. (ibid)

 Position patient every 2 hrs. To facilitate secretions movement and drainage. (ibid)

 Suction as needed. To clear secretion if the pt is unable to effectively clear the airway. (ibid)

Dependent

 Provide O2 therapy as prescribe and indicated. Increasing o2 tension in the alveoli may result in more o2 diffusion into the capillaries. ( Gulanick; 1998:203)

 Administer salbutamol ½ nebul acetylcysteine. Management of reversible airway disease due to asthma COPD (Drug guide:160)

Evaluation

Goal met. After 30 minutes of nursing intervention the patient was able to manifest effective breathing pattern as evidence of respiratory rate of 20 bpm.

Problem No. 2: Fatigue (July 29, 2007)
Assessment
Objective:
 O2 saturation of 88%
 RR of 30 bpm (N = 16-20 bpm)
 HR of 140
 Blood Pressure of 90/30
 Increase PH 7.49 (N= 7.35-.7.45) (July 28. 2007)
 Decrease PaCO2 174 (N=35-45)
 Increase PaO2 101 (N=80-100)
 Coma
 Crackles
 02 via nasal 3Lpm
 Use of accessory muscles

Nursing Diagnosis

Impaired gas exchange related to present of fluid in the alveoli secondary to the inflammation of the lungs.

Rationale: The damaged capillary and alveolar walls become more permeable allowing plasma protein and erythrocytes to enter the interstitial space. An interstitial edema increase pressure in the interstitial space rises and fluid leaks into alveoli. As a result the balance is disrupted between the osmotic force that pulls fluid from the interstitial space into the capillaries and the normal hydrostatic pressure that pusses fluid put of the capillaries.

Planning

After 30 minutes of nursing intervention the patient will manifest improve of gas exchange as evidence of O2 saturation within normal range.

Nursing Intervention

Independent

 Evaluate respiratory function. Respiratory distress and changes on vital signs occur as a result of physiologic stress and pain or may indicate development of shock due to hyposxia hemorrhage. (Doenges: 2006;153)

 Monitor synchronouse respiratory pattern when mechanical ventilator note changes in airway pressure. Difficulty of breathing with ventilator and airway suggest worsening of condition and development of complication (Ibid)

 Assess lung sound listen closely for rhonci, rates (crackles), wheezing and diminished lung sound in each lobe, assessing side to side. To compare lung sound. (Ibid)

 Auscultate breath sound. Breath sound may diminished or absent in lobe, lung segment or entire field unilateral (Ibid)

 Position patient with proper body alignment. For optimal chest excursion and breathing pattern. (Ibid)

Dependent

 Provide O2 therapy as prescribe and indicated. Increasing o2 tension in the alveoli may result in more o2 diffusion into the capillaries. ( Gulanick; 1998:203)

 Administer salbutamol ½ nebul acetylcysteine. Management of reversible airway disease due to asthma COPD (Drug guide:160)

Evaluation

Goal met. After 30 minutes of nursing intervention the patient was able to manifest improvement of gas exchange as evidence of O2 satuaration increases from 88% to 94%.

Problem No. 3: Low Blood pressure. (July 30, 2007)

Assessment

Objective:

 RR of 30 bpm (N = 16-20 bpm)

 HR of 140

 Blood Pressure of 90/30

 HGT of 112 (N= 80-120) ?

 O2 Sat 88% (N=92-100)

 Poor capillary refill 6sec <3 data-blogger-escaped-.5="" data-blogger-escaped-br="" data-blogger-escaped-seconds.="">  Pallor
Nursing Diagnosis
Decreased cardiac output related to inadequate blood the left atrium secondary to pulmonary hypertension.

Rationale: Hypoxemia is a potent pulmonary vasoconstrictor and a common initiation factor in pulmonary hypertension. (Lemone. 2004; 1134)

Planning
After 1 hour of nursing intervention the patient will manifest improve cardiac output as evidence by good capillary refill, HR, BP and normal urine output.

Nursing Intervention
Independent
 Assess skin color and temperature. Cold clammy skin is secondary to compensatory increase in sympathetic nervous system stimulate and low cardiac output and desaturation ( Gulanick. 1998; 50)
 Assess heart rate and blood pressure. Sinus tachycardia and increased atrial blood pressure are seen in the early stage. Bp drops as the condition deteriorates. (Ibid)
 Place in supine position. To increase venous return to promote diuresis (Ibid)

Dependent
 Provide O2 therapy as prescribe and indicated. Increasing o2 tension in the alveoli may result in more o2 diffusion into the capillaries. ( Gulanick; 1998:203)
 Administer Digoxin 0.25mg 1 tab. Use to slow the ventricular rate in tachyarrthymias, such as atrial fibrillation and atrial flutter (MIMS: 260)

Evaluation
Goal met. After 1 hour of nursing intervention the patient will manifest improve cardiac output as evidence by good capillary refill, HR. 75, BP 110/70 and normal urine output of 30cc/hr.
Problem No. 4: Fever (July 29-30, 2007)
Assessment
Objective:
 Temperature 38C (N= 36.5-37.5)
 RR of 37 bpm (N = 16-20 bpm)
 HR of 140
 Blood Pressure of 120/70
 Blood transfusion
 Shortness of breath
 Dry skin
 Hot flushed skin

Nursing Diagnosis
Hyperthermia related to body response to infection.

Rationale: The infection and associated inflammatory process can cause a fever in the client with pneumonia.

Planning
After 1 hour of nursing intervention the patient will demonstrate temperature within normal range from 38C to 37.5C

Nursing Intervention
Independent
 Monitor client temperature. Temperature of 102F-106F (3.9C- 41.1C suggest acute infectious disease process. (Doenges, 2007: 706)
 Monitor environment temperature, limit and add linens as indicated. Room temperature and number of blankets should be altered to maintain near normal body temperature (Ibid)
 Provide tepid sponge bath avoid use of alcohol. May help areduce fever. Alcohol may cause chills actually elevating temperature. In Addition alcohol is very drying to skin. (Ibid)
Dependent
 Administer Acetaminophen. PRN if temp increase 37.8C 1 tab 500mg. to mild moderate pain and fever (Nurse Drug guide: 5)
 Provide cooling blankets as indicated. Used to reduce fever, usually higher than 104F-105F (39.5C-40C) when brain damage and seizure can occur

Evaluation
Goal met. After 1 Hour of nursing intervention the patient demonstrate temperature within normal range from 38C to 37.5C.

Problem No. 5: Edema of the extremities (July 29, 2007)
Assessment
Objective:
 Edema on extremities Grade 2
 Orthopnea
 Bounding pulse
 Abnormal breath sound rales
 Jugular vein distention

Nursing Diagnosis
Excess fluid volume related to increase hydrostatic pressure secondary to increase venous system pressure.

Rationale: Because of hypoxemia, pulmonary artery become constricted causing pulmonary hypertension thus the right atrium and right ventricle had hard time to pump blood forward and blood flowed backward causing increase venous pressure, hydrostatic pressure at the same time causing fluid shifting and edema (Lemone 2004:1169)
Planning
After NOC shift of nursing intervention patient will maintain urine output of at least 30cc/hr .

Nursing Intervention
Independent:
 Monitor and record vital signs every 1 hour. Changes may indicate fluid or electrolyte imbalance (spark and taylor’s 2005: 115)
 Measure and record intake and output. Intake greater tan output may indicate fluid retention and possible overload (Ibid)
 Auscultate breath sound, noting decreased and adventitious sounds. Excess fluid volume often leak to pulmonary congestion (Doenges 2006:56)
 Apply antiembolism stocking or intermittent pneumatic compression stocking. To increase venous return (Ibid, 116)
 Monitor BUN, creatinine, electrolyte and Hb levels and HCT. BUN and creatinine level indicates renal function, electrolyte and Hb levels and HCT help indicate fluid status. (Ibid, 13)
Dependent
 Administer Furosemide 40mg/IV. A potent loop diuretic that inhibits sodium and chloride reabsorption at the proximal and distal tubules and the ascending loop of henle (Lippincott, Drug Guide 2006; 851)
.
Evaluation
Goal met. During NOC shift of nursing intervention patient maintained urine output of at least 30-25mL/hour

Problem No. 6: Bedsores (July 29, 2007)
Assessment
Objective:
 68 years old
 Presence of pressure sore grade 2 positive at the right ankle.
 Presence of edema
 Presence of blisters
 Cyanotic left foot

Nursing Diagnosis
Impaired skin integrity related to immobility and poor circulation.

Rationale: Immobility which leads to pressure, shear and friction, is the factor most likely to put on individual at the risk for altered skin integrity. Advance age: normal loss of elasticity inadequate nutrition, environmental moisture especially from incontinence; and vascular insufficiency potential the effect of pressure and hasten the development of skin breakdown. (Gulanick, 1998:180)

Planning
After 4 days of nursing intervention, the patient’s skin remains intact, as evidenced by no redness over bony prominences.

Nursing Interventions
Independent:
 Assess skin integrity, noting color, moisture, texture, and temperature especially pressure points. Healthy skin varies from individual to individual, but should have good turgor, an indication of moisture, feel and warm and dry to touch. (Gulanick, 1998: 181)
 Turn patient every 2 hours or prn. Because of sensory disturbance. Patient will be able to detect painful pressure. (Ibid).
 Individualize client’s bathing schedule. Daily cleansing can destroy the skin’s natural barrier, making it more susceptible to external irritants. (Smith and Deull; 690)
 Keep skin lubricated. To prevent dryness and cracking. (ibid)

Dependent:
 Apply Calmoseptin as indicated. Protects soothes and helps promoted healing in htose with impaired skin integrity. (MIMS, 2007)

Evaluation
Goal partially met. After 4 days of nursing intervention, the patient skin will remains intact as evidenced by the redness over bony prominences.


Problem # 7: Oral Lesions (July 30, 2007)
Assessment:
Objective:
 Oral pain discomfort
 Xerostomia (dry mouth)
 Oral lesion ulcers
 Edema

Nursing Diagnosis
Altered oral mucous membrane related to ineffective oral hygiene.

Rationale: Minor irritations of the oral mucous membrane occur occasionally in all person and are usually viral-related, self-limiting and easily treated. (Gulanick, 1998; 145)

Planning
After 2 days of nursing intervention, patient will be free from lip fissures and intact oral mucosa.

Nursing Interventions
Independent:
 Assess status of oral mucosa; include tongue, lips mucous membranes, gums, saliva, and teeth. Home care givers also need to be informed of the importance of these assessments. (Ibid).
 Use a moist, paddled tongue blade to gently pullback the cheeks and tongue. In order to expose all areas of oral cavity or inspections.
 Assess of extensive of ulceration involving the intraoral soft tissues, including palate, tongue, gums, and lips. Sloughing of mucosal membrane can progress to ulceration. (Ibid).
 Assess nutrition status. Malnutrition can be contributing cause. Oral fluids needed for moisture to membranes. (Ibid)
 Implement meticulous mouth care regimen after each meal and every 4 hours while awake. To prevent build up of oral plague and bacteria. (Ibid)

Dependent:
 Swab mouth with Bactidol 4-8 hours and prn. Indicated for sore throat, halitosis, general oral hygiene, improve appearance of mouth tissues protects tooth surfaces against formation of decay acid. (MIMS, 2007: 375)

Evaluation
Goal met. After 2 days of nursing intervention, patient is free from lip and intact oral mucosa.



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