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Terms in this set (35)

-Deep vein thrombosis — Deep vein thrombosis (DVT) has been reported in up to 50 percent of patients following major lower extremity amputation without prophylaxis [32]. The incidence of deep vein thrombosis is higher for above-knee amputation compared with below-knee amputation (37.5 versus 21.2 percent, respectively) [47]. This difference may contribute to the increased incidence of sudden death due to thromboembolism in patients with above-knee amputation. Thus, it is important to provide thromboprophylaxis. (See 'Thromboprophylaxis' above and 'Perioperative mortality' below.)

-Stump hematoma — Postoperative bleeding that requires reoperation occurs in 3 to 9 percent of major lower extremity amputations, and stump hematoma may lead to stump wound breakdown [9,48]. Patients on antithrombotic therapy, including DVT prophylaxis, are at a higher risk for stump hematoma. Patients with stump hematoma causing pain and stump swelling with or without drainage should have the wound opened partially, the hematoma evacuated, and the wound washed out and packed with a moist saline dressing.

-Infection — Wound infection following major lower extremity amputation occurs in 13 to 40 percent of patients [26,27,49]. Patients with diabetes, preoperative wound infection, malnutrition, malignancy, advanced age, wound hematoma, and prior prosthetic bypass grafts have an increased risk for stump wound infection. In patients with prior lower extremity bypass graft, stump infection rates are reduced by complete removal of synthetic graft material [50].

-Superficial wound infections are treated by removing the skin sutures and initiating broad-spectrum antibiotics, which are adapted to reflect the results of wound culture and sensitivities. Deeper wound infection requires operative management with removal of skin and fascial sutures, drainage and washout of the wound, and debridement of any nonviable tissue (picture 1).

-Need for re-amputation — The rate of revision following major amputation remains high despite the availability of a variety of methods to select amputation level.

-Phantom limb pain — True phantom limb pain is a complex, poorly understood pain syndrome that is described as burning, aching, or electric-type pain in the amputated limb [40]. There is no clear consensus on the mechanisms of this disorder and no standard treatment [66]. The diagnosis of phantom pain should only be made after other causes of stump pain have been eliminated, including ischemia, infection, neuroma, and pressure-related wounds. (See 'Stump pain' above.)

-Flexion contracture — Flexion contracture at the hip or knee joint (15° limitation) occurs in 3 to 5 percent of major lower extremity amputations. Although up to 15° hip contracture can be accommodated with prosthetic alignment, a more than 25° contracture will cause compensatory lumbar lordosis, leading to low back pain. Contractures are more likely to develop in older patients, particularly those with dementia or prior ipsilateral stroke. Failure to provide adequate postoperative analgesia may also result in flexion contracture. Once a significant contracture develops, it may not be possible to correct it with physical therapy or surgery [76].

Hip flexion contracture can be retarded with prone positioning; however, patients may not tolerate this position.
Cough is the cardinal symptom in patients presenting with acute bronchitis. By definition, the cough lasts at least 5 days, although, in most patients, it persists for 1 to 3 weeks, with a median duration of 18 days [3,12,26]. The cough may be associated with either purulent or nonpurulent sputum production [3,27]. The presence of purulent sputum is a nonspecific finding and does not appear to be predictive of bacterial infection or response to antibiotics [28,29].

Upper respiratory tract infection (eg, common cold) can precede the onset of acute bronchitis. During the first few days of illness, symptoms associated with these two conditions such as headache, nasal congestion, and sore throat can overlap [3,27]. With involvement of the lower respiratory tract, cough becomes the predominant symptom.

Wheezing and mild dyspnea may accompany the cough. Both wheezing and rhonchi may be auscultated on physical examination; rhonchi usually clear with coughing. Although pulmonary function testing is typically not indicated in clinical practice, bronchospasm, evidenced by reduced FEV1, has been reported in 40 percent of patients in a small case series [30], and bronchial hyperreactivity can be demonstrated with provocative testing [7]. Bronchial hyperresponsiveness is typically transient, resolving in six weeks, and is believed to be the mechanism that underlies the persistent cough [7,30].

With prolonged coughing, chest wall or substernal musculoskeletal pain can occur [3,27]. Other complications are rare; most common among them are the development of pneumonia or bacterial superinfection. For most patients, acute bronchitis is a self-limited illness that does not require specific diagnostic testing or treatment.

Certain clinical features suggest a specific cause or an alternate diagnosis that may require antimicrobial therapy (table 1). For example, paroxysms of cough accompanied by an inspiratory whoop or posttussive emesis suggest pertussis, particularly during known outbreaks. Fever, or other systemic symptoms, are rare in patients with acute bronchitis. These findings, in addition to cough and sputum production, should raise suspicion for influenza or pneumonia. On physical examination, signs of parenchymal consolidation such as dullness to percussion, decreased or bronchial breath sounds, rales, egophony, or signs of pleural inflammation such as a pleural rub suggest that disease extends beyond the bronchi, and chest imaging should be considered.
Acute bronchitis should be suspected in patients with cough for at least five days (often one to three weeks) who do not have clinical findings suggestive of pneumonia (eg, fever, tachypnea, rales, signs of parenchymal consolidation) and do not have chronic obstructive pulmonary disease. For most patients, the diagnosis can be made based upon the history and physical examination. Testing is generally reserved for cases in which pneumonia is suspected, clinical diagnosis is uncertain, or when results would change management (eg, a positive influenza test result in a patient who meets criteria for antiviral therapy).

Chest radiograph — Chest radiographs are unlikely to change management for most patients with acute cough [31,32]. In patients with acute bronchitis, chest radiographs are either normal or findings are nonspecific, though subtle changes consistent with thickening of the bronchial walls in the lower lobes are occasionally reported [31].

The primary reason for obtaining a chest radiograph is to exclude pneumonia; reasonable indications for suspecting pneumonia and obtaining imaging include the following [33-39]:

●Abnormal vital signs (pulse >100/minute, respiratory rate >24 breaths/minute, temperature >38°C [100.4°F], or oxygen saturation <95 percent)

●Signs of consolidation on chest examination (rales, egophony, or tactile fremitus)

●Mental status or behavioral changes in patients >75 years old, who may not mount a fever

Additional factors, such as moderate or severe dyspnea, hemoptysis, immunocompromise, older age, and/or dementia, raise the likelihood of pneumonia or other underlying pulmonary disorders. The decision to obtain a chest radiograph or other imaging should always take the full clinical picture into consideration
For most patients with acute bronchitis, symptoms are self-limited, resolving in about one to three weeks. Reassurance and symptom control are the cornerstones of care. Antibiotics are not recommended for routine use [1,50-52].

Patient education — We suggest having a discussion on the expected course of illness and treatment plan with all patients. Reassuring patients that acute bronchitis is a self-limited illness that typically resolves in one to three weeks without specific therapy can help improve patient satisfaction and reduce inappropriate antibiotic use

Symptom control

For cough

●Nonpharmacologic therapy - For patients with acute bronchitis who are bothered by cough, offering nonpharmacologic options for cough relief such as throat lozenges, hot tea, honey, and/or smoking cessation or avoidance of secondhand smoke is a reasonable first step. Although these interventions have not been directly evaluated in clinical trials, they may provide some benefit and expected harms are small. (See "Treatment of subacute and chronic cough in adults" and "Overview of smoking cessation management in adults".)

●Pharmacologic therapy - For patients with acute bronchitis who desire medication for cough relief, we suggest offering over-the-counter (OTC) medications, such as dextromethorphan or guaifenesin. Selection of an OTC medication should take into account patient comorbidities and drug interactions. As an example, selective serotonin reuptake inhibitors (SSRIs) may enhance the serotonergic effect of dextromethorphan (eg, precipitate serotonin syndrome). Although the benefits of these medications for symptom improvement in patients with acute bronchitis are uncertain, multiple clinical practice guidelines suggest that offering medications for symptom relief may help reduce requests for antibiotics
-Salmonella is very common in the intestines of animals and reptiles and often exists in the environment. When food is contaminated from the environment or from contact with animals, it can make humans sick when they subsequently consume that food. Contamination of food can occur on a farm, during food processing, or as a result of cross-contamination (transfer from raw meat to salad) in the home, at a restaurant, or at some other point in the supply chain. Thus, most cases of Salmonella food poisoning are due to either cross-contamination or undercooking of raw meat or poultry products or contamination of fresh produce. However, there have also been large outbreaks of Salmonella from unusual foods, such as peanut butter.

-Escherichia coli — Escherichia coli is a common cause of food poisoning and traveler's diarrhea. Infection with E. coli can occur when food or water becomes contaminated with bacteria from infected feces. Some types of E. coli infection can be very serious, resulting in kidney failure or worse

-Hepatitis A virus is transmitted in foods contaminated by an infected human such as a food handler or from raw shellfish. Symptoms do not usually appear until 15 to 50 days after infection, which can make it difficult to determine the source of infection. In nonimmune individuals, post-exposure administration of passive immune globulin might prevent or mitigate clinical infection

-Norovirus infection is the most common foodborne illness and is often acquired when infected food handlers contaminate the food they are preparing (eg, in restaurants). Norovirus is very infectious and easily passed from person to person. Symptoms usually start 24 to 48 hours after exposure with nausea, vomiting, diarrhea, and abdominal pain. Most cases resolve without medical treatment.

-Listeria monocytogenes — Listeria is a bacteria that has traditionally been found in unpasteurized or contaminated milk, soft cheese, and other dairy products or in contaminated processed/delicatessen meats, hot dogs, and smoked seafood. More recently, Listeria monocytogenes has been found in a variety of other ready-to-eat foods such as hummus, sunflower seeds, and frozen vegetables. Listeria infection may cause gastrointestinal symptoms, which usually develop within 24 hours and include fever, watery diarrhea, nausea, vomiting, headache, and pains in joints and muscles. A much more serious infection, known as listeriosis, may occur one to three weeks later if the bacteria invade the bloodstream. Listeriosis can occur without any of the gastrointestinal symptoms. Listeriosis is usually seen in pregnant women or older adults and the immunocompromised
●A weakened immune system - The immune system plays a major role in protecting against a foodborne illness; when your immune system is weakened, you become more vulnerable. A healthcare provider should be able to provide guidance on whether you fall into this group. A few examples of people with a weakened immune system include the very young, older adults, people with chronic disease, pregnant women, and people who take certain types of medication that reduce the ability to fight off foodborne infections.

●Improper food storage or handling, leaving prepared food at room temperature for more than two hours, or improperly cooking or reheating food increase the risk of food poisoning. Use a food thermometer to check internal temperatures of meat, poultry, and seafood before eating them to make sure they are properly cooked. Food should not be left out for more than two hours at room temperature. The "best before" or "use by" dates printed on food are markers of quality, not safety, and should not be used to determine if a food is "safe" to eat. Just because a food looks and smells okay does not mean that it is safe to eat.

●Cross-contamination of food can occur when one contaminated food touches another or when a food comes in contact with a contaminated food preparation surface, such as a counter or cutting board. Keep foods like meat, poultry, and raw fish separate from foods that will not be cooked, such as salads.

●Anyone who handles food should wash their hands before handling food and after using the bathroom, changing diapers, or handling pets. It is easy to pass microbes from the hands into food. Food handlers who fail to wash their hands after using the bathroom can contaminate food with fecal microorganisms.
B cells from thyroid tissue of patients with Hashimoto's thyroiditis are activated, as indicated by their ability to secrete thyroid antibodies spontaneously in vitro. T cells in patients with Hashimoto's thyroiditis react with processed thyroid antigens and peptides derived from these antigens. These activated T cells secrete cytokines which themselves activate a variety of other immune cells. T cells have three major roles in this disease: a role in antibody production (a Th2 type of function), a role in the apoptotic destruction of thyroid cells by activating cytotoxic T cells (a Th1 function), and a role in immunoregulation (Treg cells)

most common cause of hypothyroidism in iodine-sufficient areas of the world. Thyroid failure is seen in up to 10 percent of the population, and its prevalence increases with age [1]. It is characterized clinically by gradual thyroid failure, with or without goiter formation, due to autoimmune-mediated destruction of the thyroid gland involving apoptosis of thyroid epithelial cells. Nearly all patients have high serum concentrations of antibodies against one or more thyroid antigens; diffuse lymphocytic infiltration of the thyroid, which includes predominantly thyroid-specific B and T cells; and follicular destruction, which is the characteristic hallmark of thyroiditis.

The cause of Hashimoto's thyroiditis is thought to be a combination of genetic susceptibility and environmental factors. The familial association with Graves' disease and the fact that Graves' disease may sometimes evolve into Hashimoto's thyroiditis (and vice versa) indicate that the two disorders are closely related pathophysiologically, albeit not functionally