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Raynaud’s phenomenon


Description


Raynaud’s phenomenon is an episodic vasospastic disorder of the small cutaneous arteries, most frequently involving the fingers and toes. It occurs primarily in young women (typically between 15 and 40 years old). The pathogenesis is due to abnormalities in the vascular, intravascular, and neuronal mechanisms that cause an imbalance between vasodilation and vasoconstriction.


Raynaud’s phenomenon may occur in isolation or in association with an underlying disease (e.g., rheumatoid arthritis, scleroderma, or systemic lupus erythematosus). Other contributing factors include occupation-related conditions, such as use of vibrating machinery or work in cold environments, and exposure to heavy metals (e.g., lead).


Clinical manifestations


Exposure to cold, emotional upsets, tobacco use, and caffeine often bring on symptoms.



■ The disorder is characterized by vasospasm-induced color changes (white, red, and blue) of fingers, toes, ears, and nose. Decreased perfusion results in pallor (white). The digits then appear cyanotic (bluish purple). These changes are subsequently followed by rubor (red) caused by the hyperemic response that occurs when blood flow is restored.


■ The patient usually describes cold and numbness in the vasoconstrictive phase, with throbbing and aching pain, tingling, and swelling in the hyperemic phase. An episode usually lasts only minutes, but in severe cases it may persist for several hours.


■ After frequent, prolonged attacks, the skin may become thickened and the nails brittle. Complications include punctate (small hole) lesions of the fingertips and superficial gangrenous ulcers in advanced stages.


■ Diagnosis is based on persistent symptoms for at least 2 years.


Nursing and collaborative management


When conservative management is ineffective, drug therapy is considered. Sustained-release calcium channel blockers (e.g., nifedipine [Procardia]) are the first-line drug therapy. Calcium channel blockers relax smooth muscles of the arterioles by blocking the influx of calcium into the cells. This reduces the frequency and severity of vasospastic attacks.


Prompt intervention is needed for patients with digital ulceration and/or critical ischemia. Treatment options include IV prostanoid therapy (e.g., iloprost), antibiotics, analgesics, and possibly an endothelin receptor antagonist (e.g., bosentan [Tracleer]) and surgical debridement of necrotic tissue. Sympathectomy is considered only in advanced cases.


ent Patient and caregiver teaching


Teaching should be directed toward preventing recurrent episodes.



Reactive arthritis


Reactive arthritis (Reiter’s syndrome) is associated with a symptom complex that includes urethritis or cervicitis, conjunctivitis, and mucocutaneous lesions. It occurs more commonly in young men as compared with young women.



Individuals with inherited HLA-B27 are at increased risk of developing reactive arthritis after sexual contact or exposure to certain enteric pathogens, supporting the likelihood of a genetic predisposition.



Prognosis is favorable, with most patients recovering after 2 to 16 weeks. Because reactive arthritis is often associated with Chlamydia trachomatis infection, treatment of patients and their sexual partners with doxycycline (Vibramycin) is widely recommended. Drug therapy may also include nonsteroidal antiinflammatory drugs (NSAIDs), methotrexate, and sulfasalazine. Physical therapy may be helpful during disease recovery.



Refractive errors


Refractive errors are the most common visual problem. This defect prevents light rays from converging into a single focus on the retina. Defects are a result of corneal curvature irregularities, lens-focusing power, or eye length. Types of refractive errors include the following:



■ Myopia (nearsightedness), the most common refractive error, is caused by light rays focusing in front of the retina, resulting in an inability to accommodate for objects at a distance.


■ Hyperopia (farsightedness) is caused by light rays focusing behind the retina and requires the person to use accommodation to focus the light rays on the retina for near and far objects.


■ Presbyopia is a loss of accommodation resulting from age, with the crystalline lens becoming larger, firmer, and less elastic. This condition generally appears about the age of 40 years and results in an inability to focus on near objects.


■ Astigmatism is caused by an irregular corneal curvature so that incoming light rays are bent unequally and light rays do not come to a single point of focus on the retina. Astigmatism can occur in conjunction with any of the other refractive errors.


The major symptom of refractive errors is blurred vision. Additional complaints may include ocular discomfort, eye strain, or headaches. Management of refractive errors is correction, which may include eyeglasses, contact lenses, refractive surgery, or surgical implantation of an artificial lens.


Respiratory failure, acute


Description


The major function of the respiratory system is gas exchange, which involves the transfer of oxygen (O2) and carbon dioxide (CO2) between inhaled tidal volumes and circulating blood volume within the pulmonary capillary bed. Respiratory failure results when one or both of these gas-exchanging functions are inadequate.


Respiratory failure is not a disease but a symptom of an underlying pathology affecting lung tissue function, O2 delivery, cardiac output (CO), or the baseline metabolic state. It is a condition that occurs because of one or more diseases involving the lungs or other body systems (Table 73). Respiratory failure is classified as hypoxemic or hypercapnic. Many patients experience both hypoxemic and hypercapnic respiratory failure.



■ Hypoxemic respiratory failure is also referred to as oxygenation failure because the primary problem is inadequate O2 transfer between the alveoli and the pulmonary capillaries. Although no universal definition exists, hypoxemic respiratory failure is commonly defined as a partial pressure of oxygen in arterial blood (PaO2) of 60 mm Hg or less when the patient is receiving an inspired O2 concentration of at least 60%.




Pathophysiology


Hypoxemic respiratory failure


Four physiologic mechanisms may cause hypoxemia and subsequent hypoxemic respiratory failure: (1) mismatch between ventilation (V) and perfusion (Q) commonly referred to as V/Q mismatch, (2) shunt, (3) diffusion limitation, and (4) hypoventilation. The most common causes are V/Q mismatch and shunt.



■ Many diseases and conditions cause V/Q mismatch. The most common are those in which increased secretions are present in the airways (e.g., chronic obstructive pulmonary disease [COPD]) or alveoli (e.g., pneumonia) or when bronchospasm is present (e.g., asthma). V/Q mismatch may also result when alveoli collapse (atelectasis) or as a result of pain.


■ Shunt occurs when blood exits the heart without having participated in gas exchange. A shunt can be viewed as an extreme V/Q mismatch. There are two types of shunt: anatomic and intrapulmonary. O2 therapy alone may be ineffective in increasing the PaO2 if hypoxemia is caused by shunt.


■ Diffusion limitation occurs when gas exchange across the alveolar-capillary interface is compromised by a process that thickens, damages, or destroys the alveolar membrane or affects blood flow through the pulmonary capillaries. Diffusion limitation is worsened by disease states affecting the pulmonary vascular bed, such as severe emphysema or recurrent pulmonary emboli. Some diseases cause the alveolar-capillary membrane to become thicker (fibrotic), which slows gas transport. These diseases include pulmonary fibrosis, interstitial lung disease, and acute respiratory distress syndrome (ARDS). The classic sign of diffusion limitation is hypoxemia that is present during exercise but not at rest.


■ Alveolar hypoventilation is a generalized decrease in ventilation that results in an increase in the PaCO2 and a consequent decrease in PaO2. Alveolar hypoventilation may be the result of restrictive lung disease, central nervous system (CNS) disease, chest wall dysfunction, or neuromuscular disease.


Frequently, hypoxemic respiratory failure is caused by a combination of V/Q mismatch, shunt, diffusion limitation, and alveolar hypoventilation.



Hypercapnic respiratory failure


Hypercapnic respiratory failure results from an imbalance between ventilatory supply and ventilatory demand. Normally, ventilatory supply far exceeds ventilatory demand. However, patients with preexisting lung disease such as severe COPD cannot effectively increase lung ventilation in response to exercise or metabolic demands. Hypercapnic respiratory failure is sometimes called ventilatory failure because the primary problem is the inability of the respiratory system to remove sufficient CO2 to maintain a normal PaCO2.



■ Many diseases can cause a limitation in ventilatory supply (see Table 73). They can be grouped into four categories: (1) abnormalities of the airways and alveoli, (2) abnormalities of the CNS, (3) abnormalities of the chest wall, and (4) neuromuscular conditions.


Clinical manifestations


Respiratory failure may develop suddenly (minutes or hours) or gradually (several days or longer). A sudden decrease in PaO2 or a rapid rise in PaCO2 implies a serious condition that can rapidly become a life-threatening emergency.


Manifestations are related to the extent of the change in PaO2 and PaCO2, the rapidity of change (acute versus chronic), and the ability to compensate to overcome this change. When the patient’s compensatory mechanisms fail, respiratory failure occurs. Because manifestations are variable, it is important to monitor trends in arterial blood gas (ABG) values and/or pulse oximetry to evaluate the extent of change.



The patient may have a rapid, shallow breathing pattern or a respiratory rate that is slower than normal. A change from a rapid to a slower rate in a patient in acute respiratory distress suggests extreme progression of respiratory fatigue and increased possibility of respiratory arrest.



■ Respiratory behaviors such as assumption of tripod position, pursed-lip breathing, and two- or three-word dyspnea also indicate respiratory distress.



Immediately report any change in mental status, such as agitation, confusion, or a decreased level of consciousness (LOC), because this change may indicate the onset of rapid deterioration and the need for mechanical ventilation.


Diagnostic studies



In severe respiratory failure requiring endotracheal intubation, end-tidal CO2 (ETCO2) may be used to assess tube placement within the trachea immediately following intubation. ETCO2 may also be used during ventilator management to assess trends in lung ventilation. A central venous or pulmonary artery (PA) catheter is often used to measure hemodynamic parameters (e.g., central venous pressure, PA pressures, CO, pulmonary artery wedge pressure, central/mixed venous O2 saturation [ScvO2/SvO2]).


Nursing and collaborative management


Because many different problems can cause respiratory failure, specific care of these patients varies. Goals and related interventions to maximize O2 delivery are essential to improving the patient’s oxygenation and ventilation status. The primary goal is to treat the underlying cause of the respiratory failure. Other supportive goals include maintaining an adequate CO and hemoglobin concentration.


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Oct 26, 2016 | Posted by in NURSING | Comments Off on R

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