Various conditions can predispose a patient to ARDS, but they usually represent a sudden, cata- strophic situation. These conditions can be classified into two categories: direct lung injury and indirect lung injury. Direct injury occurs from situations such as gastric aspiration, near drown- ing, chemical inhalation, and oxygen toxicity. Indirect injury occurs from mediators released during sepsis, multiple trauma, thermal injury, hypoperfusion or hemorrhagic shock, dissemi- nated intravascular coagulation, drug overdose, and massive blood transfusions. The most com- mon risk factor for ARDS is sepsis from an abdominal source. Approximately 150,000 new cases of ARDS occur each year. Mortality rates vary and have been estimated to be between 40%
and 50%, but older patients and patients with severe infections have a higher rate. Survivors gen- erally have almost normal lung function a year after the acute illness.
Acute Respiratory Distress Syndrome 41
Acute Respiratory
Distress Syndrome
GENETIC CONSIDERATIONS
There may be genetic factors that influence both susceptibility and progression of ARDS. Sur- vivors are more likely to have certain alleles of the genes that code for angiotensin converting enzyme (ACE) and interleukin (IL)-6 than nonsurvivors.
GENDER, ETHNIC/RACIAL, AND LIFE SPAN CONSIDERATIONS
ARDS can occur equally across genders and at any age, including during childhood, to those who have been subjected to severe physiological stresses such as sepsis, burns, or trauma. Eth- nicity and race have no known effects on the risk for ARDS.
ASSESSMENT
HISTORY AND PHYSICAL EXAMINATION. The patient with ARDS appears in acute res- piratory distress with a marked increase in the work of breathing that may lead to nasal flaring, the use of accessory muscles to breathe, and profound diaphoresis. The respiratory rate may be more than 30 to 40 breaths per minute. If ARDS has progressed, the patient may have a dusky appearance with cyanosis around the lips and nail beds, or the patient may be very pale. Hypox- emia usually leads to restlessness, confusion, agitation, and even combative behavior.
Palpation of the peripheral pulses reveals rapid, sometimes thready, pulses. Blood pressure may be normal or elevated initially, then decreased in the later stages. Auscultation of the lungs differs, depending on the stage of ARDS. In the early stage, the lungs have decreased breath sounds. In the middle stages of ARDS, the patient may have basilar crackles or even coarse crackles. In the late stage of ARDS, if the disease has been left untreated, the patient may have bronchial breath sounds or little gas exchange with no breath sounds. If airway and breathing are not maintained, the patient becomes fatigued and apneic. When the patient is intubated and mechanically ventilated, the lungs may sound extremely congested, with wheezes and coarse crackles throughout.
Diagnosis involves excluding other causes of acute respiratory failure. A consensus confer- ence has defined ARDS as having the following features: acute bilateral lung infiltrates; a ratio of PaO2to inspired oxygen concentration (FiO2) of less than 200; no evidence of heart failure or volume overload.
PSYCHOSOCIAL. Patients may exhibit anxiety and fear because of hypoxemia and the real threat of death. Feelings of social isolation and powerlessness can occur as the patient is placed on mechanical ventilation and is unable to verbalize.
42 Acute Respiratory Distress Syndrome
General Comments:The diagnosis of ARDS can be controversial and is one of exclusion.
There are no specific markers that identify alveolar-capillary membrane damage. Early in ARDS, the pH is elevated and the PaCO2is decreased because of hyperventilation. In the later stages, the PaCO2is elevated and the pH is decreased. Other supporting tests include pulmonary function tests, pulse oximetry, and pulmonary capillary wedge pressure.
Abnormality with
Test Normal Result Condition Explanation
Diagnostic Highlights
Chest x-ray
Arterial blood gases
Clear lung fields
PaO280–100 mm Hg;
PaCO235–45 mm Hg;
SaO2!95%
Diffuse bilateral infiltrates without cardiomegaly or pul- monary vascular redistribution PaO2"80 mm Hg; PaCO2
varies; SaO2"95%
Findings reflect noncar- diogenic pulmonary edema
Poor gas exchange leads to hypoxemia and, as respiratory failure pro- gresses, to hypercapnea
PRIMARY NURSING DIAGNOSIS
Impaired gas exchange related to increased alveolar-capillary permeability, interstitial edema, and decreased lung compliance
OUTCOMES. Respiratory status: Gas exchange; Respiratory status: Ventilation; Comfort level;
Anxiety control
INTERVENTIONS. Airway insertion and stabilization; Airway management; Respiratory monitoring; Oxygen therapy; Mechanical ventilation; Anxiety reduction
PLANNING AND IMPLEMENTATION Collaborative
MECHANICAL VENTILATION. The treatment for ARDS is directed toward the underlying cause and maintaining gas exchange. To this end almost all patients with ARDS require endo- tracheal intubation and mechanical ventilation with a variety of positive-pressure modes. Com- mon methods for mechanical ventilation include pressure-controlled ventilation with an inverse inspiratory-expiratory ratio. This mode alters the standard inspiratory-expiratory ratio of 1:2 to 1:3 by prolonging the inspiratory rate and changing the ratio to 1:1. It also controls the amount of pressure in each breath to stabilize the alveoli and to re-establish the functional residual capacity (FRC) to normal levels. If possible, the physician attempts to limit the fraction of inspired oxygen (FiO) to less than 0.50 (50%) to reduce complications from oxygen toxicity.
Positive end-expiratory pressure (PEEP) is often added to the ventilator settings to increase the FRC and to augment gas exchange. Lung-protective, pressure-targeted ventilation, a method whereby controlled hypoventilation is allowed to occur, minimizes the detrimental effects of excessive airway pressures and has also been used in ARDS with positive outcomes.
Acute Respiratory Distress Syndrome 43
General Comments: Use of genetically engineered surfactant has been studied in ARDS but has not demonstrated the success that has occurred in premature infants with surfac- tant deficiency. Corticosteroids have been widely used in ARDS, yet studies have not con- sistently demonstrated any improvement in patient outcomes and remain controversial.
Some evidence exists that prolonged treatment with low-dose corticosteroids may benefit patients with unresolving ARDS, particularly by reversing the process of fibroproliferation.
If the patient is difficult to ventilate, she or he may receive skeletal muscle relaxants such as vecuronium (Norcuron), which are neuromuscular-blocking agents that paralyze the patient’s skeletal muscles. These medications are used only when the patient’s gas exchange is so poor as to threaten his or her life. Neuromuscular-blocking agents paralyze the patient without affecting mental status, so the patient requires sedation to counteract the accompanying fear and anxiety that occur when the patient is unable to move.
Medication or
Drug Class Dosage Description Rationale
Pharmacologic Highlights
Nitric oxide Inhalation route;
dosage varied Pulmonary vascular
vasodilator Decreases pulmonary vascular resistance with increased perfusion to ventilated areas
Independent
To augment gas exchange, the patient needs endotracheal suctioning periodically. Prior to suc- tioning, hyperventilate and hyperoxygenate the patient to prevent the ill effects of suctioning, such as cardiac dysrhythmias or hypotension. Turn the patient as often as possible, even every
DRG Category: 300 Mean LOS: 6.3 days
Description: MEDICAL: Endocrine Disorders with CC
hour, to increase ventilation and perfusion to all areas of the lung. If the patient has particularly poor gas exchange, consider a rocking bed that constantly changes the patient’s position. If the patient’s condition allows, even if the patient is intubated and on a ventilator, get the patient out of bed for brief periods. Evaluate the patient’s condition to determine if soft restraints are appro- priate. Although restraints are frustrating for the patient, they may be necessary to reduce the risk of self-extubation.
If the patient requires medications for skeletal muscle paralysis, provide complete care and make sure the medical management includes sedation. Use artificial tears to moisten the patient’s eyes because the patient loses the blink reflex. Provide passive range-of-motion exer- cises every 8 hours to prevent contractures. Reposition the patient at least every 2 hours for com- fort and adequate gas exchange, and to prevent skin breakdown. Provide complete hygiene, including mouth care, as needed. Assist the patient to conserve oxygen and limit oxygen con- sumption by spacing all activities, limiting interruptions to enhance rest, and providing a quiet environment.
The patient and family may be fearful and anxious. Acknowledge their fear without provid- ing false reassurance. Explain the critical care environment and technology but emphasize the importance of the patient’s humanness over and above the technology. Maintain open communi- cation among all involved. Answer all questions and provide methods for the patient and family to communicate, such as a magic slate or point board.
DOCUMENTATION GUIDELINES
• Respiratory status of the patient: respiratory rate, breath sounds, and the use of accessory mus- cles; arterial blood gas (ABG) levels; pulse oximeter and chest x-ray results
• Response to treatment, mechanical ventilation, immobility, and bedrest
• Presence of any complications (depends on the precipitating condition leading to ARDS)
DISCHARGE AND HOME HEALTHCARE GUIDELINES
PREVENTION. Prompt attention for any infections may decrease the incidence of sepsis, which can lead to ARDS.
COMPLICATIONS. If patients survive ARDS, few residual effects are seen. Complications are directed to any other conditions the patient may have.
44 Adrenal Insufficiency (Addison’s Disease)
Adrenal Insufficiency (Addison’s Disease)
A
ddison’s disease, primary adrenal insufficiency, occurs rarely. The adrenal glands consist of the medulla and the cortex. The medulla is responsible for the secretion of the cate- cholamines epinephrine and norepinephrine; the cortex is responsible for the secretion of glu- cocorticoids, mineralocorticoids, and androgen. The principal glucocorticoid, cortisol, helps regulate blood pressure, metabolism, anti-inflammatory response, and emotional behavior.The principal mineralocorticoid, aldosterone, is important for regulating sodium levels.
Adrenal insufficiency is characterized by the decreased production of cortisol, aldosterone,
and androgen. Cortisol deficiency causes altered metabolism, decreased stress tolerance, and emotional lability. Aldosterone deficiency causes urinary loss of sodium, chloride, and water, resulting in dehydration and electrolyte imbalances. Androgen deficiency leads to the loss of secondary sex characteristics.
CAUSES
Idiopathic adrenal atrophy is the most common cause of adrenal insufficiency. It is not known exactly why this occurs, but it is believed to be related to an autoimmune response that results in the slow destruction of adrenal tissue. Tuberculosis, histoplasmosis, acquired immunodeficiency syndrome (AIDS), and hemorrhage into the adrenal glands have all been associated with destruction of the adrenal glands. All patients with adrenal insufficiency or steroid-dependent disorders are at risk for an acute adrenal crisis. Secondary adrenal failure can also occur with adrenocorticotropic hormone (ACTH) deficiency caused by disorders of the pituitary or hypo- thalamus or suppression because of glucocorticoid therapy.
GENETIC CONSIDERATIONS
Susceptibility to autoimmune adrenal insufficiency sometimes runs in families. Familial gluco- corticoid insufficiency has been reported to have a recessive pattern of transmission. Adreno- myeloneuropathy has been seen to follow X-linked recessive pattern. Adrenal insufficiency is often seen in families in association with other autoimmune disorders.
GENDER, ETHNIC/RACIAL, AND LIFE SPAN CONSIDERATIONS
Addison’s disease, particularly idiopathic autoimmune Addison disease, affects females more than males and occurs in adults in midlife from ages 30 to 60 years. Ethnicity and race have no known effects on the risk for Addison’s disease.
ASSESSMENT
HISTORY. Determine if the patient has a history of recent infection, steroid use, or adrenal or pituitary surgery. Establish a history of poor tolerance for stress, weakness, fatigue, and activity intolerance. Ask if the patient has experienced anorexia, nausea, vomiting, or diarrhea as a result of altered metabolism. Elicit a history of craving for salt or intolerance to cold. Determine pres- ence of altered menses in females and impotence in males.
PHYSICAL EXAMINATION. Assess the patient for signs of dehydration such as tachycardia, altered level of consciousness, dry skin with poor turgor, dry mucous membranes, weight loss, and weak peripheral pulses. Check for postural hypotension—that is, a drop in systolic blood pressure greater than 15 mm Hg when the patient is moved from a lying to a sitting or standing position.
Inspect the skin for pigmentation changes caused by an altered regulation of melanin, noting if surgical scars, skin folds, and genitalia show a characteristic bronze color. Inspect the patient’s gums and oral mucous membranes to see if they are bluish-black. Take the patient’s temperature to see if it is subnormal. Note any loss of axillary and pubic hair that could be caused by decreased androgen levels.
PSYCHOSOCIAL. Because an acute adrenal crisis may be precipitated by emotional stress, periodic psychosocial assessments are necessary for patients with adrenal insufficiency. Patients with an adrenal insufficiency frequently complain of weakness and fatigue, which are also char- acteristic of an emotional problem. However, weakness and fatigue of an emotional origin seem to have a pattern of being worse in the morning and lessening throughout the day, while the weakness and fatigue of adrenal insufficiency seem to be precipitated by activity and lessen with Adrenal Insufficiency (Addison’s Disease) 45
PRIMARY NURSING DIAGNOSIS
Altered nutrition: Less than body requirements related to anorexia, vomiting, and nausea OUTCOMES. Fluid balance; Hydration; Nutritional status: Food and fluid intake; Nutritional status: Energy
INTERVENTIONS. Fluid/electrolyte management; Hypoglycemia management; Nutritional management; Nutritional counseling
PLANNING AND IMPLEMENTATION Collaborative
Collaborative treatment of adrenal insufficiency focuses on restoring fluid, electrolyte, and hor- mone balance. The fluid used for adrenal insufficiency will most likely be 5% dextrose in 0.9%
sodium chloride to replace fluid volume and serum sodium. Patients with adrenal insufficiency will require lifelong replacement steroid therapy. Patients with diabetes mellitus will require insulin adjustments for elevated serum glucose levels.
46 Adrenal Insufficiency (Addison’s Disease)
General Comments: To determine if a cortisol deficit exists, a plasma cortisol level is drawn in the morning; less than 10 mcg/dL suggests adrenal insufficiency; further test- ing may be needed to determine if the adrenal glands have a primary deficiency or if the pituitary cannot produce enough ACTH (secondary adrenal failure).
Abnormality with
Test Normal Result Condition Explanation
Diagnostic Highlights
Serum cortisol level
Serum electrolytes and chemistries
ACTH stimulation test
6:00 to 8:00 a.m. levels should be 5–23 mcg/dL Sodium 136–145 mEq/L;
potassium 3.5–5.1 mEq/L;
blood urea nitrogen 5–20 mg/dL;
glucose 70–105 mg/dL
Within 15–30 minutes of ACTH infusion, the adre- nal cortex releases 2–5 times its normal plasma cortisol level and the cortisol value should be above 20 mcg/dL
Decreased
Hyponatremia;
Hyperkalemia;
azotemia;
hypoglycemia
Level &20 mcg/dL in 30 or 60 minutes
Determines the ability of the adrenal gland to produce gluco- corticoids
Values reflect sodium loss from a deficit in mineralocorticoids with loss of fluids, and poor glucose control because of decreased gluconeogenesis; most consis- tent finding is elevated blood urea nitrogen due to hypo- volemia, decreased glomerular filtration rate, and decreased renal plasma flow
Adrenal glands cannot respond to the stimulation from ACTH and demonstrate that they are not functioning normally
Other Tests: Metyrapone suppression test; urine 17-hydroxycorticosteroids (17-OHCS) and 17-ketosteroids (17-KS); electrocardiogram (ECG); and computed tomography.
rest. Patients with adrenal insufficiency may show signs of depression and irritability from decreased cortisol levels.
Independent
Because of the negative effect of physical and emotional stress on the patient with adrenal insufficiency, promote strategies that reduce stress. Teach the patient to rest between activities to conserve energy and to wear warm clothing to increase comfort and limit heat loss. To limit the risk of infection, encourage the patient to use good hand-washing techniques and to limit exposure to people with infections. To prevent complications, teach the patient to avoid using lotions that contain alcohol to prevent skin dryness and breakdown and to eat a nutritious diet that has adequate proteins, fats, and carbohydrates to maintain sodium and potassium balance.
Finally, the prospect of a chronic disease and the need to avoid stress may lead patients to impaired social interaction and ineffective coping. Discuss with the patient the presence of support systems and coping patterns. Provide emotional support by encouraging the patient to verbalize feelings about an altered body image and anxieties about the disease process. Incor- porate the patient’s unique positive characteristics and strengths into the care plan. Encourage the patient to interact with family and significant others. Before discharge, refer patients who exhibit disabling behaviors to therapists, self-help groups, or crisis intervention centers.
DOCUMENTATION GUIDELINES
• Physical findings: Cardiovascular status, including blood pressure and heart rate; tissue perfusion status, including level of consciousness, skin temperature, peripheral pulses, and urine output;
fluid volume status, including neck vein assessment, daily weights, and fluid input and output
• Laboratory findings: Blood levels of potassium, sodium, hematocrit, and blood urea nitrogen (BUN)
DISCHARGE AND HOME HEALTHCARE GUIDELINES
PREVENTION. To prevent acute adrenal crisis, teach patients how to avoid stress. Emphasize the need to take medications as prescribed and to contact the physician if the patient becomes stressed or unable to take medications.
MEDICATIONS. Be sure the patient understands the reason for steroids prescribed. (See Box 2 for full explanation.)
RESOURCES. Referrals may be necessary to identify potential physical and emotional prob- lems. Notify the hospital’s social service department before patient discharge if you have identi- fied obvious environmental stressors. Initiate home health nursing to assure compliance with medical therapy and early detection of complications. If you identify emotional problems, refer the patient to therapists or self-help groups.
Adrenal Insufficiency (Addison’s Disease) 47
General Comments: Fludrocortisone promotes kidney reabsorption of sodium and the excretion of potassium. Overtreatment can result in fluid retention and possibly con- gestive heart failure; therefore, monitor serum potassium and sodium levels frequently during fludrocortisone administration.
Medication or
Drug Class Dosage Description Rationale
Pharmacologic Highlights
Glucocorticoids such as hydrocortisone, dexametha- sone and prednisone Fludrocortisone
Varies by drug
0.1 mg PO daily
Corticosteroid
Mineralocorticoid
Replacement therapy in deficiency state Replacement therapy in deficiency state
48 Air Embolism
DRG Category: 078 Mean LOS: 7.8 days
Description: MEDICAL: Pulmonary Embolism
A
n air embolism is an obstruction in a vein or artery caused by a bubble of gas. Air enters the circulatory system when the pressure gradient favors movement of air or gas from the environ- ment into the blood. A venous air embolism is the most common form of air embolism. It occurs when air enters the venous circulation, passes through the right side of the heart, and then pro- ceeds to the lungs. In relatively small amounts, the lungs can filter the air; it is absorbed without complications. When large amounts of air (80 to 100 mL) are introduced into the body, however, the lungs no longer have the capacity to filter the air, and the patient has serious or even lethal complications. One of the most serious complications is when the large air bubble blocks the outflow of blood from the right ventricle into the lungs, preventing the blood from moving for- ward. The patient develops cardiogenic shock because of insufficient cardiac output. Experts have found that the risk from air embolism increases as both the volume and the speed of air injection increase.An arterial embolism occurs when air gains entry into the pulmonary venous circulation and then passes through the heart and into the systemic arterial circulation. An arterial embolism can also form in the patient who has a venous embolism and a right-to-left shunt (often caused by a septal defect in the heart) so that the air bubble moves into the left ventricle without passing through the lungs. Pulmonary capillary shunts can produce the same effect. The arterial embolism may cause serious or even lethal complications in the brain and heart. Scientists have found that as little as 0.05 mL of air in the coronary arteries can cause death.
•BOX 2 Patient Teaching for Corticosteroids
• Emphasize the lifetime nature of taking corticosteroids.
• Provide name, dosage, and action of the prescribed medication.
• Explain the common side effects of weight gain, swelling around the face and eyes, insomnia, bruising, gastric distress, gastric bleeding, and petechiae.
• Advise the patient to take the medication with meals to avoid gastric irritation and to take the medication at the time of day prescribed, usually in the morning.
• Suggest the patient weigh self daily, at the same time each day, and call the healthcare provider if weight changes by %5 pounds.
• Emphasize that the patient should always take the medication. Not taking it can cause life- threatening complications. Tell patient to call the healthcare provider if she or he is unable to take medication for more than 24 hours.
• Explain that periods of stress require more medication. Tell the patient to call the healthcare provider for changes in dose if he or she experiences extra physical or emotional stress.
Illness and temperature extremes are considered stressors.
• Explain preventative measures. Tell the patient that, to prevent getting ill, she or he should avoid being in groups with people who are ill and environments where temperatures change from very hot to very cold.
• Teach the patient to recognize signs of undermedication: weakness, fatigue, and dizziness.
Emphasize the need to report underdosing to the healthcare provider.
• Teach the patient to avoid dizziness by moving from a sitting to a standing position slowly.
Urge the patient to always wear a medical alert necklace or bracelet to inform healthcare professionals of the diagnosis.