A

Abdominal pain, acute

Description

Acute abdominal pain is pain of recent onset. It may signal a life-threatening problem and therefore requires immediate attention. Causes include damage to organs in the abdomen and pelvis, which leads to inflammation, infection, obstruction, bleeding, and perforation. The most common causes of acute abdominal pain are listed in Table 1.

Clinical manifestations

Pain is the most common symptom of an acute abdominal problem. Patients may also complain of nausea, vomiting, diarrhea, constipation, flatulence, fatigue, fever, and bloating.

Diagnostic studies

Diagnosis begins with a complete history and physical examination. Description of the pain (frequency, timing, duration, location), accompanying symptoms, and sequence of symptoms (e.g., pain before or after vomiting) provide vital clues about the problem. Physical examination should include both a rectal and pelvic examination in addition to an abdominal examination.

■ Complete blood count (CBC), urinalysis, abdominal x-ray, and an electrocardiogram (ECG) are done initially, along with an ultrasound or computed tomography (CT) scan.

■ A pregnancy test is performed in women of childbearing age to rule out ectopic pregnancy.

Collaborative care

The goal of management is to identify and treat the cause and monitor and treat complications, especially shock. Table 43-10 in Lewis et al., Medical-Surgical Nursing, ed 9, p. 971, outlines emergency management of the patient with acute abdominal pain.

■ A minimally invasive diagnostic laparoscopy may be performed to inspect the surface of abdominal organs, obtain biopsy specimens, perform laparoscopic ultrasounds, and remove organs.

■ A laparotomy is used when laparoscopic techniques are inadequate. If the cause of the acute abdomen can be surgically removed (e.g., inflamed appendix) or surgically repaired (e.g., ruptured abdominal aneurysm), surgery is considered definitive therapy.

Nursing management

Goals

The patient will have resolution of inflammation, relief of abdominal pain, freedom from complications (especially hypovolemic shock), and normal nutritional status.

Nursing interventions

General care involves management of fluid and electrolyte imbalances, pain, and anxiety. Assess the quality and intensity of pain at regular intervals, and provide medication and other comfort measures. Maintain a calm environment and provide information to help allay anxiety. Conduct ongoing assessments of vital signs, intake and output, and level of consciousness, which are key indicators of hypovolemic shock.

Preoperative care includes the emergency care of the patient and general care of the preoperative patient (Chapter 18 and Table 43-10 Lewis et al., Medical-Surgical Nursing, ed 9, p. 971).

Postoperative care depends on the type of surgical procedure performed. Laparoscopic procedures result in lower rates of postoperative complications (e.g., poor wound healing, paralytic ileus), earlier diet advancement, and shorter hospital stays compared with open surgical procedures. A general nursing care plan (eNCP 20-1) for the postoperative patient is presented on the website for Chapter 20.

A nasogastric (NG) tube with low suction may be used to empty the stomach and prevent gastric dilation. If the upper gastrointestinal (GI) tract has been entered, drainage from the NG tube may be dark brown to dark red for the first 12 hours. Later it should be light yellowish brown or greenish. If a dark red color continues or if bright red blood is observed, notify the surgeon because of the possibility of hemorrhage. “Coffee ground” granules in the drainage indicate blood that has been modified by acidic gastric secretions.

■ Nausea and vomiting are common after a laparotomy and may be caused by the surgery, decreased peristalsis, or pain medication. Antiemetics such as prochlorperazine (Compazine), ondansetron (Zofran), or trimethobenzamide (Tigan) may be ordered (see Nausea and Vomiting, p. 432).

■ Monitor fluid and electrolyte status along with blood pressure, heart rate, and respirations.

■ Swallowed air and decreased peristalsis from decreased mobility, manipulation of abdominal organs during surgery, and anesthesia can lead to abdominal distention and gas pains. Early ambulation helps restore peristalsis and eliminate flatus and gas pain. Gradually, as intestinal activity increases, distention and gas pain disappear.

Patient and caregiver teaching

Preparation for discharge begins soon after surgery. Teach the patient and caregiver about any modifications in activity, care of the incision, diet, and drug therapy.

■ Clear liquids are given initially after surgery, and if tolerated, the patient progresses to a regular diet.

■ Normal activities should be resumed gradually with planned rest periods.

■ The patient and caregiver should be aware of possible complications after surgery and should be taught to notify the surgeon immediately if fever, pain, weight loss, incisional drainage, or changes in bowel function occur.

Acute coronary syndrome

Description

Acute coronary syndrome (ACS) develops when ischemia is prolonged and not immediately reversible. ACS encompasses the spectrum of unstable angina (UA), non–ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI) (Fig. 1). Although each remains a distinct diagnosis, this nomenclature (ACS) reflects the relationships among the pathophysiology, presentation, diagnosis, prognosis, and interventions for these disorders.

Fig. 1. Relationships among coronary artery disease, chronic stable angina, and acute coronary syndrome.

Pathophysiology

ACS is associated with deterioration of a once-stable atherosclerotic plaque. The plaque then ruptures, exposing the intima to blood and stimulating platelet aggregation and vasoconstriction with thrombus formation. This unstable lesion may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI).

What causes a coronary plaque to suddenly become unstable is not well understood, but systemic inflammation is thought to play a role.

Unstable angina

The patient with chronic stable angina may develop UA, or UA may be the first clinical manifestation of CAD. Unlike chronic stable angina, UA is unpredictable and represents an emergency.

■ The patient with previously diagnosed chronic stable angina describes a significant change in the pattern of angina. It occurs with increasing frequency and is easily provoked by minimal or no exertion, during sleep, or even at rest.

■ The patient without previously diagnosed angina describes anginal pain that has progressed rapidly in the past few hours, days, or weeks, often culminating in pain at rest.

Myocardial infarction

A myocardial infarction (MI) occurs because of sustained ischemia, causing irreversible myocardial cell death (necrosis). Thrombus formation is responsible for 80% to 90% of all acute MIs. When a thrombus develops, perfusion to the myocardium distal to the occlusion is blocked, resulting in necrosis. Contractile function of the heart stops in the necrotic areas. The degree of altered function depends on the area of the heart involved and the size of the infarction. Most MIs involve some portion of the left ventricle.

Cardiac cells can withstand ischemic conditions for approximately 20 minutes before cellular death (necrosis) begins. If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness of the heart muscle to become necrosed.

■ MIs are usually described by the location of damage (e.g., anterior, inferior, lateral, or posterior wall infarction). The location correlates with the involved coronary circulation. For example, inferior wall infarctions result from occlusions in the right coronary artery. Damage can occur in more than one location (e.g., anterolateral MI, anteroseptal MI).

■ The degree of preestablished collateral circulation also influences the severity of the infarction. An individual with a long history of CAD develops collateral circulation to provide the area surrounding the infarction site with a blood supply.

The body’s response to cell death is the inflammatory process. Within 24 hours, leukocytes infiltrate the area. Enzymes are released from the dead cardiac cells and are important diagnostic indicators of MI. Proteolytic enzymes from neutrophils and macrophages remove all necrotic tissue by the fourth day.

■ The necrotic zone is identifiable by ECG changes (e.g., ST-segment elevation, pathologic Q wave) and by nuclear scanning after the onset of symptoms.

At 10 to 14 days after an MI, the new scar tissue is still weak. The myocardium is vulnerable to increased stress because of the unstable state of the healing heart wall. Changes in the infarcted muscle also alter the unaffected myocardium. In an attempt to compensate for the infarcted muscle, the normal myocardium hypertrophies and dilates. Remodeling of normal myocardium can lead to the development of late heart failure (HF).

Clinical manifestations

Unstable angina

The chest pain associated with UA is new in onset, occurs at rest, or has a worsening pattern. Women seek medical attention for symptoms of UA more often than men. Despite national efforts to increase awareness, women’s symptoms (fatigue, shortness of breath, indigestion, anxiety) continue to go unrecognized as related to heart problems.

Myocardial infarction

Severe, immobilizing, and persistent chest pain not relieved by rest or nitrate administration is the hallmark of an MI.

■ Pain is usually described as a heaviness, pressure, burning, crushing, tightness, or constriction. The persistent pain is unlike any other pain.

■ Common locations are epigastric, substernal, or retrosternal. The pain may radiate to the neck, jaw, and arms or to the back. It may occur while the patient is active or at rest, asleep or awake, and commonly occurs in the early morning hours.

■ The pain usually lasts for 20 minutes or more and is more severe than usual anginal pain. When epigastric pain is present, the patient may take antacids without relief.

■ Some patients may not have pain but may report having “discomfort,” weakness, fatigue, or shortness of breath. Women may experience atypical discomfort, shortness of breath, or fatigue.

■ An older patient may experience a change in mental status (e.g., confusion), shortness of breath, pulmonary edema, dizziness, or a dysrhythmia.

Additional manifestations may include nausea and vomiting, diaphoresis, and the patient’s skin may be ashen, clammy, and cool (cold sweat). Fever occurs within the first 24 hours (up to 100.4° F [38° C]) and may continue for 1 week. BP and pulse rate are also elevated initially. The BP may then drop, with decreased urine output, lung crackles, hepatic engorgement, and peripheral edema. Jugular veins may be distended with obvious pulsations.

Complications

■ Dysrhythmias are the most common complication after an MI and are the most common cause of death in patients in the prehospital period. Dysrhythmias are caused by any condition that affects the myocardial cell’s sensitivity to nerve impulses, such as ischemia, electrolyte imbalances, and sympathetic nervous system stimulation. The intrinsic rhythm of the heart is disrupted, causing either a very fast heart rate (HR) (tachycardia), a very slow HR (bradycardia), or irregular HR. Life-threatening dysrhythmias occur most often with anterior wall infarction, heart failure, and shock. Complete heart block is seen in a massive infarction (see Dysrhythmias, p. 202).

■ Ventricular fibrillation, a common cause of sudden death, is a lethal dysrhythmia that most often occurs within the first 4 hours after the onset of pain. Premature ventricular contractions may precede ventricular tachycardia and fibrillation. Life-threatening ventricular dysrhythmias must be treated immediately.

■ Heart failure occurs when the heart’s pumping action is reduced. Depending on the severity and extent of the injury, HF occurs initially with subtle signs such as slight dyspnea, restlessness, agitation, or slight tachycardia. Other signs include pulmonary congestion on chest x-ray, S₃ or S₄ heart sounds on auscultation, crackles on auscultation of breath sounds, and jugular venous distention.

■ Cardiogenic shock occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe left ventricular failure. Cardiogenic shock requires aggressive management, including control of dysrhythmias, intraaortic balloon pump therapy, and support of contractility with vasoactive drugs.

Diagnostic studies

In addition to the patient’s history of pain, risk factors, and health history, the primary diagnostic studies used to determine whether a person has UA or an MI include an ECG and serum cardiac markers. Other diagnostic measures can include coronary angiography, exercise stress testing, and echocardiogram.

Thrombolytic therapy aims to stop the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium. Thrombolytic therapy (e.g., reteplase [Retavase]) is given as soon as possible, ideally within the first hour and preferably within the first 6 hours after the onset of symptoms. Mortality is reduced by 25% if reperfusion occurs within 6 hours. Contraindications and complications with thrombolytic therapy are described in Lewis et al, Medical-Surgical Nursing, ed 9, p. 751.

Coronary artery bypass graft (CABG) surgery consists of the placement of conduits to transport blood between the aorta, or other major arteries, and the myocardium distal to the obstructed coronary artery (or arteries). It requires a sternotomy (opening of the chest cavity) and the use of cardiopulmonary bypass (CPB). It is a palliative treatment for CAD and not a cure. Newer techniques include minimally invasive direct coronary artery bypass and transmyocardial laser revascularization. These surgical procedures and related nursing care are further discussed in Lewis et al, Medical-Surgical Nursing, ed 9, pp. 752 to 753.

Drug therapy includes IV nitroglycerin (Tridil), aspirin, β-adrenergic blockers, and systemic anticoagulation with either low-molecular-weight heparin given subcutaneously or IV unfractionated heparin as initial drug treatments of choice. Angiotensin-converting enzyme (ACE) inhibitors are added for select patients following MI, and calcium channel blockers may be used if the patient is already taking adequate doses of β-blockers or does not tolerate these blockers.

Nursing management

Goals

The patient with an MI will experience relief of pain, preservation of myocardium, immediate and appropriate treatment, effective coping with illness-associated anxiety, participation in a rehabilitation plan, and reduction of risk factors.

See NCP 34-1 for the patient with acute coronary syndrome, Lewis et al, Medical-Surgical Nursing, ed 9, pp. 755 to 756.

Nursing diagnoses

■ Acute pain

■ Decreased cardiac output

■ Anxiety

■ Activity intolerance

■ Ineffective self-health management

Nursing interventions

Priorities for nursing interventions in the initial phase include pain assessment and relief, physiologic monitoring, promotion of rest and comfort, alleviation of stress and anxiety, and understanding of the patient’s emotional and behavioral reactions. Proper management of these priorities decreases the O₂ needs of a compromised myocardium. In addition, you should institute measures to avoid the hazards of immobility while encouraging rest.

■ Provide nitroglycerin, morphine, and O₂ as needed to eliminate or reduce chest pain.

■ Maintain continuous ECG monitoring while the patient is in the ED and intensive care unit and after transfer to a step-down or general unit. Dysrhythmias need to be identified quickly and treated.

■ In addition to taking frequent vital signs, evaluate intake and output at least once per shift, and perform physical assessment to detect deviations from the patient’s baseline parameters. Assess lung and heart sounds and inspect for evidence of early heart failure (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins).

■ Assess the patient’s oxygenation status, especially if the patient is receiving O₂. In addition, check the nares for irritation or dryness (see Oxygen Therapy, p. 717).

■ It is important to plan nursing and therapeutic actions to ensure adequate rest periods free from interruption.

■ It is important to promote rest and comfort with any degree of myocardial injury. Bed rest may be ordered for the first few days after an MI involving a large portion of the ventricle.

■ Anxiety is present in various degrees in all patients with ACS. Your role is to identify the source of anxiety and assist the patient in reducing it. If the patient is afraid of being alone, allow a caregiver to sit quietly by the bedside or to check in frequently with the patient. If a source of anxiety is fear of the unknown, you should explore these concerns with the patient.

Patient and caregiver teaching

Patient teaching needs to occur at every stage of the patient’s hospitalization and recovery (e.g., ED, telemetry unit, home care). The purpose of teaching is to give the patient and caregiver the tools they need to make informed health decisions (Table 2).

■ Anticipatory guidance involves preparing the patient and caregiver for what to expect in the course of recovery and rehabilitation. By learning what to expect during treatment and recovery, the patient gains a sense of control over his or her life.

■ Teach the patient the parameters within which to exercise and how to check pulse rate. Tell the patient the maximum HR that should be present at any point. If the HR exceeds this level or does not return to the rate of the resting pulse within a few minutes, instruct the patient to stop. Also instruct the patient to stop exercising if pain or shortness of breath occurs. Basic physical activity guidelines following ACS are presented in Table 34-20, Lewis et al, Medical-Surgical Nursing, ed 9, p. 761.

■ Discuss participation in an outpatient cardiac rehabilitation program with all patients. These programs are beneficial, but not all patients choose or are able to participate in them (e.g., location). Home-based cardiac rehabilitation programs can be an alternative.

■ It is important to include sexual counseling for cardiac patients and their partners. Tell the patient that resumption of sex depends on the patient and his or her partner’s emotional readiness and on the physician’s assessment of the extent of recovery. It is generally safe to resume sexual activity 7 to 10 days after an uncomplicated MI.

Table 2

Patient and Caregiver Teaching Guide
Acute Coronary Syndrome

Include the following information in the teaching plan for the patient with acute coronary syndrome and the caregiver.

■ Signs and symptoms of angina and MI and what to do should they occur (e.g., take nitroglycerin)*

■ When and how to seek help (e.g., contact EMS)

■ Anatomy and physiology of the heart and coronary arteries

■ Cause and effect of CAD

■ Definition of terms (e.g., CAD, angina, MI, sudden cardiac death, heart failure)

■ Identification of and plan to decrease risk factors * (see Tables 34-2, 34-3, and 34-4, Lewis et al, Medical-Surgical Nursing, ed 9, pp. 736 and 737)

■ Rationale for tests and treatments (e.g., ECG monitoring, blood tests, angiography), activity limitations and rest, diet, and medications *

■ Appropriate expectations about recovery and rehabilitation (anticipatory guidance)

■ Resumption of work, physical activity, sexual activity

■ Measures to promote recovery and health

■ Importance of the gradual, progressive resumption of activity *

*Identified by patients as most important to learn before discharge.

Acute respiratory distress syndrome

Description

Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid. The alveoli fill with fluid, resulting in severe dyspnea, hypoxemia refractory to supplemental oxygen (O₂), reduced lung compliance, and diffuse pulmonary infiltrates.

Incidence of ARDS in the United States is estimated at more than 150,000 cases annually. Despite supportive therapy, mortality from ARDS is approximately 50%. Patients who have both gram-negative septic shock and ARDS have a mortality rate of 70% to 90%.

■ Table 3 lists conditions that predispose patients to the development of ARDS. The most common cause is sepsis. Patients with multiple risk factors are three or four times more likely to develop ARDS.

■ Direct lung injury may cause ARDS, or ARDS may develop as a consequence of the systemic inflammatory response syndrome (SIRS). ARDS may also develop as a result of multiple organ dysfunction syndrome (MODS) (see Systemic Inflammatory Response Syndrome and Multiple Organ Dysfunction Syndrome, p. 614).

Table 3

Conditions Predisposing Patients to Acute Respiratory Distress Syndrome

Direct Lung Injury	Indirect Lung Injury
Common Causes
■ Aspiration of gastric contents or other substances ■ Viral or bacterial pneumonia ■ Sepsis	■ Sepsis (especially gram-negative infection) ■ Severe massive trauma
Less Common Causes
■ Chest trauma ■ Embolism: fat, air, amniotic fluid, thrombus ■ Inhalation of toxic substances ■ Near-drowning ■ O₂ toxicity ■ Radiation pneumonitis	■ Acute pancreatitis ■ Anaphylaxis ■ Cardiopulmonary bypass ■ Disseminated intravascular coagulation ■ Nonpulmonary systemic diseases ■ Opioid drug overdose (e.g., heroin) ■ Severe head injury ■ Shock states ■ Transfusion-related acute lung injury (e.g., multiple blood transfusions)

Pathophysiology

An exact cause for damage to the alveolar-capillary membrane is not known. However, many changes are thought to be caused by stimulation of the inflammatory and immune systems, which causes an attraction of neutrophils to the pulmonary interstitium. The neutrophils cause a release of biochemical, humoral, and cellular mediators that produce changes in the lung, including increased pulmonary capillary membrane permeability, destruction of elastin and collagen, formation of pulmonary microemboli, and pulmonary artery vasoconstriction. Pathophysiologic changes in ARDS are divided into three phases: injury or exudative, reparative or proliferative, and fibrotic.

The injury or exudative phase occurs approximately 1 to 7 days (usually 24 to 48 hours) after the initial direct lung injury or host insult. The primary changes of this phase are interstitial and alveolar edema (noncardiogenic pulmonary edema) and atelectasis.

■ Initially, there is engorgement of the peribronchial and perivascular interstitial space, which produces interstitial edema. An intrapulmonary shunt develops because the alveoli fill with fluid, and blood passing through them cannot be oxygenated.

■ Alveolar cells that produce surfactant are damaged by the changes caused by ARDS. This damage, in addition to further fluid and protein accumulation, results in surfactant dysfunction. Widespread atelectasis further decreases lung compliance, compromises gas exchange, and contributes to hypoxemia.

■ Hyaline begins to line the alveolar membrane. Hyaline membranes contribute to fibrosis and atelectasis, leading to a decrease in gas exchange capability and lung compliance.

■ Severe ventilation-perfusion (V/Q) mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O₂ (refractory hypoxemia).

The reparative or proliferative phase begins 1 to 2 weeks after the initial lung injury. During this phase there is an influx of granulocytes, monocytes, and lymphocytes and fibroblast proliferation.

■ Increased pulmonary vascular resistance and pulmonary hypertension may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature.

■ Lung compliance continues to decrease, and hypoxemia worsens because of the thickened alveolar membrane.

■ If this phase persists, widespread fibrosis results. If this phase is stopped, the lesions resolve.

The fibrotic phase occurs approximately 2 to 3 weeks after the initial lung injury. This phase is also called the chronic or late phase of ARDS. By this time the lung is completely remodeled by collagenous and fibrous tissues. Diffuse scarring and fibrosis result in decreased lung compliance and decreased surface area for gas exchange. Pulmonary hypertension results from fibrosis.

Progression of ARDS varies among patients. Some patients survive the acute phase of lung injury, pulmonary edema resolves, and complete recovery occurs in a few days. Others go on to the fibrotic (late or chronic) phase requiring long-term mechanical ventilation, with a poor chance of survival.

Clinical manifestations

At the time of initial injury and for several hours to 1 to 2 days afterward, the patient may not exhibit respiratory symptoms.

■ The patient may exhibit tachypnea, dyspnea, cough, and restlessness. Chest auscultation may be normal or reveal fine, scattered crackles. Arterial blood gases (ABGs) usually indicate mild hypoxemia and respiratory alkalosis. Chest x-ray may be normal or exhibit evidence of minimal scattered interstitial infiltrates. Edema may not manifest until there is a 30% increase in lung fluid content.

As ARDS progresses, symptoms worsen because of increased fluid accumulation in the lungs and decreased lung compliance. Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor may be present. Chest auscultation usually reveals scattered to diffuse crackles and rhonchi.

■ Hypoxemia, despite increased fraction of inspired oxygen concentration (FIO₂) by mask, cannula, or endotracheal tube, is a hallmark of ARDS. Hypercapnia signifies that respiratory muscle fatigue and hypoventilation are occurring, and the patient is no longer able to maintain the level of ventilation needed to provide optimum gas exchange.

■ As ARDS progresses, profound respiratory distress occurs, requiring endotracheal intubation and positive pressure ventilation (PPV). The chest x-ray reveals whiteout or white lung because consolidation and coalescing infiltrates pervade the lungs, leaving few recognizable air spaces.

■ Pleural effusions may be present. Severe hypoxemia, hypercapnia, and metabolic acidosis, with symptoms of target organ or tissue hypoxemia, may develop if therapy is not promptly started.

Complications may develop as a result of ARDS itself or its treatment. The major cause of death in ARDS is MODS, often accompanied by sepsis. The vital organs most commonly involved are the kidneys, liver, and heart. The organ systems most often involved are the central nervous system (CNS) and hematologic and gastrointestinal systems.

Diagnostic studies

No precise criteria define ARDS. Findings that support a diagnosis of ARDS are the patient presents with refractory hypoxemia, a chest x-ray with new bilateral interstitial or alveolar infiltrates, and a pulmonary artery wedge pressure of 18 mm Hg or less with no evidence of heart failure.

Nursing and collaborative management

Goals

With appropriate therapy, the overall goals for the patient with ARDS include a partial pressure of oxygen in arterial blood (PaO₂) of at least 60 mm Hg and adequate lung volume to maintain normal pH. A patient recovering from ARDS will experience a PaO₂ within limits of normal for age or baseline values on room air, oxygen saturation in arterial blood (SaO₂) greater than 90%, a patent airway, and clear lungs on auscultation.

Nursing diagnoses

Nursing diagnoses for the patient with ARDS may include, but are not limited to, those described under Respiratory Failure, Acute (p. 534).

Collaborative care

The collaborative care for acute respiratory failure is applicable to ARDS (see Respiratory Failure, Acute, pp. 538 to 541). Patients with ARDS are commonly cared for in critical care units.

O₂ administration.

The goal of O₂ therapy is to correct hypoxemia (see Oxygen Therapy, p. 717). Initially use masks with high-flow systems that deliver higher O₂ concentrations to maximize O₂ delivery. The general standard for O₂ administration is to give the lowest concentration that results in a PaO₂ of 60 mm Hg or greater. When FIO₂ exceeds 60% for more than 48 hours, the risk for O₂ toxicity increases. Patients with ARDS need intubation with mechanical ventilation (see Artificial Airways: Endotracheal Tubes, p. 679) because the PaO₂ cannot otherwise be maintained at acceptable levels.

Mechanical ventilation.

Endotracheal intubation and positive pressure ventilation provide additional respiratory support. In patients with ARDS, positive expiratory-end pressure (PEEP) is often used. When PEEP is applied, the lung is kept partially expanded, which prevents the alveoli from totally collapsing. If hypoxemic failure persists in spite of high levels of PEEP, alternative modes and therapies may be used. These include airway pressure release ventilation, pressure-control inverse ratio ventilation, high-frequency ventilation, and permissive hypercapnia (low tidal volumes that allow PaCO₂ to increase slowly).

Extracorporeal membrane oxygenation (ECMO) and extracorporeal carbon dioxide (CO₂) removal pass blood across a gas-exchanging membrane outside the body and then return oxygenated blood back to the body.

Positioning.

Some patients with ARDS have a marked improvement in PaO₂ when turned from the supine to the prone position (e.g., PaO₂ 70 mm Hg supine, PaO₂ 90 mm Hg prone) with no change in inspired O₂ concentration. The response may be sufficient to allow a reduction in inspired O₂ concentration or PEEP.

Another positioning strategy that you can consider for patients with ARDS is continuous lateral rotation therapy, which provides continuous, slow, side-to-side turning of the patient by rotating the actual bed frame. You should maintain the lateral movement of the bed for 18 of every 24 hours to stimulate postural drainage and help to mobilize pulmonary secretions. In addition, the bed may also contain a vibrator pack that can provide chest physiotherapy to assist with secretion mobilization and removal.

Medical supportive therapy

Patients on PPV and PEEP frequently experience decreased cardiac output. Hemodynamic monitoring is essential to see trends, detect changes, and adjust therapy as needed. An arterial catheter is inserted for continuous monitoring of blood pressure (BP) and sampling of blood for ABGs. Use of inotropic drugs, such as dobutamine (Dobutrex) or dopamine (Intropin), may also be necessary. Packed red blood cells are used to increase hemoglobin and thus the O₂-carrying capacity of the blood.

Maintenance of nutrition and fluid balance is challenging in the patient with ARDS. Parenteral or enteral feedings are started to meet the high energy requirements of these patients. Increasing pulmonary capillary permeability results in fluid in the lungs and causes pulmonary edema. At the same time, the patient may be volume depleted and therefore prone to hypotension and decreased cardiac output from mechanical ventilation and PEEP. Controversy exists as to the benefits of fluid replacement with crystalloids versus colloids. The patient is usually placed on fluid restriction, and diuretics are used as necessary.

Patient and caregiver teaching

Fear of suffocation or death is not uncommon in patients with ARDS.

■ Providing reassurance, spending time with the patient, and ensuring that help can be received immediately (e.g., call light is readily available) may help to decrease patient anxiety level. Anxiety also may be reduced through instruction and use of progressive relaxation, guided imagery, and music therapy.

■ It is helpful to explain to the patient any possible sensations that may be encountered with each new experience (e.g., suctioning, drawing ABGs) so that coping strategies can be purposefully selected.

Addison’s disease

Description

Addison’s disease is a primary adrenocortical insufficiency in which all three classes of adrenal steroids (glucocorticoids, mineralocorticoids, and androgens) are reduced because of hypofunction of the adrenal cortex.

In secondary adrenocortical insufficiency, which is caused by a lack of pituitary adrenocorticotropic hormone (ACTH) secretion, corticosteroids and androgens are deficient but mineralocorticoids rarely are.

The most common cause of Addison’s disease in the United States is an autoimmune response in which adrenal tissue is destroyed by antibodies against the patient’s own adrenal cortex. Often other endocrine conditions are present and Addison’s disease is considered a component of autoimmune polyglandular syndrome. Other causes include infarction, fungal infections (e.g., histoplasmosis), acquired immunodeficiency syndrome (AIDS), and metastatic cancer.

Addison’s disease may be caused by adrenal hemorrhage (often related to anticoagulant therapy), antineoplastic chemotherapy, ketoconazole therapy for AIDS, or bilateral adrenalectomy.

Clinical manifestations

Manifestations have a slow (insidious) onset and include progressive weakness, fatigue, weight loss, and anorexia. Skin hyperpigmentation, a striking feature due to increased ACTH, is seen primarily in sun-exposed areas of the body, at pressure points, over joints, and in creases, especially palmar creases.

■ Other frequent manifestations are orthostatic hypotension, hyponatremia, hyperkalemia, nausea and vomiting, and diarrhea.

Patients with adrenocortical insufficiency are at risk for acute adrenal insufficiency (addisonian crisis), which is a life-threatening emergency caused by insufficient adrenocortical hormones or a sudden, sharp decrease in these hormones.

■ The most dangerous feature is hypotension, which may cause shock, especially during stress. Circulatory collapse is often unresponsive to the usual treatment (vasopressors and fluid replacement).

■ Addisonian crisis may be triggered by stress (e.g., from infection, surgery, trauma, or psychologic distress), sudden withdrawal of corticosteroid hormone therapy (often done by a patient who lacks knowledge regarding replacement therapy), adrenal surgery, or sudden pituitary gland destruction.

Diagnostic studies

■ Plasma cortisol levels are subnormal or fail to rise over basal levels with an ACTH stimulation test. A positive response to ACTH stimulation indicates a functioning adrenal gland and points to pituitary disease rather than adrenal disease.

■ Urine levels of free cortisol and aldosterone are low.

■ Serum electrolytes show hyperkalemia, hypochloremia, and hyponatremia.

■ CT and MRI are used to localize causes other than autoimmune, including tumors, fungal infections, or tuberculosis.

Collaborative care

Treatment is focused on management of the underlying cause when possible. The mainstay of treatment is hormone therapy with corticosteroids (e.g., hydrocortisone) with glucocorticoid and mineralocorticoid activity. Mineralocorticoid replacement with fludrocortisone acetate (Florinef) is administered daily with increased salt in the diet.

■ During stressful situations, the glucocorticoid dosage is increased to prevent addisonian crisis. The patient usually is instructed to take 2 to 3 times the usual dose.

The patient in addisonian crisis requires immediate aggressive management. Treatment must be directed toward shock management and high-dose hydrocortisone replacement. Large volumes of 0.9% saline solution and 5% dextrose are administered to reverse hypotension and electrolyte imbalances until BP returns to normal.

Nursing management

When the patient with Addison’s disease is hospitalized, nursing management focuses on monitoring the patient while correcting fluid and electrolyte balance.

■ Assess vital signs and signs of fluid volume deficit and electrolyte imbalance. Monitor trends in serum glucose, sodium, and potassium.

■ Nursing interventions include daily weights, protection against exposure to infection (reverse isolation), and assistance with daily hygiene.

■ Protect the patient from noise, light, and environmental temperature extremes. The patient cannot cope with these stresses because corticosteroids cannot be produced.

■ If hospitalization was due to an adrenal crisis, patients usually respond by the second day and can start oral corticosteroid replacement.

■ Because discharge frequently occurs before the usual maintenance dose of corticosteroids is reached, the patient should be instructed on the importance of keeping scheduled follow-up appointments.

Patient and caregiver teaching

The serious nature of the disease and the need for lifelong hormone therapy necessitate a comprehensive teaching plan (Table 4).

■ Patients must be taught the signs and symptoms of corticosteroid deficiency and excess and to report these to their health care provider so that the dosage can be adjusted.

■ It is critical that the patient wear an identification bracelet (Medic Alert) and carry a wallet card stating the patient has Addison’s disease so that appropriate therapy can be initiated in case of an emergency.

■ Patients should carry an emergency kit with 100 mg of intramuscular (IM) methylprednisolone (Solu-Medrol), syringes, and instructions for use. Instruct the patient and significant others to give an IM injection if hormone therapy cannot be taken orally. Have the patient verbalize instructions, practice IM injections with saline, and have written instructions on when the dosage should be changed.

Table 4

Patient and Caregiver Teaching Guide
Addison’s Disease

Include the following information in the teaching plan for Addison’s disease.

■ Names, dosages, and actions of drugs

■ Symptoms of overdosage and underdosage

■ Conditions requiring increased medication (e.g., trauma, infection, surgery, emotional crisis)

■ Course of action to take relative to changes in medication

■ Increase in dose of corticosteroid

■ Administration of large dose of corticosteroid intramuscularly, including demonstration and return demonstration

■ Consultation with health care provider

■ Prevention of infection and need for prompt and vigorous treatment of existing infections

■ Need for lifelong replacement therapy

■ Need for lifelong medical supervision

■ Need for medical identification device

■ Prevention of falls

■ Adverse effects of corticosteroid therapy and prevention techniques

■ Special instruction for patients who are diabetics and management of blood glucose when taking corticosteroids

Alzheimer’s disease

Description

Alzheimer’s disease (AD) is a chronic, progressive, degenerative disease of the brain. It is the most common form of dementia, accounting for about 60% to 80% of all cases of dementia (see Dementia, p. 171). Approximately 5.2 million people in the United States have AD. Ultimately the disease is fatal, with death typically occurring 4 to 8 years after diagnosis, although some patients live for 20 years. AD is the sixth leading cause of death in the United States.

Pathophysiology

The exact etiology of AD is unknown. AD is not a normal part of aging. When AD develops in someone younger than 60 years, it is referred to as early-onset AD. AD that becomes evident in individuals after the age of 60 years is called late-onset AD.

Characteristic findings in AD relate to changes in the brain’s structure and function, including amyloid plaques, neurofibrillary tangles, loss of connections between neurons, and neuron death.

■ Amyloid plaques consist of insoluble deposits of a protein called β-amyloid, other proteins, remnants of neurons, nonnerve cells such as microglia, and other cells. In AD the plaques develop first in brain areas used for memory and cognitive function. Eventually the cerebral cortex, especially the areas responsible for language and reasoning, is affected.

■ Neurofibrillary tangles are abnormal collections of twisted protein threads inside nerve cells. The main component of these structures is a protein called tau. Normally tau proteins maintain cellular structure by holding intracellular microtubules together. In AD the tau protein is altered, and as a result, the microtubules twist together in a helical fashion, ultimately forming neurofibrillary tangles.

Plaques and neurofibrillary tangles are not unique to patients with AD or dementia. They are also found in the brains of individuals without evidence of cognitive impairment. However, they are more abundant in the brains of individuals with AD.

The other features of AD are the loss of connections between neurons and neuron death. These processes result in structural damage. Affected parts of the brain begin to shrink in a process called brain atrophy. By the final stage of AD, brain tissue has shrunk significantly.

Genetic factors may play a critical role in the way that the brain processes the β-amyloid protein. Overproduction of β-amyloid appears to be an important risk factor for AD. Abnormally high levels of β-amyloid cause cell damage either directly or through eliciting an inflammatory response and ultimately neuron death.

Diabetes mellitus, hypertension, current smoking, hypercholesterolemia, obesity, and trauma are associated with an increased risk of dementia including AD.

Clinical manifestations

Pathologic changes often precede clinical manifestations of dementia by 5 to 20 years. (Early warning signs of AD are listed in Table 5.) The rate of progression from mild to severe is highly variable and ranges from 3 to 20 years.

Table 5

Patient and Caregiver Teaching Guide
Early Warning Signs of Alzheimer’s Disease

Include the following information in the teaching plan for the patient with Alzheimer’s disease and the family caregiver.
Warning Sign	Description
1. Memory loss that affects job skills	■ Frequent forgetfulness or unexplainable confusion at home or in the workplace may signal that something is wrong. ■ This type of memory loss goes beyond forgetting an assignment, colleague’s name, deadline, or phone number.
2. Difficulty performing familiar tasks	■ It is normal for most people to become distracted and to forget something (e.g., leave something on the stove too long). ■ People with AD may cook a meal but then forget not only to serve it but also that they made it.
3. Problems with language	■ Most people have trouble finding the “right” word from time to time. ■ People with AD may forget simple words or substitute inappropriate words, making their speech difficult to understand.
4. Disorientation to time and place	■ Most individuals occasionally forget the day of the week or what they need from the store. ■ People with AD can become lost on their own street, not knowing where they are, how they got there, or how to get back home.
5. Poor or decreased judgment	■ Many individuals from time to time may choose not to dress appropriately for the weather (e.g., not bringing a coat or sweater on a cold evening). ■ A person with AD may dress inappropriately in more noticeable ways, such as wearing a bathrobe to the store or a sweater on a hot day.
6. Problems with abstract thinking	■ For the person with AD, this goes beyond challenges such as balancing a checkbook. ■ A person with AD may have difficulty recognizing numbers or doing even basic calculations.
7. Misplacing things	■ For many individuals, temporarily misplacing keys, purses, or wallets is a normal albeit frustrating event. ■ A person with AD may put items in inappropriate places (e.g., eating utensils in clothing drawers) but have no memory of how they got there.
8. Changes in mood or behavior	■ Most individuals experience mood changes. ■ A person with AD tends to exhibit more rapid mood swings for no apparent reason.
9. Changes in personality	■ As most individuals age, they may demonstrate some change in personality (e.g., become less tolerant). ■ A person with AD can change dramatically, either suddenly or over time. For example, someone who is generally easygoing may become angry, suspicious, or fearful.
10. Loss of initiative	■ A person with AD may become and remain uninterested and uninvolved in many or all of his or her usual pursuits.

Adapted from Alzheimer’s Association: Early warning signs, Chicago, The Association.

Initial manifestations are usually related to changes in cognitive functioning. Patients may have complaints of memory loss, mild disorientation, and/or trouble with words and numbers. Often it is a family member, in particular the spouse, who reports the patient’s declining memory to the health care provider.

■ Memory loss initially relates to recent events, with remote memories still intact. With time and progression of AD, memory loss includes both recent and remote memory and ultimately affects the ability to perform self-care.

■ Behavioral manifestations (e.g., agitation, aggression) result from changes that take place within the brain. The person’s behaviors are neither intentional nor controllable by the individual with the disease. Some patients develop delusions and hallucinations.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Tags: Clinical Companion to Medical-Surgical Nursing

Oct 26, 2016 | Posted by admin in NURSING | Comments Off

■ Abdominal compartment syndrome	■ Gastroenteritis ■ Pelvic inflammatory disease
■ Acute pancreatitis	■ Perforated gastric or duodenal ulcer
■ Appendicitis	■ Perforated gastric or duodenal ulcer
■ Bowel obstruction	■ Peritonitis
■ Cholecystitis	■ Ruptured abdominal aneurysm
■ Diverticulitis	■ Ruptured ectopic pregnancy

Nurse Key

Fastest Nurse Insight Engine

A

A

Abdominal pain, acute

Description

Clinical manifestations

Diagnostic studies

Collaborative care

Nursing management

Goals

Nursing interventions

Patient and caregiver teaching

Acute coronary syndrome

Description

Pathophysiology

Unstable angina

Myocardial infarction

Clinical manifestations

Unstable angina

Myocardial infarction

Complications

Diagnostic studies

ECG

Cardiac markers

Collaborative care

Nursing management

Goals

Nursing diagnoses

Nursing interventions

Patient and caregiver teaching

Acute respiratory distress syndrome

Description

Pathophysiology

Clinical manifestations

Diagnostic studies

Nursing and collaborative management

Goals

Nursing diagnoses

Collaborative care

O2 administration.

Mechanical ventilation.

Positioning.

Medical supportive therapy

Patient and caregiver teaching

Addison’s disease

Description

Clinical manifestations

Diagnostic studies

Collaborative care

Nursing management

Patient and caregiver teaching

Alzheimer’s disease

Description

Pathophysiology

Clinical manifestations

Share this:

Related

Related posts:

Stay updated, free articles. Join our Telegram channel

Full access? Get Clinical Tree

O₂ administration.