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Manifestaciones de Esclerosis Sitémica

Aca va lo de esclerosis Overview of the clinical manifestations of systemic sclerosis (scleroderma) in adults Author John Varga, MD Section Editor John S Axford, DSc, MD, FRCP Deputy Editor Paul L Romain, MD Last literature review version 16.3: octubre 2008 This topic last updated: agosto 19, 2008 (More) INTRODUCTION — The term scleroderma, is used to describe the presence of thickened, hardened skin (from the Greek "scleros") [1]. Scleroderma is the hallmark feature of a heterogeneous group of conditions, the classification of which is discussed in more detail separately. (See "Classification of scleroderma disorders"). To summarize briefly, scleroderma may be a clinical feature of limited anatomic extent affecting only the skin and adjacent tissues or it may be associated with systemic involvement. When the characteristic skin disorder is associated with internal organ involvement, the disease is termed systemic sclerosis (SSc). SSc is subcategorized further into diffuse cutaneous SSc (dcSSc) and limited cutaneous SSc (lcSSc) on the basis of the extent and distribution of skin involvement. LcSSc is generally associated with the CREST syndrome (see "Limited cutaneous SSc" below) [2]. Other disorders that may either have typical scleroderma skin changes or those that have scleroderma-like cutaneous involvement are considerations in the differential diagnosis of SSc. (See "Diagnosis and differential diagnosis of systemic sclerosis (scleroderma) in adults"). The manifestations of SSc are diverse. Most prominent are abnormalities of the circulation (most notably Raynaud phenomenon) and involvement of multiple organ systems, including the musculoskeletal, renal, pulmonary, cardiac, and gastrointestinal systems, with fibrotic and/or vascular complications. The prevalence rates of diseases that share scleroderma as a clinical feature are reported to range from 4 to 489 cases per million individuals [3,4]. Incidence figures for SSc are 0.6-122 per million persons/year; the actual prevalence is probably at the high end of the range noted above [4]. There are regional differences in incidence, as examples: higher rates are seen in the United States and Australia than in Japan or Europe and higher rates in blacks than whites [4]. A brief overview of the characteristic sclerodermatous skin changes and of other organ involvement in adults is presented here. The pathogenesis, diagnosis, and treatment of SSc are discussed separately. (See "Pathogenesis of systemic sclerosis (scleroderma)", and see "Diagnosis and differential diagnosis of systemic sclerosis (scleroderma) in adults", and see "Overview of the treatment and prognosis of systemic sclerosis (scleroderma) in adults"). Localized forms of scleroderma, and scleroderma in childhood are discussed separately. (See "Localized scleroderma in childhood"). SKIN INVOLVEMENT — Skin involvement is characterized by variable thickening and hardening of the skin. The fingers, hands and face are generally the earliest areas of the body involved. Edematous swelling and erythema of the skin may precede skin induration. Other prominent skin manifestations include: • Pruritus in the early stages • Edema in the early stages • Sclerodactyly • Digital ulcers • Pitting at the fingertips • Telangiectasia • Calcinosis cutis The assessment of skin involvement includes semiquantitative estimation of skin thickness, pliability (hardness), and fixation or tethering to underlying structures (tethering). The modified Rodnan skin score, commonly used in clinical trials, score the severity of these features in 17 distinct areas of the body from 0 (normal) to 3 (most severe). Objective approaches to measuring skin disease, such as ultrasonography [5,6], and use of a durometer, are under investigation. The distribution of skin lesions and the accompanying pattern of internal organ involvement forms the basis for the current classification system of SSc into limited and diffuse forms of the disease (show table 1 and show table 2). (See "Classification of scleroderma disorders"). Radiographs of the hands may reveal calcinosis and resorption of the distal phalangeal tufts (acro-osteolysis); articular erosions, joint space narrowing, and demineralization are other radiographic findings that may be present [7]. Limited cutaneous SSc — Patients with limited cutaneous SSc (lcSSc) typically have skin sclerosis restricted to the hands, and to a lesser extent, the face and neck. With time some patients develop scleroderma of the distal forearm. Patients with limited cutaneous SSc generally have prominent vascular manifestations, including severe Raynaud phenomenon and cutaneous telangiectasia. Many of these patients have other manifestations of what has been referred to as the CREST syndrome (Calcinosis cutis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia). Diffuse cutaneous SSc — Sclerotic skin on the chest, abdomen, or upper arms and shoulders is indicative of diffuse cutaneous SSc (dcSSc). Patients with dcSSc are more likely to have, or to develop, internal organ damage due to ischemic injury or fibrosis than those with lcSSc. Systemic sclerosis sine scleroderma — Not all patients with SSc have skin manifestations. SSc sine scleroderma, is characterized by typical vascular and/or fibrotic features of systemic disease (eg, renal crisis, pulmonary hypertension, or interstitial lung disease) but without clinically evident skin sclerosis. VASCULAR DISEASE — The most obvious clinical manifestation of vascular dysfunction is Raynaud phenomenon, defined as sequential color changes in the digits precipitated by cold, stress or even change in temperatures. Raynaud phenomenon is due to arterial vasoconstriction in the digits. The color changes of pallor ("white"), acrocyanosis ("blue"), and reperfusion hyperemia ("red") are characteristic. (See "Clinical manifestations and diagnosis of the Raynaud phenomenon"). Vascular injury and subsequent chronic damage underlies other serious complications of SSc, including pulmonary artery hypertension, scleroderma renal crisis and gastric antral vascular ectasia, and also contributes to the pathogenesis of cardiac and gastrointestinal complications. Raynaud phenomenon — Although Raynaud phenomenon is classically viewed as reversible vasospasm, many patients with SSc develop progressive structural changes in the small blood vessels, with permanently impaired flow. Episodes of Raynaud phenomenon may be prolonged and can result in digital ulceration or infarction. It is important to realize that persons presenting with Raynaud phenomenon may have primary (no definable underlying disease) or secondary Raynaud phenomenon. Whereas Raynaud phenomenon is seen in SSc, other connective tissue diseases, or a number of disorders which result in abnormal blood flow (show table 3), primary Raynaud phenomenon is common in the general population, occurs in otherwise healthy individuals, and almost always has a benign course. In patients with lcSSc, Raynaud phenomenon generally precedes other disease manifestations, sometimes by years or even decades. In contrast, in patients with dcSSc, the onset of Raynaud phenomenon generally coincides with, or may even follow, the appearance of characteristic skin or musculoskeletal manifestations. ORGAN INVOLVEMENT — Extracutaneous organ involvement is common in SSc. The lungs, kidneys, gastrointestinal tract, and heart are commonly affected (show table 4). Gastrointestinal involvement — Nearly 90 percent of patients with either subtype of SSc (dcSSc or lcSSc) have some degree of gastrointestinal involvement [8,9]. Nearly half of these patients may be asymptomatic. Esophageal hypomotility and incompetence of the lower esophageal sphincter disease was the earliest visceral manifestation of SSc described. Symptoms principally result from chronic gastroesophageal reflux, with subsequent chronic esophagitis and stricture formation, and abnormal motility. Any part of the gastrointestinal tract from mouth to anus may be affected. Thus, a variety of signs and symptoms are seen in patients with SSc, including dysphagia ad choking, heartburn, cough after swallowing, bloating, alternating constipation and diarrhea, pseudo-obstruction and bacterial small bowel overgrowth with malabsorption, and fecal incontinence. Chronic gastroesophageal reflux and recurrent episodes of aspiration may contribute to the development of interstitial lung disease [10]. Vascular ectasia in the stomach ("watermelon stomach") is frequent, and may cause chronic gastrointestinal bleeding and anemia. (See "Gastrointestinal manifestations of systemic sclerosis (scleroderma)"). Pulmonary disease — Pulmonary involvement is seen in more than 70 percent of patients with SSc. The two principal clinical manifestations of lung involvement are interstitial lung disease (also called fibrosing alveolitis or pulmonary fibrosis) and pulmonary vascular disease, leading to pulmonary arterial hypertension (show table 5). These issues are discussed in detail separately but will be briefly reviewed here. (See "Clinical manifestations of systemic sclerosis (scleroderma) lung disease"). Interstitial lung disease — Some degree of interstitial lung disease occurs in more than three-quarters of patients with SSc. Fibrosis is commonly preceded by alveolitis. The most common symptoms are breathlessness on exertion (which may progress to dyspnea at rest), and a nonproductive cough. Chest pain is infrequent and hemoptysis is rare. On examination, auscultation over the lungs reveals fine "Velcro" rales most prominent at the lung bases. Pulmonary vascular disease — Pulmonary vascular disease occurs in 10 to 40 percent of patients with SSc, and is more common in patients with limited cutaneous disease. It may occur in the absence of significant interstitial lung disease, a setting it which it resembles idiopathic pulmonary hypertension. Dyspnea with exertion and diminished exercise tolerance are the most common initial symptoms of pulmonary arterial hypertension. Pulmonary arterial hypertension is generally a late complication of SSc, is typically progressive and, if severe, can lead to cor pulmonale and right-sided heart failure. (See "Cor pulmonale"). Thrombosis of the pulmonary vessels is a common complication of late-stage pulmonary arterial hypertension, and is a frequent cause of death. Lung cancer — The risk of lung cancer is increased in patients with SSc, and is similar in lcSSc and dcSSc. The incidence rate of malignant lung neoplasms is approximately five fold higher than for an age and gender matched subset of the general population. (See "Cancer risk" below). Renal disease — Autopsy studies suggest that 60 to 80 percent of patients with dcSSc have pathologic evidence of kidney damage [11,12]. Impaired renal reserve may be present in the absence of clinical renal disease [13]. Some degree of proteinuria, a mild elevation in the plasma creatinine concentration, and/or hypertension are observed in as many as 50 percent of patients [14,15]. Scleroderma renal crisis — Severe and life-threatening renal disease develops in approximately 10 to 15 percent of patients. This type of renal involvement is more frequent in patients with dcSSc than those with lcSSc. Scleroderma renal crisis is discussed in more detail separately. (See "Scleroderma renal crisis"). To summarize briefly, this form of renal involvement is characterized by: • Acute onset of renal failure • Urine analysis reveals only mild proteinuria with few cells or casts • Abrupt onset of moderate to marked or malignant hypertension (although some patients remain normotensive) Other features of scleroderma renal crisis may be due to the effects of severe hypertension or vasculopathy and include: microangiopathic hemolytic anemia, pulmonary edema, headache, blurred vision, and hypertensive encephalopathy, often complicated by generalized seizures. Cardiac disease — Patients with symptomatic cardiac involvement due to SSc have a poor prognosis, with two and five year mortality rates of approximately 60 and 75 percent, respectively [16]. Cardiac complications secondary to systemic or pulmonary hypertension are most common in SSc, but primary cardiac involvement also occurs. The manifestations of primary cardiac involvement include pericarditis, pericardial effusion, myocardial fibrosis, heart failure, myocarditis associated with myositis, conduction disturbances, and arrhythmias [16,17]. Pericardial disease — Symptomatic pericarditis occurs in 7 to 20 percent of patients with SSc, but pathologic evidence of pericardial involvement is observed in 70 to 80 percent at autopsy. Pericardial effusions may be small or large, and can develop rapidly. There is an association between pericardial effusion and the development of acute renal failure. Two potential explanations for this association have been suggested. First, pericardial effusion may simply be a marker of active and/or severe SSc. Second, the presence of a large pericardial effusion could compromise cardiac output, resulting in renal hypoperfusion, triggering a cascade of events culminating in scleroderma renal crisis. (See "Scleroderma renal crisis"). Myocardial disease — Patchy myocardial fibrosis is a hallmark of cardiac involvement in SSc [18]. It is distinguishable from the fibrosis associated with coronary atherosclerotic disease and is independent of the secondary cardiac involvement that may result from pulmonary hypertension. It is thought to result from recurrent vasospasm of small vessels (similar to Raynaud phenomenon), and is often associated with contraction band necrosis, a histological lesion indicative of myocardial ischemia followed by reperfusion. The degree of myocardial fibrosis may be increased in SSc patients with a long history of Raynaud phenomenon [18]. The myocardial disease can lead to systolic or more often diastolic ventricular dysfunction. This was illustrated in a Doppler echocardiography study of 570 patients with SSc in which left ventricular systolic and diastolic dysfunction were present in 1 and 18 percent, respectively [19]. Higher rates of myocardial dysfunction have been reported with tissue Doppler studies in which the abnormalities were independent of pulmonary artery hypertension or interstitial lung disease [20]. (See "Tissue Doppler echocardiography"). Arrhythmias — Conduction system disease and arrhythmias are common. They are likely to result from fibrosis of the myocardium and conduction system. Many deaths among SSc patients are sudden, some of which may result from a ventricular arrhythmia. Musculoskeletal disease — The earliest manifestations of diffuse SSc often are edema and swelling of the hands, arthralgia and myalgia. True inflammatory arthritis is uncommon in SSc. Joint pain, immobility and contractures develop as the result of fibrosis around tendons and other periarticular structures. Contractures of the fingers from this process are most common, but large joint contractures involving the wrists, elbows and ankles may also occur. The process is sometimes associated with palpable and/or audible deep tendon friction rubs. Tendon friction rubs occur predominantly in patients with dcSSc. The most common sites of involvement are the extensor and flexor tendons of the fingers and wrist, tendons over the elbow (triceps), knees (patellar), and ankle (anterior and posterior tibial, peroneal and Achilles). Some studies suggest that the presence of tendon friction rubs is a marker for aggressive disease and increased risk of developing internal organ involvement [21]. Deposits of hydroxyapatite crystals may occasionally be observed, with resultant severe joint damage. Destructive joint disease in a patient with SSc may suggest an overlap syndrome with rheumatoid arthritis. (See "Undifferentiated systemic rheumatic (connective tissue) diseases and overlap syndromes"). Neuromuscular involvement — Neuromuscular involvement in SSc is discussed in more detail elsewhere. (See "Neuromuscular manifestations of systemic sclerosis (scleroderma)"). The following is a brief summary of the types of neurologic and muscle disorders that have been noted in case reports and series: • Cranial, entrapment, peripheral, cutaneous, autonomic neuropathies • Myopathy • Central nervous system involvement, including headache, seizures, stroke, vascular disease, radiculopathy, and myelopathy Genitourinary — SSc in men is very frequently associated with erectile dysfunction. This was illustrated in a survey that compared 43 SSc patients to 23 patients with rheumatoid arthritis (RA) [22]. Among the SSc patients, 81 percent had self-reported erectile dysfunction versus 48 percent of those with RA. While Raynaud phenomenon was more prevalent in SSc than in RA (86 versus 19 percent), it was not an independent predictor of erectile dysfunction. Women with SSc also have sexual dysfunction. This is related to decreased vaginal lubrication or constriction of the vaginal introitus. In one study, dyspareunia was present in 56 percent of 60 women with SSc [23]. Pregnancy — A detailed discussion of issues related to pregnancy in SSc is presented separately. (See "Systemic sclerosis (scleroderma) and pregnancy"). CANCER RISK — There have been several reports examining cancer in association with SSc [24-29]. The most significant association appears to be with lung cancer, which may account for approximately one-third of the cancers seen in SSc patients [26], however a significantly increased incidence was not noted in a population with a high background rate of lung cancer [29]. In a study of 632 Australian patients with SSc, 19 developed lung cancer [30]. Those who smoked were seven times as likely to develop cancer as those who did not. Pulmonary fibrosis and antitopoisomerase antibodies were not risk factors for lung cancer. The issue of malignancy in SSc was assessed in a population based, retrospective cohort analysis from Sweden performed between 1965 and 1983; 917 patients with SSc and 102 with localized scleroderma were compared to a cohort from the Swedish National Cancer Registry [24]. The ratio of cancers in SSc patients to expected cancers (the standardized incidence ratio, SIR) was 1.5 overall. Particular elevations were noted for lung cancer (SIR 4.9), skin cancer (SIR 4.2), hepatoma (SIR 3.3), and hematopoietic malignancies (SIR 2.3). In comparison to SSc, the cancer risk in patients with localized scleroderma was not different from that of the general population. A similar, modest increase in the overall risk of malignant disease (SIR 1.55) was also seen in a cohort of 769 patients seen from 1987-2002 [31]. There was, however, a marked increase in the risk of esophageal carcinoma (SIR 15.9 [95% CI 4.2-27.6]) and oropharyngeal carcinoma (SIR 9.63 [95%CI 2.97-16.3]). The cause of an increased cancer risk in SSc is not well understood. The association with lung and skin cancers suggests that sites of disease activity may be prone to malignant transformation. There are conflicting data on whether the presence of antibodies to topoisomerase-I (Scl-70) identifies a population of SSc patients who are more likely to have, or develop, cancer [32,33] In summary, the information available indicates a possible increased risk of malignancy in patients with SSc. The relationship cannot be considered proven due to the small number of patients. The author and editors wish to acknowledge contributions of Dr. Carol Black and Dr. Joseph Korn (deceased) to earlier versions of this topic review.

Nodulo pulmonar solitario

Aca les mando los criterios de valuacion de nódulo pulmonar solitario Diagnostic evaluation and initial management of the solitary pulmonary nodule Author Steven E Weinberger, MD Section Editors Nestor Muller, MDTalmadge E King, Jr, MDJames R Jett, MD Deputy Editor Kevin C Wilson, MD Last literature review version 16.3: octubre 2008 This topic last updated: enero 4, 2008 (More) INTRODUCTION — A solitary pulmonary nodule (SPN), or "coin lesion", is a common clinical problem [1]. It is usually detected incidentally on a plain chest radiograph or computed tomographic (CT) scan [2]. The major question that follows detection of a SPN is whether the lesion may be malignant, with management varying accordingly. In this topic review, a SPN is defined and its differential diagnosis is summarized. A general approach is then outlined, followed by detailed descriptions of the diagnostic evaluation and initial management. Radiographic evaluation of pulmonary nodules is discussed in greater detail separately. (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules"). DEFINITION — A SPN is a lesion that is both within and surrounded by pulmonary parenchyma. The size at which a "nodule" becomes a "mass" is arbitrary, although 3 or 4 cm is typically used [3,4]. DIFFERENTIAL DIAGNOSIS — The causes of a SPN can be categorized as benign or malignant (show table 1). The estimated frequency of each etiology varies substantially among studies, reflecting differences in the population studied, the methodology used, and the age of the study [4-10]. As an example, a higher prevalence of malignant etiologies among resected nodules is generally reported by newer studies, likely due to improved preoperative prediction of which nodules are malignant and require resection. Malignant etiologies — Common causes of a malignant SPN include primary lung cancer, carcinoid tumors, and lung metastases. Primary lung cancer — All types of primary lung cancer can present as a SPN. Adenocarcinoma (including the subtype bronchioloalveolar cell carcinoma) is the histologic subtype that most commonly presents as a SPN, followed by squamous cell carcinoma and large cell carcinoma. Both adenocarcinoma and large cell carcinoma share a tendency to originate as a peripheral lesion, whereas squamous cell carcinoma presents more frequently as a central lesion than as a peripheral nodule. Rarely, malignant lymphomas can present as a SPN. Carcinoid tumors — Carcinoid tumors tend to be centrally located endobronchial lesions; however, approximately 20 percent arise peripherally and present as a SPN. These tumors are generally well circumscribed radiographically. (See "Bronchial carcinoid tumors"). Metastatic cancer — Extrapulmonary malignancies that are most likely to produce a SPN due to metastasis include malignant melanoma, sarcomas, and carcinomas of the colon, breast, kidney, and testicle [11]. The probability of metastasis is approximately 25 percent when a SPN is detected on a chest radiograph in a patient with a history of extrathoracic malignancy [12]. Most metastases present as multiple pulmonary nodules. Benign etiologies — Common causes of a benign SPN include infectious granulomas and hamartomas. Less common causes include pulmonary abscesses, vasculitic lesions (as in Wegener's granulomatosis), and pulmonary dirofilariasis. Infectious Granulomas — Infectious granulomas cause approximately 80 percent of benign nodules [2,8,9]. Endemic fungi (eg, histoplasmosis, coccidioidomycosis) and mycobacteria (either tuberculous or nontuberculous mycobacteria) are the most frequently recognized causes of infectious granulomas presenting as a SPN. When nontuberculous mycobacterial disease presents as a solitary peripheral nodule, the cause of the nodule is typically unrecognized until the lesion is resected as a presumed primary lung cancer [13]. In patients with acquired immunodeficiency syndrome, pneumocystis jirovecii (previously called pneumocystis carinii) infection can present as a SPN and may cavitate [14]. (See "Clinical presentation and diagnosis of Pneumocystis carinii (P. jirovecii) infection in HIV-infected patients"). Hamartomas — Hamartomas are generally considered benign tumors of the lung. They cause approximately 10 percent of benign nodules [2,8,9]. Hamartomas typically present in middle age, grow slowly over years, and are histologically heterogeneous. Cartilage (with scattered calcification), fat, muscle, myxomatous tissue, and fibroblastic tissue may all exist (show picture 1, show histology 1A-1B) [15]. The characteristic appearance of a hamartoma on a chest radiograph is a SPN with "popcorn" calcification, although this pattern is observed in less than 10 percent of cases (show radiograph 1). High resolution CT scanning of the lesion is particularly useful because it may demonstrate focal areas of fat, or calcification alternating with fat, which are virtually diagnostic of a hamartoma [16]. Dirofilariasis — Pulmonary infestation with the dog heartworm, Dirofilaria immitis, is a rare but well-recognized cause of a SPN [17,18]. Dogs are the usual animal host, but cats, wolves, coyotes, and foxes can also harbor the organism. The greatest concentration of human cases in the United States is found in eastern, southeastern, and southern coastal states. (See "Miscellaneous nematodes"). The organism is transmitted to humans by Aedes, Anopheles, Culex, or Myzorhynchus mosquitoes, which ingest blood-containing microfilariae from affected dogs [19]. Larvae in humans embolize to the lungs (the larvae are dead because the human is not a suitable host for the organism), where antigens from the dead organism initiate endarteritis and a granulomatous response. The typical finding with Dirofilaria immitis affecting the lungs is a noncalcified, pleural-based nodule [17]. Pulmonary dirofilariasis can be indistinguishable from other causes of a SPN; therefore, it is often resected as a presumed primary lung cancer. Once the diagnosis is made, no further therapy is indicated. GENERAL APPROACH — The ideal approach to a SPN would result in definitive resection of all malignant nodules, while avoiding resection of all benign nodules that do not require therapy. Unfortunately, a foolproof means to implement such a strategy does not exist. Approaches that remove most malignant nodules tend to result in frequent removal of benign nodules, whereas approaches that leave most benign nodules intact tend to leave some malignant nodules unresected. The former approach is generally preferred because: The five year survival rate may be as high as 70 to 80 percent for patients who have had a stage 1A (T1N0M0) non-small cell lung cancer resected [20-23]. In contrast, unresected lung cancer is often fatal. The operative mortality rate is less than 1 percent among patients with benign nodules early stage lung cancer [2,24]. Patients who have a SPN undergo an initial diagnostic evaluation. During the evaluation, clinical features, radiographic features, and, occasionally, quantitative models are used to determine the probability that the nodule is malignant. Once the probability that the SPN is malignant has been formulated, initial management must be chosen. There are many reasonable approaches to the initial management of a SPN and significant variation exists among institutions. When decisions are uncertain, initial management should carefully consider the patient's preference [25,26]. DIAGNOSTIC EVALUATION — In this section, the clinical features, radiographic features, and quantitative models used to determine the likelihood that a nodule is malignant are discussed. Clinical features — Clinical features associated with an increased probability that a SPN is malignant include advanced patient age and underlying risk factors. Patient age — The probability of a SPN being malignant rises with increasing patient age [5,7,27]. As an example, one study stratified the percentage of SPNs that were malignant according to the patient's age [7]: - Three percent in patients between ages 35 and 39 - 15 percent between ages 40 and 49 - 43 percent between ages 50 and 59 - 50 percent or higher at age 60 or above Another study similarly found malignant nodules more frequently in patients 50 years of age or older, compared to patients less than 50 years of age (65 versus 33 percent) [5]. Despite the association between age and malignancy, a SPN should not be automatically assumed to be benign in a young patient [27]. Risk factors — The possibility of lung cancer is always a concern when a SPN is detected in a patient with a history of smoking, because of the strong association between cigarette smoking and primary lung cancer. Other risk factors for lung cancer (eg, asbestos exposure, family history) should also be considered when evaluating a patient with a SPN. Previously diagnosed malignancy increases the likelihood that a SPN is a metastasis [28]. (See "Overview of the risk factors, pathology, and clinical manifestations of lung cancer", section on Risk factors and See "Cigarette smoking and other risk factors for lung cancer"). Radiographic features — Radiographic features that can be used to predict whether a nodule is malignant include size, border, calcification, density, growth, and metabolic activity. Size — Larger lesions are more likely to be malignant than smaller lesions. In one study, the likelihood of malignancy was 0.2 percent for nodules smaller than 3 mm, 0.9 percent for nodules 4 to 7 mm, 18 percent for nodules 8 to 20 mm, and 50 percent for nodules larger than 20 mm [29,30]. (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules", section on Size). Border — Malignant lesions tend to have more irregular and spiculated borders, whereas benign lesions often have a relatively smooth and discrete border. (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules", section on Border). Calcification — The presence of calcification does not exclude malignancy. As an example, "eccentric" calcification (ie, asymmetric calcification) should raise concern about carcinoma arising in an old granulomatous lesion (ie, a "scar" carcinoma). Certain patterns of calcification, however, strongly suggest that a SPN is likely benign. These patterns include "popcorn" calcification (show radiograph 1), laminated (concentric) calcification, central calcification (show radiograph 2), and diffuse, homogeneous calcification (show radiograph 3). (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules", section on Calcification). Density — Increased density of a SPN argues against malignancy. As an example, one study measured the CT density of 58 malignant nodules and 33 benign nodules [31]. All of the malignant nodules were less than 147 Hounsfield units and most of the benign nodules were greater than 164 Hounsfield units. The likelihood of incorrectly identifying a malignant nodule as benign decreases if a higher cutoff value is used, although benign nodules then become more likely to be characterized as indeterminant [32]. Although density measurement was at one time considered to be a promising technique, it is no longer used as part of the routine evaluation of a SPN. (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules", section on Density). Growth — Review of available prior imaging studies is a critical part of the diagnostic evaluation. Lesions that are malignant tend to have a volume doubling time between 20 and 400 days, where volume doubling of a nodule corresponds to a 30 percent increase in its diameter [2,4,22,33]. Therefore, a SPN whose size has increased very rapidly or has remained stable for a prolonged duration is likely benign. Volume doubling time also varies according to the CT appearance of malignant SPNs. As an example, nodules described as ground glass, ground glass with a solid component, or solid had volume doubling times of 813, 457, and 149 days, respectively, in one study [29,34]. (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules", section on Growth). Quantitative models — Quantitative models (based upon Bayes' theorem) use likelihood ratios (LRs) to estimate the probability that a nodule is malignant [2,35]. LRs are defined as the prevalence of a specific finding among all subjects with a malignant nodule, divided by the prevalence of the same finding among all patients with a benign nodule. To estimate the probability of malignancy, LRs are first determined for nodule size, patient age, smoking history, and overall prevalence of malignancy in the population (show table 2) [36]. The odds of malignancy are then calculated by multiplying the LRs (show table 3). Finally, the probability of malignancy is calculated from the odds of malignancy (show table 3). This method of estimating the probability of malignancy was subsequently modified to include more LRs, thereby accounting for more radiographic and clinical characteristics (show table 4) [37].An alternative method of estimating the probability of malignancy has also been reported (show table 5) [38,39]. INITIAL MANAGEMENT — An initial management decision should be made once the probability that the SPN is malignant has been assessed. There is significant variation among institutions regarding what is considered optimal initial management of a SPN; one reasonable approach is as follows (show figure 1): A nodule that has a low probability of being malignant can be followed with serial CT scans. A nodule that is 1 cm or larger and has an intermediate probability of being malignant should be evaluated by FDG-PET. Nodules that are negative on FDG-PET can be followed with serial CT scans, while nodules that are positive should be excised. Sampling of the nodule should be performed if FDG-PET is unavailable. A nodule that is smaller than 1 cm and has an intermediate probability of being malignant can be followed by serial CT scans. A nodule that has a high probability of being malignant should be excised. It must be emphasized that this is just one of many reasonable approaches to the initial management of a SPN. Optimal management is individualized and carefully considers the patient's preference. Serial CT scans — Traditionally, a nodule that remained stable for two years or longer on a chest radiograph was considered likely benign. Several arguments have been used to challenge this practice, including: The two year cutoff is arbitrary. A small retrospective study reported that lack of appreciable growth on a chest radiograph over a two year duration had a positive predictive value of only 65 percent for a benign lesion [2,40,41]. In addition, certain cell types (bronchioloalveolar carcinoma and carcinoid) can maintain a stable size for two years or longer [2]. CT scans are preferable to chest radiographs. Growth is more readily detected by CT than chest radiography. Specifically, 3 to 5 mm of growth is necessary for detection on a chest radiograph, compared to only 0.5 mm on a high-resolution CT scan [2]. Different strategies should be used for nodules of different sizes. Nearly 50 percent of smokers older than 50 years have at least one nodule [29,42]. Moreover, approximately 10 percent of these patients develop new nodules over a one year period. The vast majority of these nodules are small and unlikely to be malignant [29,30,42]. Thus, the traditional approach of performing CT scans every three months during the first year and every six months during the second year is both unnecessary and impractical. The following guidelines, proposed by the Fleischner Society, advocate different frequencies of CT scans based upon the size of the nodule and the patient's risk for lung cancer (show table 6) [29]. Patients are considered low risk if they have no history or minimal history of smoking and other risk factors; otherwise, patients are considered high risk. Times refer to the duration from initial detection of the SPN: For nodules ≤4 mm, serial CT scans are not required if the patient is low risk. Patients who are high risk should have a CT scan performed at 12 months with no further follow-up if the nodule is unchanged. For nodules 4 to 6 mm, a CT scan should be performed at 12 months if the patient is low risk, with no further follow-up if the nodule is unchanged. Patients who are high risk should have a CT scan performed at six to 12 months and at 18 to 24 months if the nodule is unchanged. For nodules 6 to 8 mm, a CT scan should be performed at six to 12 months and at 18 to 24 months if the nodule is unchanged and the patient is low risk. Patients who are high risk should have a CT scan performed at three to six months, nine to 12 months, and 24 months if the nodule remains unchanged. For nodules greater than 8 mm, a CT scan should be performed at three, nine, and 24 months if the nodule remains unchanged, regardless of whether the patient is low or high risk. These guidelines are not applicable to young patients (less than 35 years old), or patients with an extrathoracic malignancy or unexplained fever [29]. Metabolic imaging — 18-flourodeoxyglucose positron emission tomography (FDG-PET) can help distinguish malignant and benign lesions because cancers are metabolically active and take up FDG avidly. It is indicated for patients whose SPN is 1 cm or greater in size and has an intermediate probability of malignancy, especially if the patient has increased surgical risk. (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules", section on Positron emission tomography). Approximately 95 percent of patients with a malignant nodule will have an abnormal FDG-PET (ie, sensitivity) and 78 percent of patients with a benign lung nodule will have a normal FDG-PET (ie, specificity) [43]. As a result, a negative FDG-PET will correctly exclude cancer in most cases (ie, high negative predictive value), but a positive FDG-PET will incorrectly identify infectious, inflammatory, or granulomatous nodules as malignant with considerable frequency (ie, poor positive predictive value) [44]. False-negative results can occur with tumors that have low metabolic activity (eg, bronchioloalveolar tumors, carcinoids, and some well-differentiated adenocarcinomas), small lesions (a critical mass of metabolically active malignant cells is required for detection by PET), and uncontrolled hyperglycemia because the uptake of FDG is retarded by the hyperglycemia [44]. An additional benefit of FDG-PET is the acquisition of staging data if the nodule is malignant. Nodule sampling — Consultation with a pulmonologist is warranted to decide whether and how the nodule should be sampled or excised if the clinical features, radiographic features, and quantitative models do not provide sufficient evidence that a lesion is either benign or malignant. Sampling of the nodule can be performed through the airway (fiberoptic bronchoscopy) or through the chest wall (percutaneous needle aspiration or biopsy). The choice of sampling procedure varies according to the size of the nodule, the location of the nodule, the availability of the procedure, and local expertise. Bronchoscopy — Fiberoptic bronchoscopy is a reasonable approach for the diagnostic evaluation of large, central nodules and masses; however, it is much less useful for small SPNs. When bronchoscopy is performed, specimens can be collected by washing or lavage of the airway supplying the lesion, or by direct sampling of the lesion with brushings or transbronchial biopsy. With all of these techniques, however, it is often difficult for the bronchoscopist to be certain about optimal positioning of the bronchoscope and placement of the brush or forceps within the lesion itself. As a result, the yield of bronchoscopy performed for diagnosis of a SPN is lower than other techniques, especially if the SPN is small. A systematic review of studies that examined the diagnosis of peripheral lung cancer using bronchoscopy with washing, brush, or biopsy, found an overall sensitivity of 69 percent [45]. The yield for diagnosing peripheral lesions smaller than 2 cm by brushing or biopsy was 33 percent, whereas the yield for lesions larger than 2 cm was 62 percent. The small amount of material provided by fiberoptic bronchoscopy is a limiting factor; thus, several approaches aimed at improving the diagnostic yield of bronchoscopy have been studied: - Fluoroscopy or endobronchial ultrasound can optimize localization of the lesion and increase the diagnostic yield of transbronchial biopsy (to greater than 70 percent) [46-49]. Unfortunately, these techniques require additional equipment and expertise and are not widely available. (See "Endobronchial ultrasound: Indications, advantages, and complications" and see "Endobronchial ultrasound: Technical aspects"). - Combining fluorescence in situ hybridization (FISH) and cytology may improve the sensitivity compared to cytology alone for both washings (61 versus 44 percent) and brushings (75 versus 51 percent); however, specificity is unaltered [50]. Validation of this technique is necessary before its routine use can be recommended. Percutaneous needle aspiration — Percutaneous needle aspiration (also called fine needle aspiration) of a SPN can be performed through the chest wall using either fluoroscopy or CT scanning to guide placement of the needle within the lesion. Its diagnostic yield is higher than fiberoptic bronchoscopy, since placement of the needle is more reliable. The overall diagnostic yield of percutaneous needle aspiration for suspected lung cancer is approximately 90 percent, and is higher when a cytologist attends the procedure than when a cytologist is not present to review the specimens [51,52]. Optimization of needle placement is particularly beneficial when evaluating a small SPN. An older study estimated that the diagnostic yield of percutaneous needle aspiration was 60 percent for SPNs smaller than 2 cm [53]. This was supported by a more recent study that reported a diagnostic yield of 64 percent for SPNs smaller than 3 cm [54]. In this study, the sensitivity and specificity of percutaneous needle aspiration for such nodules were 67 and 100 percent, respectively. Percutaneous needle aspiration obtains material for cytology, but does not biopsy a core of tissue. As a result, it is more helpful for confirming malignancy than establishing a specific benign diagnosis [33]. The former only requires the detection of malignant cells, while the latter usually requires evaluation of tissue architecture [33]. Percutaneous needle aspiration may be complicated by pneumothorax, which can be clinically significant in patients with coexisting emphysema. Bleeding is a less frequent complication. Percutaneous needle biopsy — An increasing number of centers are performing transthoracic needle biopsy to obtain a core of tissue, thereby improving the diagnostic yield of benign nodules. In this procedure, a core of tissue is obtained using a cutting needle. Up to 97 percent of patients with a malignant or benign lung nodule will obtain a definitive diagnosis using this procedure [55]. Surgical resection — Surgical excision of the nodule is indicated if the likelihood of malignancy is high (according to clinical and radiographic characteristics), an FDG-PET is positive, or a nodule has proven to be malignant by a sampling procedure. Excision can be performed by thoracotomy or thoracoscopy (also called video assisted thoracic surgery or VATS) if the lesion is located close enough to pleural surface to allow VATS resection [56,57]. The SPN is usually located by visual inspection. In some cases, however, the nodule is localized and marked preoperatively by placement of a hook wire (as used for localizing non-palpable breast lesions prior to biopsy) or by staining of the lesion with percutaneous injection of methylene blue [58]. For nodules sufficiently close to the pleura to be accessible to a video-assisted approach, VATS has essentially replaced thoracotomy, which has greater morbidity (eg, post-thoracotomy pain syndrome). VATS is very safe in experienced hands and can be performed as a day procedure at many centers. It has also replaced percutaneous needle aspiration or biopsy as a sampling technique in many medical centers, but recent studies have shown that approximately 50 percent of SPNs resected by VATs are benign lesions. That percentage of benign nodule resection is too high and dictates more rigorous preoperative evaluation. SUMMARY AND RECOMMENDATIONS A solitary pulmonary nodule (SPN) is a lesion that is both within and surrounded by pulmonary parenchyma. It is typically smaller than 3 or 4 cm. (See "Definition" above). The most common causes of a malignant SPN are primary lung cancer, carcinoid tumors, and lung metastases. Infectious granulomas and hamartomas are the most common causes of a benign SPN. (See "Differential diagnosis" above). Diagnostic testing cannot distinguish malignant and benign nodules unequivocally in all cases. An approach that leads to the excision of most malignant nodules is generally preferred, even if the cost is frequent resection of benign nodules. (See "General approach" above). During the diagnostic evaluation of a SPN, clinical features, radiographic features, and, occasionally, quantitative models are used to determine the probability that a nodule is malignant. (See "Diagnostic evaluation" above). Once the probability that a SPN is malignant has been formulated, initial management must be chosen. This choice should carefully consider patient preference. We propose the following approach to initial management, although we recognize that many reasonable alternative approaches exist (show figure 1): - We recommend surgical resection of a nodule that has a high probability of being malignant (Grade 1B). This recommendation reflects our belief that surgical resection is the only intervention that is potentially curative. (See "Initial management" above and see "Surgical resection" above). - We suggest following a nodule with serial CT scans if it has a low probability of being malignant, rather than surgically resecting the nodule immediately (Grade 2C). The frequency of CT scans varies according to the nodule's size and the patient's risk for lung cancer (show table 6). FDG-PET or sampling of the nodule are acceptable alternatives for patients who are uncomfortable with a strategy of observation. (See "Initial management" above and see "Serial CT scans" above). - We believe that a nodule that is 1 cm or larger with an intermediate probability of being malignant should be evaluated by FDG-PET, rather than followed with serial CT scans or surgically resected. We recommend that nodules that are positive on FDG-PET be excised (Grade 1B). Nodules that are negative on FDG-PET can be followed with serial CT scans. Sampling of the nodule should be performed if FDG-PET is unavailable. Sampling techniques include percutaneous needle aspiration, percutaneous needle biopsy, thoracoscopy, and bronchoscopy. (See "Initial management" above, see "Metabolic imaging" above, and see "Nodule sampling" above). - We suggest that a nodule smaller than 1 cm with an intermediate probability of malignancy be followed by serial CT scans, rather than excised, sampled, or evaluated by FDG-PET (Grade 2C). This suggestion reflects our recognition that the diagnostic yield of both sampling and FDG-PET is relatively poor for nodules smaller than 1 cm, and that there are risks associated with excision or sampling. (See "Initial management" above and see "Serial CT scans" above).

Fué un placer

Estimados udeanos. Espero que el viernes todos hallan salido airosos en el examen. Suerte en lo que les resta del años Saludos Micaela PD para aquellos que se engolosinaron introduciéndose en la era blogger siempre habrá un espacio, para aquellos que dominan siempre habrá nuevos desafíos.

Respuestas a las dudas sobre los riesgos de contagio de HIV

Hola: Les escribo ésta entrada para comentarles que colgué en: sitios de interés la dirección de la Sociedad Argentina de Infectología donde encontrarán varias guias , entre ellas la actualizada de tto y prevención de HIV, vayan a la pag 101 y lean las cifras, verán que interesantes y mañana lo charlamos. Saludos a todos los del grupete y lectores aficionados Vivián

Mobbing

En la última consulta, vino al consultorio una chica de 21 años, que refería acúfenos y otalgia en ambos oídos, pero sobre todo en el izquierdo. La paciente trabaja todos los días durante 10hs, atendiendo el teléfono en el sector de legales de una compañía de seguros. Pero refiere que los síntomas le aparecen siempre alrededor de las 16 hs. El médico le revisó los oídos, y al examen físico eran totalmente normales. A pesar de hacerle una orden para que se haga una audiometría y una logometría, siguió interrogando a la paciente sobre su contexto laboral. Ante esa pregunta, la chica respondió que el ambiente era bastante hostil, que había mucho recambio de personal (lo que le generaba inestabilidad) y que había maltrato generalizado por parte de los jefes con todo el personal, que no era algo particular con ella. Pero que por esta situación muchas veces tenía ganas de ir al baño a llorar. Cuando terminó de relatar esta situción, el médico le dijo que se hiciera los estudios que le había ordenado, pero que para él era estrés laboral, que le dijo que se llamaba Mobbing (que es: tanto la acción de un hostigador u hostigadores conducente a producir miedo o terror en el trabajador afectado hacia su lugar de trabajo, como el efecto o la enfermedad que produce en el trabajador). Como la paciente empezaba en una semana la facultad, le pidió al médico si le podía hacer un certificado para faltar al trabajo, para saber si después de unos días de no ir a trabajar mejoraba. Si bien el médico le ordenó reposo diagnosticando un cuadro de ansiedad, le explicó a la paciente que para que el su estrés laboral desaparezca tendría que producirse un cambio en el ambiente laboral o bien debería renunciar. Alejandra Ponsiglione

Exposición a líquidos corporales

En la UDA pasada me quedé pensando en los casos de ITS que habíamos discutido, y encontré info. acerca de la estratificación de los pacientes según el riesgo de exposición a sangre o líquidos contaminados. Hay 3 categorías básicas: Exposición tipo 1 (E1) Exposición sobre mucosas o piel no intacta (por ej., dermatitis, abrasiones o heridas) con volúmenes pequeños de sangre (pocas gotas y durante poco tiempo). Exposición tipo 2 (E2) Exposición sobre mucosas o piel no intacta con un volumen más grande o de mayor duración que la considerada para la E1, así como a la exposición percutánea leve (con una aguja sólida o a través de una erosión superficial). Exposición tipo 3 (E3) Exposición percutánea grave (por ej., aguja hueca, de uso intravascular, de punción profunda, o con sangre visible en el dispositivo). Cuando el contacto se produce sobre piel intacta, no se considera la profilaxis post-exposición, salvo que haya habido un gran volumen de líquido, una gran superficie expuesta, o un contacto prolongado. Se aclara que los líquidos contaminados (por ej., pleural, ascítico, amniótico, etc.) se consideran, en general, de bajo riesgo, a menos que contengan sangre visible. La exposición a hemoderivados como el plasma o el suero debe considerarse de manera similar a la exposición a sangre. En la tabla siguiente se muestra el Odds ratio para seronversión de HIV estratificado por factores de riesgo de exposición.