Palliative Care and Pain Managemet
The focus of palliative care is to improve symptoms and quality of life at any stage of illness. At the end of life, palliative care often becomes the only focus of care, but a palliative care approach is applicable throughout the course of both serious chronic and terminal illnesses.
Whether the goal is to cure disease or manage chronic illness, clinicians have a responsibility to help ameliorate patients’ suffering. “To cure sometimes, to relieve often, to comfort always” is the crux of palliative care.
The World Health Organization defines palliative care as “an approach that improves the quality of life of patients and their families facing the problem associated with lifethreatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment and treatment of pain and other problems, physical, psychosocial and spiritual.” Palliative care commonly involves management of pain, but treatment of all symptoms is pursued, including physical symptoms, such dyspnea, nausea and vomiting, constipation, and agitation; emotional distress, such as depression, anxiety, and interpersonal strain; and existential distress, such as spiritual crisis. While palliative care has been recognized formally as a medical specialty by the American Board of Medical Specialties, all clinicians should possess the basic skills to be able to manage pain, treat dyspnea, identify possible depression, communicate about important issues (such as prognosis and patient preferences for care), and help address spiritual distress. While palliative care experts are increasingly available in hospital and outpatient settings and while expert consultation may be helpful for many patients, recognizing the importance of symptom management and quality of life is a necessary step for all clinicians in helping patients face serious illness.
Symptoms that cause significant suffering can be considered a type of medical emergency and managed aggressively by frequent elicitation, continuous reassessment, and individualized treatment. While patients at the end of life may experience a host of distressing symptoms, pain, dyspnea, and delirium are reported to be among the most feared and burdensome. The principles of excellent palliative care dictate that comfort is the main focus of care and that properly informed patients or their surrogates may decide to pursue aggressive symptom relief even if, as a known but unintended consequence, the treatments preclude further curative interventions or even hasten death. That said, there is a growing awareness that scrupulous symptom control for patients with end-stage illness may actually prolong life.
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Community-Acquired Pneumonia
Definition & Pathogenesis
Community-acquired pneumonia is diagnosed outside of the hospital or is diagnosed within 48 hours after admission to the hospital in a patient who has not been hospitalized in an acute care hospital for 2 or more days within 90 days of the infection; or has resided in a long-term care facility; or has received intravenous antimicrobial therapy, chemotherapy, or wound care within the 30 days prior to the current infection; or has attended a hospital or hemodialysis clinic.
Pulmonary defense mechanisms (cough reflex, mucociliary clearance system, immune responses) normally prevent the development of lower respiratory tract infections following aspiration of oropharyngeal secretions containing bacteria or inhalation of infected aerosols. Community-acquired pneumonia occurs when there is a defect in one or more of the normal host defense mechanisms or when a very large infectious inoculum or a highly virulent pathogen overwhelms the host.
Prospective studies have failed to identify the cause of community-acquired pneumonia in 40–60% of cases; two or more causes are identified in up to 5% of cases.
Bacteria are more commonly identified than viruses. The most common bacterial pathogen identified in most studies of community-acquired pneumonia is Spneumoniae, accounting for approximately two-thirds of bacterial isolates. Other common bacterial pathogens include H influenzae, Mycoplasma pneumoniae, Chlamydia pneumoniae, S aureus, Neisseria meningitidis, M catarrhalis, Klebsiella pneumoniae, other gram-negative rods, and Legionella species. Common viral causes of community-acquired pneumonia include influenza virus, respiratory syncytial virus, adenovirus, and parainfluenza virus. A detailed assessment of epidemiologic risk factors may aid in diagnosing pneumonias due to the following causes: Chlamydia psittaci (psittacosis), Coxiella burnetii (Q fever), Francisella tularensis (tularemia), endemic fungi (Blastomyces, Coccidioides, Histoplasma), and sin nombre virus (hantavirus pulmonary syndrome).
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_ Clinical Findings
A. Symptoms and Signs
Most patients with community-acquired pneumonia experience an acute or subacute onset of fever; cough with or without sputum production, and dyspnea. Other common symptoms include rigors, sweats, chills, chest discomfort, pleurisy, hemoptysis, fatigue, myalgias, anorexia, headache, and abdominal pain.
Common physical findings include fever or hypothermia, tachypnea, tachycardia, and mild arterial oxygen desaturation. Many patients will appear acutely ill. Chest examination is often remarkable for altered breath sounds and rales. Dullness to percussion may be present if a parapneumonic pleural effusion is present.
The differential diagnosis of lower respiratory tract symptoms and signs is extensive and includes upper respiratory tract infections, reactive airway diseases, congestive heart failure, COP, lung cancer, pulmonary vasculitis, pulmonary thromboembolic disease, and atelectasis.
B. Laboratory Findings
Controversy surrounds the role of Gram stain and culture analysis of expectorated sputum in patients with community-acquired pneumonia. Most reports suggest that these tests have poor positive and negative predictive value in most patients. Some argue, however, that the tests should still be performed to try to identify etiologic organisms in the hope of reducing microbial resistance to drugs, unnecessary drug costs, and avoidable side effects of empiric antibiotic therapy. Expert panel guidelines suggest that sputum Gram stain should be attempted in all patients with community-acquired pneumonia and that sputum culture should be obtained for all patients who require hospitalization. Sputum should be obtained before antibiotics are initiated except in a case of suspected antibiotic failure. The specimen is obtained by deep cough and should be grossly purulent. Culture should be performed only if the specimen meets strict cytologic criteria, eg, more than 25 neutrophils and fewer than 10 squamous epithelial cells per low power field. These criteria do not apply to cultures of legionella or mycobacteria.
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Additional testing is generally recommended for patients who require hospitalization: preantibiotic blood cultures (at least two sets with needle sticks at separate sites), arterial blood gases, complete blood count with differential, and a chemistry panel (including serum glucose, electrolytes, urea nitrogen, creatinine, bilirubin, and liver enzymes). The results of these tests help assess the severity of the disease and guide evaluation and therapy. HIV serology should be obtained from all hospitalized patients.
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Peptic Ulcer Disease
Essentials of Diagnosis
_ History of nonspecific epigastric pain present in 80 – 90% of patients with variable relationship to meals.
_ Ulcer symptoms characterized by rhythmicity and periodicity.
_ Ten to 20 percent of patients present with ulcer complications without antecedent symptoms.
_ Most NSAID-induced ulcers are asymptomatic.
_ Upper endoscopy with antral biopsy for H pylori is the diagnostic procedure of choice in most patients.
_ Gastric ulcer biopsy or documentation of complete healing necessary to exclude gastric malignancy.
_ General Considerations
Peptic ulcer is a break in the gastric or duodenal mucosa that arises when the normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid and pepsin. By definition, ulcers extend through the muscularis mucosae and are usually over 5 mm in diameter. In the United States, there are about 500,000 new cases per year of peptic ulcer and 4 million ulcer recurrences; the lifetime prevalence of ulcers in the adult population is approximately 10%. Ulcers occur five times more commonly in the duodenum, where over 95% are in the bulb or pyloric channel. In the stomach, benign ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser curvature (25%). Ulcers occur slightly more commonly in men than in women (1.3:1). Although ulcers can occur in any age group, duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years, whereas gastric ulcers are more common in patients between the ages of 55 and 70 years. Ulcers are more common in smokers and in patients taking NSAIDs on a long-term basis (see below). Alcohol, dietary factors, and stress do not appear to cause ulcer disease. The incidence of duodenal ulcer disease has been declining dramatically for the past 30 years, but the incidence of gastric ulcers appears to be increasing as a result of the widespread use of NSAIDs and low-dose aspirin.
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_ Etiology
Three major causes of peptic ulcer disease are now recognized: NSAIDs, chronic H pylori infection, and acid hypersecretory states such as Zollinger-Ellison syndrome. Evidence of H pylori infection or NSAID ingestion should be sought in all patients with peptic ulcer. NSAID- and H pylori–associated ulcers will be considered in the present section; Zollinger-Ellison syndrome will be discussed subsequently. Uncommon causes of ulcer disease include CMV (especially in transplant recipients), systemic mastocytosis, Crohn’s disease, lymphoma, and medications (eg. alendronate). Up to 10% of ulcers are idiopathic.
H pylori – Associated Ulcers
H pylori appears to be a necessary cofactor for the majority of duodenal and gastric ulcers not associated with NSAIDs. Overall, it is estimated that one in six infected patients will develop ulcer disease. The prevalence of H pylori infection in duodenal ulcer patients is 75–90%. Most H pylori– infected duodenal ulcer patients have infection predominantly in the gastric antrum, which is associated with increased gastric acid secretion and decreased duodenal mucosal bicarbonate secretion. It is hypothesized that increased acid exposure can give rise to small islands of gastric metaplasia in the duodenal bulb. Colonization of these islands by H pylori may lead to duodenitis or duodenal ulcer. The association with gastric ulcers is lower, but H pylori is found in the majority of patients in whom NSAIDs cannot be implicated. H pylori–associated gastric ulcers tend to form at the junction of the gastric body and antrum—the site of transition from oxyntic to pyloric epithelium. Most H pylori–infected gastric ulcer patients have infection that predominates in the gastric body and is associated with decreased acid secretion. It is hypothesized that chronic inflammation overwhelms the gastric mucosal defense mechanisms.
The natural history of H pylori–associated peptic ulcer disease is well defined. In the absence of specific antibiotic treatment to eradicate the organism, 85% of patients will have an endoscopically visible recurrence within 1 year. Half of these will be symptomatic. After successful eradication of H pylori with antibiotics, ulcer recurrence rates are reduced dramatically to 5–20% at 1 year. Some of these ulcer recurrences may be due to NSAID use or reinfection with H pylori.
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