Pharmacie française en ligne: Acheter des antibiotiques sans ordonnance en ligne prix bas et Livraison rapide.

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2002 Lippincott Williams & Wilkins, Inc. Coyne, Patrick J. MSN, RN, CS; Lyne, Marjorie E. MSN, RN, OCN; Watson, Ashby C. MS, RN, OCN, CS Patrick J. Coyne is the clinical director of the Thomas Palliative Care Unit, Virginia Commonwealth University Health System, Richmond, and an instructor in the End of Life Nursing Education Consortium (ELNEC) project. Marjorie E. Lyne is the program director of the Institutionalizing Effective Pain Management Practices program, Virginia Cancer Pain Initiative, Richmond. Ashby C. Watson is a clinical nurse specialist in psychosocial oncology, Massey Cancer Center, Virginia Commonwealth University Health System, Richmond. Contact author: Patrick J. Coyne, P.O. Box 980007, Richmond, VA 23298. This article is the third in a series on palliative nursing that is supported in part by a grant from the Robert Wood Johnson Foundation. Betty R. Ferrell, PhD, RN, FAAN (bferrell@coh.org), and Nessa Coyle, MS, NP, FAAN (coylen@mskcc.org), are the series editors. • Abstract • ASK, BELIEVE, COMPILE, DIFFERENTIATE • DYSPNEA • COUGH • DEMENTIA AND DELIRIUM • CASE REVISITED • ABCD Assessment of People with HIV or AIDS • The 14th International Congress on Care of the Terminally Ill • REFERENCES Assessing and differentiating dyspnea, cough, dementia, and delirium. “I can't breathe.” That is all Amalia Kreuzer says to anyone who comes close to her bedside. The 32-year-old single mother of three is dying of overwhelming infections and lymphoma caused by AIDS. In the past hour she has been coughing more often, and her breathing has become more labored. Agitated and disoriented, she picks and pulls at her sheets and gown. Her parents, her three sons, and her older sister try to comfort her by speaking in gentle tones, but it's clear that they're extremely distressed by Ms. Kreuzer's agitation. How will you assess Ms. Kreuzer? What interventions might be appropriate in this case, for both dying patient and exhausted family? New drugs and aggressive prevention programs have given many who have access to them an increased chance of survival, and many with HIV and AIDS in the United States are living longer and are more reliant on health care services than ever.(1) Yet at the end of 2001, according to a report by the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO), an estimated 40 million people worldwide were living with HIV or AIDS. (2) Although the over-all prevalence rate among adults worldwide last year was 1.2%, it varied greatly by region, from as high as 8.4% in the countries of sub-Saharan Africa to as low as 0.1% in Australia, New Zealand, and the East Asian and Pacific nations. (2) But the report warns that the lower national prevalence rates often obscure local, population-specific, or resurgent HIV epidemics.(2) In this country, which has an overall prevalence rate of 0.6%, (2) deaths from AIDS are disproportionately high among African Americans and women and in low-income communities.(1,2) AIDS is a chronic illness characterized by frequent and sometimes life-threatening exacerbations that can include infections, malignancies, and neurologic consequences. Late-stage AIDS may be defined as CD4+ counts below 200, and end-stage AIDS as CD4+ counts below 50, both with frequently occurring opportunistic infections, often with more than one pathogen. Symptoms of these advanced stages include pain, diarrhea, nausea and vomiting, fever, dyspnoea, cough, congestive heart failure, anemia, skin disorders, dementia and delirium, wasting, depression, anxiety, fatigue, and fear, (3) and people with AIDS have great need of palliation. Palliative care, which the Institute of Medicine defines as care that “seeks to prevent, relieve, reduce, or soothe the symptoms of disease or disorder without effecting a cure,” (4) is integral to AIDS care and should begin at the initial diagnosis of HIV. Diagnostic testing should be determined by how a test's results are likely to affect the treatment plan and the patient's quality of life. Figure 1. Three Men, by Deidre Scherer, fabric and thread, 36" × 30", 2001; photo by Jeff Baird. This piece is one of six panels in the series Surrounded by Family and Friends. For more about the artist and her work, go to www.dscherer.com . The main goal of palliative care is the enhancement of the quality of the patient's life through a reduction of the distress caused by symptoms and the promotion or maintenance of autonomy. Therefore, it's important that nurses know their patients and their patients' families, as well as their desires and intentions. Yet little clinical research has been performed into either pharmacologic or non-pharmacologic palliative care interventions. Palliative nursing care requires highly specialized physical assessment and communication skills. And because fewer invasive procedures and examinations are performed near the end of life, most clinical decisions and interventions rely solely upon these assessments, making them crucial to symptom management. Unfortunately, most nurses are unprepared for this challenge.5 This article outlines four steps that can help enhance symptom assessment and management by focusing on four symptoms common in late- and end-stage AIDS: dyspnea, cough, dementia, and delirium. When assessing the symptoms of a patient with HIV or AIDS (as with any patient), remember “ABCD,” a mnemonic device representing four crucial steps: ask the patient about himself, believe what he says, compile the information, and differentiate the symptoms described. Ask your patient to describe each of his symptoms, incorporating techniques of active listening such as asking open-ended questions (a “what, where, when, how” format is often best) and noting the patient's tone of voice and body movements as well as his words. This will help in analyzing the patient's responses, compiling the appropriate data, and developing the best plan of care. Pasero and McCaffery note that believing the patient's report of symptoms, especially pain, is paramount. Yet, although clinicians have often invoked McCaffery's 1968 definition of pain (“Pain is whatever the experiencing person says it is, existing whenever he says it does”), many still do not believe the patient's report. (6) The current recommendation to clinicians is to accept the report and move forward with treatment. (6) Strong assessment and data compilation skills allow the clinician to differentiate symptoms and devise a treatment plan. For example, for a patient with cognitive impairment, one must consider whether the patient's medications may be contributing to that dysfunction or whether it's caused by the HIV virus or by an opportunistic infection. Both treatment and outcome depend largely on etiology. Understanding this is crucial in order to treat symptoms adequately. Communication among all team members, the patient, and the family must also be an ongoing priority, so that everyone understands the plan and goals of care as they evolve. (See ABCD Assessment of People with HIV or AIDS, page 51.) Pathophysiology and assessment. Dyspnea, or shortness of breath, is a subjective awareness of difficulty or distress associated with breathing. Unfortunately, the mechanisms that lead to it aren't well understood, and it's often ignored by health professionals. (7) The patient's report is the best indicator of both dyspnea and distress-respiratory rate and oxygenation status are not reliable indicators of either. Dyspnea has both physical and affective symptoms (such as suprasternal notch retraction and anxiety), and it often takes a chronic course of respiratory decline, punctuated by episodes of acute shortness of breath that increase anxiety. Patients with dyspnea usually limit their activities, which can lead to social isolation and loss of independence. (8) The patient's experience with dyspnea influences his perception of subsequent bouts. Dyspnea is a cardinal symptom of pulmonary complications in people with AIDS,9 who may experience opportunistic infections caused by bacteria, viruses, and fungi. For example, AIDS increases susceptibility to Mycobacterium tuberculosis infection and makes its reactivation more likely, and Pneumocystis carinii accounts for 70% of opportunistic infections in such patients. (9) Bacterial and nosocomial infections such as P. carinii and Pseudomonas can cause dyspnea as well as fever, cough, chest pain, and other symptoms. Pulmonary malignancies, bronchitis, pneumothorax, asthma, bronchiectasis, and pulmonary embolism can cause dyspnea with associated cough. Severe anemia, congestive heart failure, and debilitation associated with wasting can cause dyspnea without cough. If the causative infection is correctly diagnosed soon after dyspnea arises, the symptom can be alleviated; early diagnosis is therefore crucial. Assessment involves obtaining a history of acute or chronic dyspnea, smoking, allergies, cardiovascular disease, and lung disease. Other conditions present and the patient's perception of his own physical status should also be noted. Factors that improve or worsen symptoms (such as respiratory treatments, the patient's level of activity) and those that affect the patient's functional status (such as fractures, deep vein thrombosis, gout) also should be assessed. Physical examination involves auscultating lungs and heart, monitoring respiratory rate and depth, noting whether respiration involves use of accessory muscles, noting the presence of pain on breathing, monitoring heart rate and rhythm, noting the presence of extra heart sounds (such as a third heart sound, S3), and assessing functional status. Diagnostic tests may include chest X-ray, pulmonary function tests, complete blood count, oxygen saturation reading, arterial blood gas analysis, electrolyte tests, and electrocardiogram; whether these tests are performed depends on the risk-benefit ratio, the patient's desires, and the prognosis. Nonpharmacologic treatment of dyspnea includes positioning for comfort; for example, using pillows to prop the patient in a forward sitting position allows the lungs to expand and may improve air exchange. Cool air coming through an open window or circulated by a fan or an air conditioner may also help. The presence of family members and caregivers who may be reassuring, soothing, relaxing music, and pursed-lip breathing can reduce anxiety, slow respiration, and reduce dyspnea. (10) Guided imagery and meditation, massage, and prayer also can promote relaxation. (10,11) Oxygen therapy titrated to comfort for patients who are terminally ill, hypoxic, and dyspneic has been recommended, (12) and Janson and Carrieri-Kohlman cited it as a potentially appropriate treatment of “unrelenting severe dyspnea in end-stage AIDS.” (9) But its role in treating patients who are not hypoxic is less clear, (7) necessitating further study. That said, many patients and families believe that oxygen can alleviate shortness of breath. If it does no harm, oxygen administration may confer a psychological benefit. Pharmacologic treatment should consist primarily of opioids, which have been used to relieve dyspnea effectively for more than a century, although their mechanism of action isn't clearly understood. (8) As a general guideline, a starting dose for an opioid naive patient would be either 5 to 10 mg PO morphine or 2 to 4 mg IV or SC morphine. If the patient is already receiving opioids for pain, his dosage might be adjusted upward, toward the higher end of the dosing range. Starting opioids early in treatment helps the patient develop tolerance to side effects such as respiratory depression, allowing rapid titration to levels that can comfort the patient and reduce anxiety. (13) Around-the-clock dosing thereafter and ongoing nursing assessment are also vital. Anxiolytics should be considered as a second-line intervention when a “true” anxiety (psychological rather than physiologic in origin) is perceived as the main cause of dyspnea that does not respond to opioids, usually in acute cases of it. Depending on the underlying or suspected etiology, bronchodilators, diuretics, steroids, or antibiotics may also be used. (11,14) Pathophysiology and assessment. Cough, the violent expiration of air through the glottis, is thought to result from irritation and inflammation of sensory receptors in the tracheobronchial tree. (7) It's usually related to increased mucus production, aspiration of mucus or gastric contents, irritation caused by gastrointestinal reflux, or anxiety. Major causes in patients with HIV are inflammatory processes caused by infections (particularly tuberculosis), bronchial lesions, lung parenchymal disease, and treatments such as radiation. Assessment involves determining causes, history of gastroesophageal reflux disease or asthma, time of onset and frequency of cough, sputum production and characteristics, pharmacologic or non-pharmacologic treatments the patient has attempted, and history of recent respiratory illness or contact with people afflicted with them. Physical assessment involves listening to the cough, noting its quality (for example, wet or dry, deep or weak) and frequency. Also, note any presenting factors such as deep breathing. Inspect the upper airway: examine the throat for drainage (such as of blood), erythema, and edema, and palpate the sinuses for tenderness. Perform a thorough lung examination, as well, with special attention to any adventitious breath sounds. Sputum analysis and sinus and chest X-rays may be considered when an infection appears to be the cause. A new cough should be evaluated for the development of pneumonia, bronchitis, or esophageal infection. Several types of cough and likely causes have been identified, including the following (9): • Chronic cough may result from exposure to allergens or from chronic disease processes such as bronchitis or airway inflammation. • Acute cough may be caused by exposure to allergens, environmental irritants, postnasal drip, aspiration of gastric contents, pulmonary lesions, pneumonia, tuberculosis, or the presence of foreign objects. • Nocturnal cough suggests gastroesophageal reflux disease, asthma, or congestive heart failure. • Cough with haemoptysis (bloody sputum) suggests pneumonia, small capillary erosion caused by pulmonary lesions, or pulmonary embolism. • Cough with dark green or yellow sputum suggests bacterial or viral infection (such as bronchitis or pneumonia). • Cough with fever or night sweats indicates tuberculosis or bacterial pneumonia. • Cough induced by deep breathing or laughing may be caused by interstitial lung processes or airway inflammation. Patients should avoid stimuli that may induce coughing, such as smoke, cold air, and exercise. Patients receiving nebulized pentamidine to treat P. carinii should receive a [beta]-agonist bronchodilator such as albuterol to relieve cough and enhance pentamidine distribution in the lungs. (15) Interventions for cough include chest physiotherapy to mobilize secretions in frail patients, elevating the head of the bed to help clear secretions and to reduce gastroesophageal reflux, and teaching patients to use the forced expiratory technique to clear secretions, (9) which involves huffing several times (a huff is a rapid, forced exhalation made with less than full effort, as in breathing on eyeglasses to fog the lenses), then inhaling deeply and holding for a few seconds before exhaling forcefully with a strong cough. Caffeinated beverages may promote dilation of pulmonary vessels. When there's no therapeutic reason to stimulate coughing (such as to clear airways of mucus), the goal is to suppress the cough. Demulcents, agents that soothe and reduce irritation, are found in many over-the-counter cough medicines. Opioids act in the central nervous system to suppress cough and are widely used for that purpose (although how they do this is unknown, it's thought that they suppress the respiratory center within the medulla oblongata). Bronchodilators relax smooth muscle and decrease coughing in reactive airway disease. Steroids lessen inflammation or compression of airways caused by tumors. Nebulized local anesthetics such as lidocaine can suppress chronic cough, but they can also increase risk of choking and aspiration. (16) Use of cool humidified air may comfort patients while helping to thin secretions. Two major forms of cognitive dysfunction that usually occur during end-stage AIDS are AIDS dementia complex and delirium. AIDS dementia complex is associated with severe immunosuppression and other AIDS-defining illnesses. Although advances in treatment have reduced its incidence, (17,18) it's estimated that 15% to 20% of patients with advanced disease will develop AIDS-related dementia.19 Its prevalence is likely to increase as people with HIV live longer. Delirium has been reported as the most frequent diagnosis in hospitalized patients who are HIV positive and in need of psychiatric consultation. (20) One study revealed that delirium was present in 30% to 40% of hospitalized HIV-positive patients. (21) Yet although nurses are often the first to become aware of either a change in a patient's status or a new symptom, several studies have revealed that delirium often goes unrecognized. (22-24) Pathophysiology and assessment of AIDS-related dementia. This subcortical dementia is associated with the morbidity and poor prognosis characteristic of late-stage AIDS. Like other dementias, it's marked by a persistent cognitive decline with alertness intact. And AIDS dementia complex involves the central nervous system more significantly, with greater degrees of cognitive impairment, motor performance, and behavioral changes than occur in other dementias. HIV attacks the central nervous system early, before symptoms appear. (25) Cognitive changes progress in stages. Basic attentiveness remains intact in a person with early AIDS dementia complex, but forgetfulness, loss of concentration, slowed cognition, and reduced performance of “executive” mental functions (such as planning and coping with new situations) may occur. The ability to process information is preserved, but recollection of it may be impaired. Psychomotor speed may be slowed. Emotional spontaneity and responsiveness are reduced, and social withdrawal increases. The person may lose track of his own thoughts and conversation. Late-stage effects include marked memory impairment, disorientation, and severe speech and language impairments. (21) The patient often forgets to take medications and turn off appliances, and wandering and becoming lost are also common. Motor disturbances, such as ataxia, dyskinesia, and spasticity, can result in significant loss of function, with symptoms including clumsiness, leg weakness, and loss of coordination and balance. Hallucinations and seizures may occur. (26) Patients with end-stage dementia may be completely bedridden and indifferent to their illness and surroundings, and they may be grossly aphasic or mute. In many patients, antiretroviral therapy has reduced severity of AIDS-related dementia,27,28 but various studies have revealed this therapy to be ineffective in about 20% to 50%. (27-29) Pathophysiology and assessment of delirium. Delirium, an acute confusional state characterized by “concurrent disturbances of level of consciousness, attention, thinking, perception, memory, and psychomotor behavior,” (30) progresses rapidly over hours or days. Early symptoms are often nonspecific and may include irritability and disturbances in the sleep-wake cycle. (20) Level of functioning declines dramatically, and level of consciousness fluctuates. Thoughts are disorganized, speech may be impaired or incoherent, and finding words and naming objects becomes difficult. Perceptual disturbances range from misinterpretation of the environment to hallucinations. Orientation to time and place is affected, but in most cases the patient can identify himself. Short-term and recent memory are impaired and the patient may be agitated, labile, or apathetic. (31) The condition can be reversed. When assessing for the presence of delirium, it's important to consult family members and friends who know the patient well and can tell you whether they've noticed sudden changes in behavior and cognition. Standard neuropsychological tests are more sensitive to subtle cognitive dysfunction but may be impractical for use in patients with advanced disease. One exception to this is the Folstein Mini-Mental Status Examination (MMSE), which can be performed in only 15 minutes. (32) The MMSE tests abilities in all major cognitive domains-orientation; attention and concentration; and executive, linguistic, spatial, and memory functions-and can help clinicians detect the presence of delirium or combined delirium and dementia and track its progression. The etiology of delirium is determined in fewer than 50% of terminally ill patients with AIDS. (33,34) The use of neuroleptics to treat dementia is controversial, and some clinicians are concerned about the side-effect profiles of these drugs. An extensive review of 16 randomized, controlled trials revealed that neuroleptics have a small but significant efficacy advantage in treating dementia, when compared with placebo. (35) Comparison of different neuroleptics demonstrated similar efficacy, side effects, and drop-out rates. (35) A more recent literature review revealed haloperidol to be effective in reducing aggression in elderly patients with dementia; however, it was ineffective in alleviating agitation in this group, and it actually exacerbated some symptoms. (36) The authors recommend that haloperidol not be used routinely to treat patients with agitated dementia, and they also emphasized the importance of individualizing treatment and monitoring patients for side effects of therapy. Apathy and social withdrawal in patients with mild-to-moderate cognitive impairment can be treated with methylphenidate 5 mg PO at 8 AM and 2 PM,20 which can be increased to as much as 20 mg in early morning, mid-morning, and early afternoon, but it shouldn't be taken after 2 PM because it interferes with sleep. Other side effects include jitteriness, nausea, loss of appetite, tachycardia, elevated blood pressure, and rarely, nightmares and psychosis. (37) Stimulating antidepressants such as fluoxetine and venlafaxine have also been prescribed for apathy in such patients. If the cause of delirium can't be determined or pharmacologic treatment isn't indicated, focus care on managing symptoms and enhancing comfort. And again, the treatment of agitation with neuroleptic medications in people with delirium is controversial. Some clinicians prefer to use other medications that they believe are better tolerated. The only randomized trial of neuroleptics in patients who were both HIV positive and agitated revealed that haloperidol (a highly potent neuroleptic) and chlorpromazine (a less potent neuroleptic) are both effective and tolerated well when compared with lorazepam (a benzodiazepine). (21) (Benzodiazepines actually have been shown to aggravate delirium. (21)) Haloperidol has a short half-life, produces no metabolites, produces few anticholinergic and cardiovascular effects, and causes less sedation. It can be administered orally, subcutaneously, or intravenously. An intravenous dose is twice as potent as an oral one; subcutaneous dosing is equivalent in potency to intravenous dosing, but absorption of the drug is slower. The recommended dosage of oral haloperidol in the treatment of delirium is 0.5 mg to 5 mg PO every two to 12 hours. Karasic and Dilly found that highly potent neuroleptics such as haloperidol and fluphenazine are more likely than less potent ones to cause extrapyramidal symptoms in HIV-positive patients. (20) Low-potency neuroleptics such as chlorpromazine are also believed to produce adverse effects, particularly anticholinergic effects and orthostasis, in this population. (38) The researchers recommend administering olanzapine 2.5 mg PO BID or 5 mg PO QHS, which can be increased to as much as 20 mg PO QHS as necessary and as tolerated. Olanzapine, an atypical antipsychotic, has greater efficacy and is associated with fewer extrapyramidal symptoms than typical antipsychotics, but it can lower the seizure threshold. Risperidone is also tolerated well at 0.5 mg PO BID or 1 mg PO QHS, which can be increased to as much as 3 mg PO BID if necessary. Medium-potency neuroleptics such as molindone (12.5 mg PO BID) and perphenazine (4 mg PO BID, which may be increased to a total of 24 mg QD) are also useful, but they require monitoring for dystonic reactions. In an emergency, intravenous administration of haloperidol is acceptable at low doses (0.5 to 2 mg IV BID). Intravenous lorazepam may be added at 0.5 to 1 mg IV every three to eight hours, but this drug can heighten confusion, disinhibition, and ataxia. The main goal of nursing care for patients and families is providing a calm, safe, supportive environment. It's difficult for families and friends to witness the patient's distress. Nurses can help reassure patients by using a calming touch and voice. Familiar objects and the presence of loved ones can alleviate anxiety and may lessen perceptual disturbances, such as misinterpretation of the environment. When possible, the same staff members should be assigned to the patient on a regular basis. Placing the patient in a room with a window may reinforce the diurnal cycle. Serene music familiar to the patient may promote a sense of peace. Turning off television sets and shutting doors can reduce overstimulation. In cases of severe or persistent dementia or delirium, there's no benefit in trying to reorient the patient to time and place; in fact, reminding the patient repeatedly that, for example, “Today is Tuesday,” will probably only increase agitation. Orientation in this instance should focus on reassurance, using comments such as, “We are here with you. You are safe.” Family members can be taught to observe and evaluate the patient's responses to such comments. (31) In some patients who are cognitively impaired, these techniques may not relieve agitation, and sedation may be necessary. When possible, discontinue drugs that aren't absolutely necessary. If more than 20 mg to 30 mg a day of a highly potent neuroleptic is required to manage agitation, it may be necessary to change to a more sedating drug. If symptoms of delirium remain intractable despite aggressive titration of these medications, greater sedation with agents such as midazolam may be indicated. Family members of people with AIDS may face the challenge of caring for a physically debilitated, cognitively impaired patient at home. Caregiving responsibilities only increase as the disease progresses. End-stage disease may necessitate hospitalization for aggressive symptom management and caregiver respite. Family members of patients who are dying of AIDS may need special kinds of support, as well. It may have come as a surprise, for instance, that their loved one is gay; or perhaps they had been unaware that he had contracted HIV through the sharing of needles. There are many such familial issues to which nurses should be sensitive, and they must be prepared to deal with a variety of emotions. A quick assessment of Ms. Kreuzer indicates two areas of concern: the respiratory symptoms, which take first priority, and her mental status. Although dyspnea and coughing make it difficult for her to speak, she manages to say that she feels unable to take a full breath and rates her chest pain at 7 on a 0 to 10 scale. She picks and pulls at the bedclothes with increasingly erratic gestures. Ms. Kreuzer's sons are visibly disturbed by her agitation. When you ask her parents and sister if anything has happened in the past few hours that may have made it harder for her to breathe, her sister replies, “I think she slipped down on the pillow.” As you continue assessing Ms. Kreuzer, you raise the head of the bed and adjust the pillows to support her in a forward sitting position, and this relives the dyspnea somewhat. You obtain an oxygen saturation reading noninvasively: pulse oximetry at the finger indicates 88% saturation. Because the goal is Ms. Kreuzer's comfort, further laboratory tests and procedures such as arterial blood gas analysis aren't indicated. You auscultate her lungs and heart, and determine that she's tachypneic and tachycardic. You hear crackles at both lung bases and note the presence of pink, frothy sputum. According to her family, the exacerbation occurred fairly quickly, and you suspect new-onset pulmonary edema. The interdisciplinary team is notified, and Ms. Kreuzer, who is opioid naive, is started on morphine 2.5 mg IV Q1H PRN. Nebulizer treatments with a bronchodilator are also initiated. Anxiolytics aren't indicated because Ms. Kreuzer's anxiety appears to stem from dyspnea and cough. The team physician orders furosemide and, at her parents' request, oxygen via nasal cannula (usually more comfortable than a face mask). But Ms. Kreuzer becomes more agitated and pulls the cannula off. Reinsertion only increases her distress, so the team decides to leave it off. You check to see that her urinary catheter is still in place. With encouragement, Ms. Kreuzer's father sits at the bedside and strokes her hand, and this seems to calm her. Her sister speaks to her in a soothing tone, saying, “Amalia, we're here, we're not going anywhere.” You ask the oldest son to turn on the ceiling fan, explaining that this may ease the dyspnea, and then explain to the family that if these interventions don't decrease her agitation, a low-potency neuroleptic such as haloperidol (0.5 to 5 mg Q2H to Q12H, PO or IV or SC) can be administered. Within 20 minutes, though, Ms. Kreuzer's agitation decreases and breathing improves. One of the boys asks, “Will Mom be all right?” You explain to Ms. Kreuzer's sons, and to her parents and sister, that although her ability to breathe is diminishing overall, their presence is one of the best treatments she can receive. ABCD Assessment of People with HIV or AIDS I. The patient's report-ASK the following questions with regard to each symptom. BELIEVE (accept) the patient's responses. 1. What is it? (Ask the patient to identify the symptom.) 2. Where is it? (Ask about localized symptoms, and examine the site.) 3. When does it occur? When did it start? 4. How does it feel? (Ask the patient to describe the symptom.) 5. How would you rate its intensity on a scale of 0-10? 6. How much does it interfere with daily life? (Ask the patient to rate interference on a scale of 0-10.) 7. What remedies have you already tried? (Ask about prescribed and over-the-counter medications, herbal and nutritional supplements, and complementary or alternative therapies.) 8. What makes it better or worse? (Ask about factors such as time of day and the effects of activities of daily life.) 9. What is your goal in the treatment of this symptom? (For example, the treatment goal for cough might be to reduce or eliminate it so that the patient can sleep through the night.) II. History and Physical Assessment-COMPILE information. • History taking includes listing all past and current prescribed and over-the-counter medications and herbal and nutritional supplements that the patient has taken or is taking for HIV or AIDS, all other past and current conditions, and past and current treatments (such as radiation therapy) for HIV, AIDS, and any other condition. • Physical assessment includes focusing on specific symptoms. (For example, perform a respiratory assessment for dyspnea or cough. Include pertinent diagnostic laboratory test results.) III. Treatment-DIFFERENTIATE and treat symptoms. Optimally, treatment should address both the cause of the symptom and the relief of it. With dying patients, the treatment goal may be comfort alone. Reassess the patient's symptoms and document response to each treatment intervention. Inform all members of the health care team of the results. Reassessment should be performed on either a periodic or ongoing basis, as appropriate. 1. O'Neill JF, et al. Improving HIV/AIDS services through palliative care: an HRSA perspective. J Urban Health 2000;77(2):244-54. 2. AIDS epidemic update 2001: Joint United Nations Programme on HIV/AIDS, World Health Organization [2001]. http://www.unaids.org/worldaidsday/2001/Epiupdate2001/Epiupdate2001_en.pdf 3. Neill K. HIV/AIDS. In: Smith S, editor. Hospice and palliative care clinical practice monograph: treatment of end-stage non-cancer diagnoses. Pittsburgh (PA): Hospice and Palliative Nurses Association; 2001. 4. Field MJ, et al., editors. Approaching death: improving care at the end of life. Washington (DC): National Academy Press; 1997. 5. White KR, et al. Are nurses adequately prepared for end-of-life care? J Nurs Scholarsh 2001;33(2):147-51. Ovid Full Text Bibliographic Links 6. McCaffery M, Pasero C. Pain: clinical manual. 2nd ed. St. Louis: Mosby; 1999. 7. Dudgeon D. Dyspnea, death rattle and cough. In: Ferrell B, Coyle N, editors. Textbook of palliative nursing. New York: Oxford University Press; 2001. p. 164-74 8. Coyne PJ, et al. Nebulized fentanyl citrate improves patients' perception of breathing, respiratory rate, and oxygen saturation in dyspnea. J Pain Symptom Manage 2002;23(2):157-60. Bibliographic Links 9. Janson S, Carrieri-Kohlman V. Respiratory changes. In: Ropka M, Williams A, editors. HIV nursing and symptom management. Sudbury (MA): Jones and Bartlett; 1998. p. 361-86. 10. Corner J, et al. Non-pharmacological intervention for breathlessness in lung cancer. Palliat Med 1996;10(4):299-305. Bibliographic Links 11. End of Life Nursing Education Consortium [web site]. 2002. http://www.aacn.nche.edu/ELNEC/index.htm . 12. Bruera E, et al. Effects of oxygen on dyspnoea in hypoxaemic terminal-cancer patients. Lancet 1993;342(8862):13-4. Bibliographic Links [Context Link] 13. Twycross RG. Pain relief in advanced cancer. New York: Churchill Livingstone; 1994. [Context Link] 14. Newshan G, Sherman DW. Palliative care: pain and symptom management in persons with HIV/AIDS. Nurs Clin North Am 1999;34(1):131-45. 15. Harrison KS, Laube BL. Bronchodilator pretreatment improves aerosol deposition uniformity in HIV-positive patients who cough while inhaling aerosolized pentamidine. Chest 1994;106(2):421-6. Bibliographic Links 16. Dudgeon D, Rosenthal S. Pathophysiology and assessment of dyspnea in the patient with cancer. In: Portenoy RK, Bruera E, editors. Topics in palliative care. New York: Oxford University Press; 2000. vol. 4. p. 237-54. 17. Dore GJ, et al. Changes to AIDS dementia complex in the era of highly active antiretroviral therapy. AIDS 1999;13(10):1249-53. 18. Sacktor NC, et al. Psychomotor slowing in HIV infection: a predictor of dementia, AIDS and death. J Neurovirol 1996;2(6):404-10. Bibliographic Links 19. McArthur JC, et al. Human immunodeficiency virusassociated dementia. Semin Neurol 1999;19(2):129-50. Bibliographic Links 20. Karasic D, Dilly J. HIV-associated psychiatric disorders. In: Cohen PT, et al., editors. The AIDS knowledge base: a textbook on HIV disease from the University of California, San Francisco School of Medicine, and San Francisco General Hospital. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 577-84. 21. Breitbart W, et al. A double-blind trial of haloperidol, chlorpromazine, and lorazepam in the treatment of delirium in hospitalized AIDS patients. Am J Psychiatry 1996;153(2):231-7. 22. Lacko L, et al. Changing clinical practice through research: the case of delirium. Clin Nurs Res 1999;8(3):235-50. Bibliographic Links 23. Rockwood K, et al. Increasing the recognition of delirium in elderly patients. J Am Geriatr Soc 1994;42(3):252-6. 24. Inouye SK, et al. Nurses' recognition of delirium and its symptoms: comparison of nurse and researcher ratings. Arch Intern Med 2001;161(20):2467-73. Bibliographic Links 25. Brew BJ. AIDS dementia complex. Neurol Clin 1999;17(4):861-81. Bibliographic Links 26. Meehan RA, Brush JA. An overview of AIDS dementia complex. Am J Alzheimers Dis Other Demen 2001;16(4):225-9. 27. Palella FJ, Jr., et al. Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. N Engl J Med 1998;338(13):853-60. 28. Fatkenheuer G, et al. Virological treatment failure of protease inhibitor therapy in an unselected cohort of HIV-infected patients. AIDS 1997;11(14):F113-6. 29. Rausch DM, Stover ES. Neuroscience research in AIDS. Prog Neuropsychopharmacol Biol Psychiatry 2001;25(1):231-57. Bibliographic Links 30. American Psychiatric Association. Diagnostic and statistical manual of mental disorders: DSM-IV. 4th ed. Washington (DC): The Association; 1994. 31. Kuebler K, et al. Delirium, confusion, agitation, and restlessness. In: Ferrell B, Coyle N, editors. Textbook of palliative nursing. New York: Oxford University Press; 2001. p. 290-308. 32. Malloy PF, et al. Cognitive screening instruments in neuropsychiatry: a report of the Committee on Research of the American Neuropsychiatric Association. J Neuropsychiatry Clin Neurosci 1997;9(2):189-97. Bibliographic Links 33. Bruera E, et al. Cognitive failure in patients with terminal cancer: a prospective study. J Pain Symptom Manage 1992;7(4):192-5. Bibliographic Links 34. De Stoutz ND, et al. Reversible delirium in terminally ill patients. J Pain Symptom Manage 1995;10(3):249-53. Bibliographic Links 35. Lanctot KL, et al. Efficacy and safety of neuroleptics in behavioral disorders associated with dementia. J Clin Psychiatry 1998;59(10):550-63. Bibliographic Links 36. Lonergan E, et al. Haloperidol for agitation in dementia (Cochrane Review). The Cochrane Library. Oxford (UK): Update Software; 2002. 37. Rosenfeld B. HIV infection and AIDS-associated neoplasms. In: Holland JC, Breitbart W, editors. Psycho-oncology. New York: Oxford University Press; 1998. p. 417-26. 38. Morrow G, et al. Nausea and vomiting. In: Holland JC, Breitbart W, editors. Psycho-oncology. New York: Oxford University Press; 1998. p. 476-84.

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