Inflammation of the synovium-like cellular membrane overlying bony prominences may be secondary to trauma, infection, or arthritic conditions such as gout, rheumatoid arthritis, or osteoarthritis. The most common locations are the subdeltoid, olecranon, ischial, trochanteric, semimembranous-gastrocnemius (Baker's cyst), and prepatellar bursae.

There are several ways to distinguish bursitis from arthritis. Bursitis is more likely than arthritis to begin abruptly and cause focal tenderness and swelling. Olecranon bursitis, for example, causes an oval (or, if chronic, bulbous) swelling at the tip of the elbow, whereas elbow joint inflammation produces more diffuse swelling. Similarly, a patient with prepatellar bursitis has a small focus of swelling over the kneecap but no distention of the knee joint itself. Active and passive ranges of motion are usually much more limited in arthritis than in bursitis. A patient with trochanteric bursitis will have normal internal rotation of the hip, whereas a patient with hip arthritis will not. Bursitis caused by trauma responds to local heat, rest, NSAIDs, and local corticosteroid injections.
Bursitis can result from infection. The two most common sites are the olecranon and prepatellar bursae. Acute swelling and redness at either of these two sites calls for aspiration to rule out infection. The absence of fever does not exclude infection; and onethird of those with septic olecranon bursitis are afebrile. A bursal fluid white blood cell count of greater than 1000/mcL indicates inflammation from infection, rheumatoid arthritis, or gout. In septic bursitis, the white cell count averages over 50,000/mcL. Most cases are caused by Staphylococcus aureus; the Gram stain is positive in two-thirds. Treatment involves antibiotics and repeated aspiration for tense effusions.

Chronic, stable olecranon bursa swelling unaccompanied by erythema or other signs of inflammation does not suggest infection and does not require aspiration. Aspiration of the olecranon bursa in rheumatoid arthritis and in gout runs the risk of creating a chronic drainage site, which can be reduced by using a small needle (25-gauge if possible) and pulling the skin over the bursa before introducing it. Applying a pressure bandage may also help prevent chronic drainage. Surgical removal of the bursa is indicated only for cases in which repeated infections occur. Repetitive minor trauma to the olecranon bursa should be eliminated by avoiding resting the elbow on a hard surface or by wearing an elbow pad.

A bursa can also become symptomatic when it ruptures. This is particularly true for Baker's cyst, whose rupture can cause calf pain and swelling that mimic thrombophlebitis. Ruptured Baker's cysts are imaged easily by sonography or MRI. In most cases, imaging is unnecessary because the cyst and an associated knee effusion are detectable on physical examination. It may be important to exclude a deep venous thrombosis, which can be mimicked by a ruptured Baker's cyst. Treatment of a ruptured cyst includes rest, leg elevation, and injection of triamcinolone, 20–40 mg into the knee (which communicates with the cyst). Rarely, Baker's cyst can compress vascular structures and cause leg edema and true thrombophlebitis.
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Dyspnea is a common symptom. It is analogous to hunger or nausea in that sensory input from multiple sites is integrated in the cerebral cortex. In general, dyspnea increases with the level of functional impairment as measured by spirometry. However, there is only a weak correlation between the severity of dyspnea and quantitative measures of airflow limitation or exercise tolerance.
Several pathophysiologic processes contribute to dyspnea. The most important is the increased respiratory effort that accompanies many different diseases: airflow obstruction (asthma; chronic obstructive pulmonary disease [COPD]), changes in pulmonary compliance (interstitial fibrosis, congestive heart failure) or chest wall compliance (obesity, pleural disease), intrinsic respiratory muscle weakness (inanition, neuromuscular disease, chronic respiratory failure), or the weakness conveyed by the mechanical disadvantage of hyperinflation (asthma or emphysema).

Dyspnea is magnified by increased respiratory drive. Acute hypercapnia is therefore a potent stimulus to dyspnea, while hypoxemia is usually a weak one. Stimulation of irritant receptors in the airways intensifies dyspnea, while stimulation of pulmonary stretch receptors decreases it. In mechanically ventilated patients, failure to provide adequate inspiratory flow rates to patients with heightened respiratory drive commonly results in dyspnea that may present as agitation.

Clinical Findings
The history should focus on onset and timing of symptoms, the patient's position at onset of symptoms, the relationship of symptoms to activity, and any factors that may improve or exacerbate symptoms. The clinician can assess dyspnea and response to treatment with a numeric rating scale by asking the patient, “On a scale of zero to ten, with zero being no shortness of breath and ten being the worst shortness of breath you can imagine, how short of breath are you?” Exertional dyspnea should be quantified, but the absolute level of exertion that precipitates dyspnea is less important than acute changes in the threshold level of activity. Complete allergic, occupational, and smoking histories are essential.

Acute dyspnea has a short list of causes, most of which are readily identified: asthma, pulmonary infection, pulmonary edema, pneumothorax, pulmonary embolus, metabolic acidosis, or acute respiratory distress syndrome (ARDS). Panic attacks may present as a respiratory complaint. Orthopnea (dyspnea on recumbency) and nocturnal dyspnea suggest asthma, gastroesophageal reflux disease (GERD), left ventricular dysfunction, or obstructive sleep apnea. Rapid onset of severe dyspnea when supine suggests phrenic nerve impairment leading to diaphragmatic weakness or paralysis. Platypnea (dyspnea that worsens in the upright position) is a rare complaint associated with arteriovenous malformations at the lung bases or with hepatopulmonary syndrome, resulting in increased shunting and hypoxemia in the upright position (orthodeoxia).

Chronic dyspnea is invariably progressive. Symptoms often first appear during exertion; patients learn to limit their activity to accommodate their diminished pulmonary reserve until dyspnea occurs with minimal activity or at rest. Episodic dyspnea suggests congestive heart failure, asthma, acute or chronic bronchitis, or recurrent pulmonary emboli. Constant dyspnea is most commonly due to COPD but may indicate interstitial lung disease (eg, pulmonary fibrosis), pulmonary vascular disease, or fixed airflow obstruction from severe asthma.
Evaluation should include a complete blood count, renal function tests, chest radiograph, spirometry, and noninvasive oximetry. Patients over 40 years of age or with a family history of early coronary disease should have an electrocardiogram. Arterial blood gases, measurement of lung volumes, ventilation-perfusion ([V with dot above]/[Q with dot above]) scanning, echocardiography, and cardiopulmonary exercise testing are reserved for cases that elude diagnosis on initial evaluation.

In patients with advanced lung disease, the responsible condition may be easily identified but treatment only partially effective. Oxygen improves survival in those
who are hypoxemic and can improve the exercise tolerance of all patients. Its effect on dyspnea is variable. Opioids reduce respiratory drive and blunt dyspnea. They can be titrated safely even in patients with advanced lung disease. Anxiety can play an important role in the distress caused by dyspnea and may be relieved by judicious use of benzodiazepines such as lorazepam, 0.5–1 mg orally every 6–8 hours. Pulmonary rehabilitation can improve respiratory function and train patients in energy conservation and breathing techniques that help moderate their sense of respiratory effort. Finally, fresh air or a fan may offer additional relief. Smokers with progressive exertional dyspnea should know that they can limit future loss of function through smoking cessation.

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Syphilis is a complex infectious disease caused by Treponema pallidum, a spirochete capable of infecting almost any organ or tissue in the body and causing protean clinical manifestations Transmission occurs most frequently during sexual contact (including oral sex), through minor skin or mucosal lesions; sites of inoculation are usually genital but may be extragenital. The risk of developing syphilis after unprotected sex with an individual with early syphilis is approximately 30–50%. The organism is extremely sensitive to heat and drying but can survive for days in fluids; therefore, it can be transmitted in blood from infected persons. Syphilis can be transferred via the placenta from mother to fetus after the tenth week of pregnancy (congenital syphilis).
The immunologic response to infection is complex, but it provides the basis for most clinical diagnoses. The infection induces the synthesis of a number of antibodies, some of which react specifically with pathogenic treponemes and some with components of normal tissues (see below). If the disease is untreated, in most cases these immune reactions fail to eradicate existing infection and may contribute to tissue destruction in the late stages. Patients treated early in the disease are fully susceptible to reinfection.
The natural history of acquired syphilis is generally divided into two major clinical stages: early (infectious) syphilis and late syphilis. The two stages are separated by a symptom-free latent phase during the first part of which (early latency) the infectious stage is liable to recur. Infectious syphilis includes the primary lesions (chancre and regional lymphadenopathy), the secondary lesions (commonly involving skin and mucous membranes, occasionally bone, central nervous system, or liver), relapsing lesions during early latency, and congenital lesions. The hallmark of these lesions is an abundance of spirochetes; tissue reaction is usually minimal. Late syphilis consists of so-called benign (gummatous) lesions involving skin, bones, and viscera; cardiovascular disease (principally aortitis); and a variety of central nervous system and ocular syndromes. These forms of syphilis are not contagious. The lesions contain few demonstrable spirochetes, but tissue reactivity (vasculitis, necrosis) is severe and suggestive of hypersensitivity phenomena.
As a result of intensive public health efforts during and after World War II, there was a reduction in the incidence of infectious syphilis. With the marked increase in all sexually transmitted diseases since the 1970s, there has been a rise in the number of reported cases of syphilis. In the early 1980s, the incidence of infectious syphilis increased, with a particularly high rate among homosexual men. In the mid-1980s, there was a slight decrease, primarily a result of changes in sexual practices in response to the acquired immunodeficiency syndrome (AIDS) epidemic. Between 1985 and 1990, there was again a dramatic increase in infectious syphilis, with 50,223 cases of primary and secondary syphilis reported in 1990. This increase was broad based, affecting both men and women in inner city, urban, and rural areas, particularly in the southern regions of the United States. Although adolescent and young adult blacks were primarily affected, increases were seen in other ethnic groups also, as well as adults over 60 years of age. Limited access to health care, decreases in health department clinical services, increased use of illicit drugs (especially “crack cocaine”), the exchange of sex for drugs or money to buy drugs, and the difficulty of contact tracing when multiple sexual partners are involved all contributed to the dramatic increase. Concomitantly with the increase in acquired syphilis, there has also been an increase in congenital syphilis, particularly in urban areas. In response to this increase in infectious syphilis in 1998, the United States Congress allocated funds for a syphilis elimination program. This included intensive syphilis control programs targeting high-risk populations (women of childbearing age, sexually active teens, drug users, inmates of penal institutions, persons with multiple sexual partners or those who have sex with prostitutes) emphasizing screening, early treatment, contact tracing, and condom use. The effort has been successful, as evidenced by a decrease in the number of primary and secondary cases reported in 2001 (6103 cases) compared with 1998 (7035 cases). However, for the first time since 1990, the number of cases increased between 2000 (5979) and 2001 and increased 

again between 2001 and 2002 (6862 cases). These increases occurred only among men (suggesting that the increase is likely in the group of men having sex with men), whereas the number of cases actually declined among women and non-Hispanic blacks. Most cases are still reported from the South, but urban outbreaks (New York City, San Francisco) are being reported with increasing frequency, primarily among men having sex with men. Despite the increase in primary and secondary syphilis in men who have sex with men, there has not been a concomitant increase in the number of human immunodeficiency virus (HIV) cases.

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Assessment & Complications
Hypertension may be due to poisoning with amphetamines, anticholinergics, cocaine, ephedrine-containing performance-enhancing products, monoamine oxidase (MAO) inhibitors, and other drugs.
Severe hypertension (eg, diastolic blood pressure > 105–110 mm Hg in a person who does not have chronic hypertension) can result in acute intracranial hemorrhage, myocardial infarction, or aortic dissection. Patients often present with headache, chest pain, or encephalopathy.
Treat hypertension if the patient is symptomatic or if the diastolic pressure is greater than 105–110 mm Hg—especially if there is no prior history of hypertension.
Hypertensive patients who are agitated or anxious may benefit from a sedative such as lorazepam, 2–3 mg intravenously. For persistent hypertension, administer phentolamine, 2–5 mg intravenously, or nitroprusside sodium, 0.25–8 mcg/kg/min intravenously. If excessive tachycardia is present, add propranolol, 1–5 mg intravenously, or esmolol 25–100 mcg/kg/min intravenously. Caution: Do not give β-blockers alone, since doing so may paradoxically worsen hypertension.

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Assessment & Complications
Hypotension may be due to poisoning by many different drugs and poisons. The most common drugs causing hypotension are antihypertensive drugs, bblockers, calcium channel blockers, disulfiram (ethanol interaction), iron, theophylline, and antidepressants. Poisons causing hypotension include cyanide, carbon monoxide, hydrogen sulfide, arsenic, and certain mushrooms.
Hypotension in the poisoned or drug-overdosed patient may be caused by venous or arteriolar vasodilation, hypovolemia, depressed cardiac contractility, or a combination of these effects. The only certain way to determine the cause of hypotension in any individual patient is to insert a pulmonary artery catheter and calculate the cardiac output and peripheral vascular resistance. Alternatively, a central venous pressure (CVP) monitor may indicate a need for further fluid therapy.

Most patients respond to empiric treatment (200 mL intravenous boluses of 0.9% saline or other isotonic crystalloid up to a total of 1–2 L. If fluid therapy is not successful, give dopamine, 5–15 mcg/kg/min by intravenous infusion in a large peripheral or central line. Consider pulmonary artery catheterization if hypotension persists.
Hypotension caused by certain toxins may respond to specific treatment. For hypotension caused by overdoses of tricyclic antidepressants or related drugs, administer sodium bicarbonate, 50–100 mEq by intravenous bolus injection. Norepinephrine is more effective than dopamine in some patients with overdoses of tricyclic antidepressants or of drugs with predominantly vasodilating effects. For β-blocker overdose, glucagon (5–10 mg intravenously) may be of value. For calcium channel blocker overdose, administer calcium chloride, 1–2 g intravenously (repeated doses may be necessary; doses of 5–10 g and more have been given in some cases).

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Patients with drug overdoses or poisoning may initially have no symptoms or they may have varying degrees of overt intoxication. The asymptomatic patient may have been exposed to or may have ingested a lethal dose of a poison but not yet have any manifestations of toxicity. It is always important to (1) quickly assess the potential danger, (2) perform gut decontamination to prevent absorption, and (3) observe the patient for an appropriate interval.
Assess the Danger
If the toxin is known, the danger can be assessed by consulting a text or computerized information resource (eg, Poisindex) or by calling a regional poison control center. (Dialing 800-222-1222 will direct the call to the appropriate United States regional poison control center.) Assessment will usually take into account the dose ingested (in milligrams per kilogram of body weight); the time interval since ingestion; the presence of any clinical signs; preexisting cardiac, respiratory, renal, or liver disease; and, occasionally, specific serum drug or toxin levels. Be aware that the history given by the patient or family may be incomplete or unreliable.
The manufacturer or its local representative may be able to provide information over the phone concerning the toxic ingredients in question and can be contacted directly or via the regional poison control center (800-222-1222).
Gut Decontamination
The choice of gut decontamination procedure depends on the toxin and the circumstances. (See below for more discussion of methods.)
Observation of the Patient
Asymptomatic or mildly symptomatic patients should be observed for at least 4–6 hours. Longer observation is indicated if the ingested substance is a sustained-release preparation or is known to slow gastrointestinal motility or if there may have been exposure to a poison with delayed onset of symptoms (such as acetaminophen, colchicine, or hepatotoxic mushrooms). After that time, the patient may be discharged if no symptoms have developed and adequate gastric decontamination has been provided. Before discharge, psychiatric evaluation should be performed to assess suicidal risk. Intentional ingestions in adolescents should raise the possibility of unwanted pregnancy or sexual abuse.

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Over the past two and a half decades, numerous authorities have published dietary guidelines that make specific nutritional recommendations. Dietary Guidelines for Americans were published by the U.S. Department of Health and Human Services and the U.S. Department of Agriculture in January 2005. These guidelines reinforce many longstanding nutritional principles while also placing greater emphasis on several recent observations. Key recommendations in the new guidelines include the following: limit the intake of saturated fat, trans fat, cholesterol, added sugars, salt, and alcohol; balance calories from food and beverages with calories expended; engage in regular physical activity at least 30–60 minutes most days of the week; consume greater quantities (up to 9 servings per day) and more varieties of fruits and vegetables per day; consume at least half of the daily grains as whole grains; consume 3 cups per day of low fat milk or milk products; consume less than 10% of calories as saturated fat, less than 300 mg/d of cholesterol, and as little trans-fatty acids as possible; consume fiber-rich fruits, vegetables, and whole grains; use little added sugars or caloric sweeteners; consume less than 2300 mg of sodium per day; use alcohol sensibly and in moderation; and prepare food safely. 
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Dietary fat is the most concentrated source of food energy. Like energy from dietary carbohydrate, energy derived from fat can support protein synthesis. Dietary fat also provides the essential fatty acid linoleic acid. Other than the need for adequate quantities of linoleic acid, there is no specific requirement for dietary fat as long as the diet provides adequate nutrients oxidizable for energy. Although the average American diet contains 35–40% of calories as fat, most current recommendations are to limit dietary fat to 30% or less of total calories. Diets containing as little as 5–10% of total calories as fat appear to be safe and well tolerated.
Dietary fats are composed primarily of fatty acids and dietary cholesterol. Fatty acids contain either no double bonds (saturated), one double bond (monounsaturated), or more than one double bond (polyunsaturated). Saturated fatty acids are associated with increased serum cholesterol, whereas polyunsaturated and monounsaturated fatty acids lower serum cholesterol. Trans-fatty acids, a particular form of unsaturated fat found in partially hydrogenated vegetable oils, also raise serum cholesterol levels. Saturated fats are solid at room temperature and in general are derived from animal foods; unsaturated fats are liquid at room temperature and in general are derived from plant foods.
The polyunsaturated fatty acid linoleic acid is an essential nutrient, required by the body for the synthesis of arachidonic acid, the major precursor of prostaglandins. Deficiency of linoleic acid results in dermatitis, hair loss, and impaired wound healing. For individuals with average energy requirements, approximately 5 g of linoleic acid per day—1–2% of total calories—is required to prevent essential fatty acid deficiency.
Cholesterol is a major constituent of cell membranes. It is synthesized by the body and is not an essential nutrient. Diets that contain large amounts of cholesterol partially inhibit endogenous cholesterol synthesis but result in a net increase in serum cholesterol concentrations because of suppression of synthesis of low-density lipoprotein receptors. Average American diets contain approximately 450 mg/d of cholesterol, but 200 mg or less per day is recommended.

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The body requires energy to support normal functions and physical activity, growth, and repair of damaged tissues. Energy is provided by oxidation of dietary protein, fat, carbohydrate, and alcohol. Oxidation of 1 g of each provides 4 kcal of energy from protein and carbohydrate, 9 kcal from fat, and 7 kcal from alcohol.
In healthy adults, energy expenditure is primarily determined by three factors: basal energy expenditure (BEE), thermic effect of food (TEF), and physical activity.
The BEE is the amount of energy required to maintain basic physiologic functions. It is measured while the subject is resting in a warm room, not having eaten for 12 hours. In healthy persons, the BEE (in kcal/24 h) can be estimated by the Harris—Benedict equation, which will correctly predict measured BEE in 90% ± 10% of healthy subjects. In clinical practice, patients rarely meet the strict criteria for BEE measurement. Instead, energy expenditure is measured in individuals at rest without food for 2 hours. This measurement, the resting energy expenditure (REE), is about 10% greater than BEE.
TEF, the amount of energy expended during and following the ingestion of food, averages approximately 10% of the BEE.
Physical activity has a major impact on energy expenditure. The average energy expenditure per hour by adults engaged in typical activities

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Approximately 40 nutrients are required by the human body. Nutrients are essential if they cannot be synthesized by the body and if a deficiency causes recognizable abnormalities that disappear when the deficit is corrected. Required nutrients include the essential amino acids, water-soluble vitamins, fat-soluble vitamins, minerals, and the essential fatty acids. The body also requires an adequate energy substrate, a small amount of metabolizable carbohydrate, indigestible carbohydrate (fiber), additional nitrogen, and water.
Nutritional requirements have been most commonly expressed by recommended dietary allowances (RDAs). Published and periodically reviewed by the Food and Nutrition Board of the National Academy of Sciences, the RDAs were initially designed to meet the known nutritional needs of practically all healthy persons. RDAs have been established for carbohydrate and protein; the water-soluble vitamins thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B12, and vitamin C; the fat-soluble vitamins A, C, and E; and the minerals copper, phosphorus, magnesium, iron, zinc, iodine, molybdenum, and selenium.
Recently, the Food and Nutrition Board has developed a broader approach to defining nutritional adequacy. Known as dietary reference intakes (DRIs), these new guidelines go beyond the prevention of classic nutritional deficiency diseases and address the role of nutrients and other food components in long-term health and the reduction of risk of chronic diseases. The DRIs consist of four reference intakes: the RDA, the estimated average requirement (EAR), the tolerable upper intake level (UL), and the adequate intake (AI). The RDA remains the dietary intake that is sufficient to meet the nutritional requirements of nearly all individuals in an ageand gender-specific group. RDAs are intended as goals for individuals. The EAR is the intake value that is estimated to meet the requirements of 50% of individuals in an ageand gender-specific group. The UL is the maximum level of daily nutrient intake that is unlikely to pose health risks to most individuals. The AI is determined when insufficient data are available to establish the EAR and RDA for a given nutrient. It is based on fewer data and more expert opinion but is also intended as goals for individuals. 

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Both general and spinal or epidural anesthetic agents usually cause peripheral vasodilation, and most of the commonly used general anesthetic regimens also decrease myocardial contractility. These effects often result in transient mild hypotension or, less frequently, prolonged or more severe hypotension. The decrease in tidal volume caused by general and spinal-epidural anesthesia can close small airways and lead to atelectasis. Epinephrine, norepinephrine, and cortisol levels increase during surgery and remain elevated for 1–3 days. Serum antidiuretic hormone levels may be elevated for up to 1 week postoperatively. There is some evidence that general anesthesia may be associated with a relative hypercoagulable state during the perioperative period. This does not occur with spinal or epidural anesthesia. The degree to which this hypercoagulability contributes to perioperative morbidity is not known.
There is no evidence that spinal or epidural anesthesia is preferable to general anesthesia in terms of cardiac outcomes or overall surgical outcomes. Similarly, there is no conclusive evidence that the routine use of invasive hemodynamic monitoring with pulmonary artery catheters improves surgical outcomes. In general, the choice of anesthetic technique or agent and the decision to use invasive hemodynamic monitoring should be left to the anesthesiologist.

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Tinea Versicolor (Pityriasis Versicolor)

Velvety, tan, or pink macules or white macules that do not tan.
Fine scales that are not visible but are seen by scraping the lesion.
Central upper trunk the most frequent site.
Yeast and short hyphae observed on microscopic examination of scales.
General Considerations
Tinea versicolor is a mild, superficial Malassezia furfur infection of the skin (usually of the trunk). This yeast is a colonizer of all humans, which accounts for the high recurrence rate after treatment. It is not understood why some patients manifest the spore and hyphal form of the organism and the clinical disease. The eruption is often called to patients' attention by the fact that the involved areas will not tan, and the resulting hypopigmentation may be mistaken for vitiligo. A hyperpigmented form is not uncommon.
Clinical Findings
Lesions are asymptomatic, but a few patients note itching. The lesions are velvety, tan, pink, or white macules that vary from 4–5 mm in diameter to large confluent areas. The lesions initially do not look scaly, but scales may be readily obtained by scraping the area. Lesions may appear on the trunk, upper arms, neck, face, and groin.
Large, blunt hyphae and thick-walled budding spores (“spaghetti and meatballs”) may be seen when skin scales have been cleared in 10% KOH. Fungal culture is not useful.
Differential Diagnosis
Vitiligo usually presents with larger periorificial lesions. Vitiligo (and not tinea versicolor) is characterized by total depigmentation, not just a lessening of pigmentation. Vitiligo does not scale. Pink and red-brown lesions on the chest are differentiated from seborrheic dermatitis of the same areas by the KOH preparation.
Treatment & Prognosis
Topical treatments include selenium sulfide lotion, which may be applied from neck to waist daily and left on for 5–15 minutes for 7 days; this treatment is repeated weekly for a month and then monthly for maintenance. Ketoconazole shampoo, 1% or 2%, lathered on the chest and back and left on for 5 minutes may also be used weekly for maintenance. Clinicians must stress to the patient that the raised and scaly aspects of the rash are being treated; the alterations in pigmentation may take months to fade or fill in. Tinver lotion (contains sodium thiosulfate) is effective. Irritation and odor are common complaints from patients. Relapses are common.
Sulfur-salicylic acid soap or shampoo or zinc pyrithrone-containing shampoos used on a continuing basis may be effective prophylaxis.
Ketoconazole, 200 mg daily orally for 1 week or 400 mg as a single oral dose, results in short-term cure of 90% of cases. Patients should be instructed not to shower for 8–12 hours after taking ketoconazole, because it is delivered in sweat to the skin. The single dose may not work in more hot and humid areas, and more protracted therapy carries a small but finite risk of druginduced hepatitis for a completely benign disease. Without maintenance therapy, recurrences will occur in over 80% of “cured” cases over the subsequent 2 years. Treatment with a single dose of 400 mg of oral fluconazole is also effective but more expensive.
Newer imidazole creams, solutions, and lotions are quite effective for localized areas but are too expensive for use over large areas such as the chest and back.
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Tinea Manuum & Tinea Pedis (Dermatophytosis, Tinea of Palms & Soles, “Athlete's Foot”)

Most often presenting with asymptomatic scaling.
May progress to fissuring or maceration in toe web spaces.
Itching, burning, and stinging of interdigital web; scaling palms, and soles; vesicles of soles in inflammatory cases.
The fungus is shown in skin scrapings examined microscopically or by culture of scrapings.
General Considerations
Tinea of the feet is an extremely common acute or chronic dermatosis. Certain individuals appear to be more susceptible than others. Most infections are caused by Trichophyton species.
Clinical Findings
The presenting symptom may be itching, burning, or stinging. Pain may indicate secondary infection with complicating cellulitis. Interdigital tinea pedis is the most common cause of leg cellulitis in healthy individuals. Tinea pedis has several presentations that vary with the location. On the sole and heel, tinea may appear as chronic noninflammatory scaling, occasionally with thickening and fissuring. This may extend over the sides of the feet in a “moccasin” distribution. The KOH preparation is usually positive. Tinea pedis often appears as a scaling or fissuring of the toe webs, perhaps with sodden maceration. As the web spaces become more macerated, the KOH preparation and fungal culture are less often positive because bacterial species begin to dominate. Finally, there may also be grouped vesicles distributed anywhere on the soles, generalized exfoliation of the skin of the soles, or nail involvement in the form of discoloration and thickening and crumbling of the nail plate.
Hyphae can be demonstrated microscopically in skin scales treated with 10% KOH. KOH and culture does not always demonstrate pathogenic fungi from macerated areas.
Differential Diagnosis
Differentiate from other skin conditions involving the same areas, such as interdigital erythrasma (use Wood's light). Psoriasis may be a cause of chronic scaling on the palms or soles and may cause nail changes. Repeated fungal cultures should be negative, and the condition will not respond to antifungal therapy. Contact dermatitis (from shoes) will often involve the dorsal surfaces and will respond to topical or systemic corticosteroids. Vesicular lesions should be differentiated from pompholyx (dyshidrosis) and scabies by proper scraping of the roofs of individual vesicles. Rarely, gram-negative organisms may cause toe web infections in the setting of prior tinea or in its absence. Culture is not very specific, because gramnegative organisms can be cultured from normal toe webs. This entity is treated with aluminum salts (see below) and imidazole antifungal agents or ciclopirox.
The essential factor in prevention is personal hygiene. Wear open-toed sandals if possible. Use of rubber or wooden sandals in community showers and bathing places is often recommended, though the effectiveness of this practice has not been studied. Careful drying between the toes after showering is essential. A hair dryer used on low setting may be used. Socks should be changed frequently, and absorbent nonsynthetic socks are preferred. Apply dusting and drying powders as necessary. The use of powders containing antifungal agents (eg, Zeasorb-AF) or chronic use of antifungal creams may prevent recurrences of tinea pedis.
Macerated stage—Treat with aluminum subacetate solution soaks for 20 minutes twice daily. Broadspectrum antifungal creams and solutions (containing imidazoles or ciclopirox instead of tolnaftate and haloprogin) will help combat diphtheroids and other grampositive organisms present at this stage and alone may be adequate therapy. If topical imidazoles fail, often 1 week of once-daily allylamine treatment (terbinafine or butenafine) will result in clearing.
Dry and scaly stage—Use any of the agents listed in the section on tinea corporis. The addition of urea 10% lotion or cream may increase the efficacy of topical treatments in thick (“moccasin”) tinea of the soles.
Griseofulvin should be used only for severe cases or those recalcitrant to topical therapy. If the infection is cleared by systemic therapy, the patient should be encouraged to begin maintenance with topical therapy, since recurrence is common. Itraconazole, 200 mg daily for 2 weeks or 400 mg daily for 1 week, or terbinafine, 250 mg daily for 2–4 weeks, may be used in refractory cases.
For many individuals, tinea pedis is a chronic affliction, temporarily cleared by therapy only to recur.
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Tinea Cruris (Jock Itch)

Marked itching in intertriginous areas, usually sparing the scrotum.
Peripherally spreading, sharply demarcated, centrally clearing erythematous lesions.
May have associated tinea infection of feet or toenails.
Laboratory examination with microscope or culture confirms diagnosis.
General Considerations
Tinea cruris lesions are confined to the groin and gluteal cleft. Intractable pruritus ani may occasionally be caused by a tinea infection.
Clinical Findings
Itching may be severe, or the rash may be asymptomatic. The lesions have sharp margins, cleared centers, and active, spreading scaly peripheries. Follicular pustules are sometimes encountered. The area may be hyperpigmented on resolution.
Hyphae can be demonstrated microscopically in KOH preparations. The organism may be cultured readily.
Differential Diagnosis
Tinea cruris must be distinguished from other lesions involving the intertriginous areas, such as candidiasis, seborrheic dermatitis, intertrigo, psoriasis of body folds (“inverse psoriasis”), erythrasma, and rarely tinea versicolor. Candidiasis is generally bright red and marked by satellite papules and pustules outside of the main border of the lesion. Candida typically involves the scrotum. Tinea versicolor can be diagnosed by the KOH preparation. Seborrheic dermatitis also often involves the face, sternum, and axillae. Intertrigo tends to be more red, less scaly, and present in obese individuals in moist body folds with less extension onto the thigh. Inverse psoriasis is characterized by distinct plaques. Other areas of typical psoriatic involvement should be checked, and the KOH examination will be negative. Erythrasma is best diagnosed with Wood's light—a brilliant coral-red fluorescence is seen.
Drying powder (eg, miconazole nitrate [Zeasorb-AF]) should be dusted into the involved area in patients with excessive perspiration or occlusion of skin due to obesity. Underwear should be loose-fitting.
Any of the preparations listed in the section on tinea corporis may be used. There is great variation in expense, with miconazole, clotrimazole, butenafine, and terbinafine available over the counter and usually at a lower price. Terbinafine cream is curative in over 80% of cases after once-daily use for 7 days.
Griseofulvin ultramicrosize is reserved for severe cases. Give 250–500 mg orally twice daily for 1–2 weeks. One week of either itraconazole, 200 mg daily, or terbinafine, 250 mg daily, is also effective.
Tinea cruris usually responds promptly to topical or systemic treatment. It may leave behind postinflammatory hyperpigmentation.
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Tinea Corporis or Tinea Circinata (Body Ringworm)


Ring-shaped lesions with an advancing scaly border and central clearing or scaly patches with a distinct border.
On exposed skin surfaces or the trunk.
Microscopic examination of scrapings or culture confirms the diagnosis.
General Considerations
The lesions are often on exposed areas of the body such as the face and arms. A history of exposure to an infected cat may occasionally be obtained, usually indicating microsporum infection. All species of dermatophytes may cause this disease, but Trichophyton rubrum is the most common pathogen, usually representing extension onto the trunk or extremities of tinea cruris, pedis, or manuum.
Clinical Findings
Itching may be present. In classic lesions, rings of erythema have an advancing scaly border and central clearing, occasionally with hyperpigmentation.
Hyphae can be demonstrated by removing scale and examining it microscopically using KOH. The diagnosis may be confirmed by culture.
Differential Diagnosis
Positive fungal studies distinguish tinea corporis from other skin lesions with annular configuration, such as the annular lesions of psoriasis, lupus erythematosus, syphilis, granuloma annulare, and pityriasis rosea. Psoriasis has typical lesions on elbows, knees, scalp, and nails. Secondary syphilis is often manifested by characteristic palmar, plantar, and mucous membrane lesions. Tinea corporis rarely has the large number of lesions seen in pityriasis rosea. Granuloma annulare lacks scales.
Complications include extension of the disease down the hair follicles (in which case it becomes
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Mycotic infections are traditionally divided into two principal groups—superficial and deep. 

The diagnosis of fungal infections of the skin is usually based on the location and characteristics of the lesions and on the following laboratory examinations: (1) Direct demonstration of fungi in 10% KOH of scrapings from suspected lesions. “If it's scaly, scrape it” is a time-honored maxim. (2) Cultures of organisms from skin scrapings. (3) Histologic sections of nails stained with periodic acid-Schiff (Hotchkiss-McManus) technique may be diagnostic if scrapings and cultures are negative.

Principles of Treatment
In general, treatment follows a diagnosis confirmed by KOH preparation or culture, especially if systemic antifungal therapy is to be used. Many other diseases cause scaling, and use of an antifungal agent without a firm diagnosis makes subsequent diagnosis more difficult. In general, fungal infections are treated topically except for those involving the nails or those deep in hair follicles on the face or body.
Griseofulvin is safe and effective for treating dermatophyte infections of the skin (except for the scalp and nails). Itraconazole, an azole antifungal, accumulates in the nail plate from the matrix and nail bed and persists for 3 months after oral administration is discontinued.
Terbinafine is an allylamine oral antifungal. It has excellent activity against dermatophytes. In vitro activity against yeast forms is variable, but the drug is active against hyphal forms. It is well delivered to the nail plate and persists in the nail for 6–9 months after treatment has ended.
Fluconazole has excellent activity against yeasts and may be the treatment of choice for many forms of mucocutaneous candidiasis. Fluconazole is less effective than itraconazole or terbinafine for the treatment of dermatophytosis.
Itraconazole, fluconazole, and terbinafine can all cause elevation of liver function tests and—though rarely in the dosing regimens used for the treatment of dermatophytosis—clinical hepatitis. Ketoconazole is no longer recommended for the treatment of dermatophytosis (except for tinea versicolor) because of the higher rate of hepatitis when it is used for more than a month.
General Measures & Prevention
Since moist skin favors the growth of fungi, dry the skin carefully after bathing or after perspiring heavily. Talc or other drying powders may be useful. The use of topical corticosteroids for other diseases may be complicated by intercurrent tinea or candidal infection, and topical antifungals are often used in intertriginous areas with corticosteroids to prevent this.
 much more difficult to cure), pyoderma, and dermatophytid.
Treat infected household pets (microsporum infections).

The following applied topically are effective against dermatophyte infections other than those of the nails: miconazole, 2% cream; clotrimazole, 1% solution, cream, or lotion; ketoconazole, 2% cream; econazole, 1% cream or lotion; sulconazole, 1% cream; oxiconazole, 1% cream; ciclopirox, 1% cream; naftifine, 1% cream or gel; butenafine cream; and terbinafine, 1% cream. Miconazole, clotrimazole, butenafine and terbinafine are available over the counter. Allylamines (especially terbinafine and butenafine) require shorter courses and lead to the most rapid response and prolonged remissions. Treatment should be continued for 1–2 weeks after clinical clearing. Betamethasone dipropionate with clotrimazole (Lotrisone) is overused by nondermatologists. In general, short-term use of betamethasone-clotrimazole does not justify the expense, and long-term improper use may result in side effects from the high-potency corticosteroid component, especially in body folds. Cases of tinea that are clinically resistant to this combination have been reported.
Griseofulvin (ultramicrosize), 250–500 mg twice daily, is used. Typically, only 4–6 weeks of therapy are required. Itraconazole as a single week-long pulse of 200 mg daily is also effective in tinea corporis. Terbinafine, 250 mg daily for 1 month, is an alternative.
Body ringworm usually responds promptly to conservative topical therapy or to griseofulvin by mouth within 4 weeks.
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Body Mass Index (BMI)

BMI is perhaps the most common anthropometric measure used to predict relative overweight. However, the value of the measurement in children and adolescents is regularly questioned. The natural course of growth and maturation in children, plus the individual variability during the same period mean that indices of weight-for-height, including the BMI (W/H2) are not very good indices of adiposity. In children younger than 15 years of age, BMI is not totally independent of height and thus should be used with caution. Both Schey et al. and Michielutte et al. examined the value of various

Hills/Lyell/Byrne 8weight-for-height indices and found that BMI was the most useful. However, in paediatric populations there is a correlation with height that is not oted in adult populations. BMI was found to correlate less strongly with the triceps skinfold measure at younger ages. Both papers concluded by suggesting that practitioners be cautious in using BMI as a measure of adiposity in children and that, if possible,multiple criteria should be used in assessing bodycomposition.Deurenberg et al. stated that BMI could accurately predict body fat percentage using equations however the SEE in children was 4.4%BF which is above the cut-off (3–4%BF) proposed by Reilly to indicate acceptable accuracy. This finding indicates that BMI is useful as a classifying tool in epidemiological studies, but, however, has limited use in body composition assessment.

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Magnetic Resonance Imaging (MRI)

Magnetic Resonance Imaging (MRI)

MRI provides a visual image of adipose tissue and non-fat tissue within the sections of the body scanned. The subject must lie enclosed in a scanner Hills/Lyell/Byrne 4 until sufficient images are obtained to predict total body fat. The weight of fat is then estimated using the known volume and density of fat. It must be noted that the non-fat components of fat (protein and water) will be included in areas of fat and thus the FFM estimate from this technique will be less
than that measured using DXA or hydrodensitometry. The benefits of MRI are the ability to measure regional fat distribution and inter-abdominal fat content, and the high degree of accuracy and reliability [18]. Several limitations exist, especially when working with children. The subject must be enclosed in the MRI scanner for a long period of time that may be traumatic, especially for younger children. The method is expensive, time consuming, not accessible to all practitioners and therefore has limited application for work with paediatric populations.

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Indications for Intubation

Indications for Intubation
Intubation is reserved for those patients who continue to show signs of inadequate
respiration after basic interventions or those in whom these interventions
alone are not likely to sustain appropriate respiration (12).

Absolute Indications for Intubation:
1. Airway obstruction unrelieved with basic interventions,
2. Apnea or near apnea,
3. Respiratory distress, and
4. Severe neurologic deficit or decreased consciousness (i.e., focal deficit
or GCS rating less than 9) due to head trauma or any other cause.

Urgent Indications for Intubation:
1. Penetrating neck injury (with any signs of airway compromise or
expanding hematoma),
2. Persistent or refractory hypotension, especially due to active hemorrhage,
3. Chest wall injury with respiratory dysfunction, and
4. Moderate altered mentation, especially after head trauma, including
both combative and mildly obtunded patients.

Relative Indications for Nonemergent Intubation:
1. Oromaxillofacial injury,
2. Impending respiratory failure,
3. Need for diagnostic or therapeutic procedures [e.g., computed tomography
(CT) or angiography] in patients with risk for deterioration or
those unable to remain motionless during the examination, and
4. Potential respiratory failure after sedative-analgesic use. read more......

Foot Disorders

Calcaneovalgus Foot

Calcaneovalgus foot is generally considered a uterine-packing problem in which the foot is markedly dorsiflexed at birth so the dorsum of the foot sits against the anterior surface of the tibia. The hindfoot is usually in moderate eversion (valgus) as well. Although some flexibility is present with the deformity, there is resistance to full motion, and most cases do not allow ankle plantar flexion beyond a right angle.

Despite its dramatic appearance, calcaneovalgus foot corrects spontaneously within 2–3 months. Although some orthopedists brace or apply serial casts and many recommend stretching exercises, all true calcaneovalgus feet resolve without treatment.

Congenital Vertical Talus

Calcaneovalgus foot must be differentiated from a much rarer condition known as congenital vertical talus (congenital rocker-bottom foot, congenital complex pes valgus). In this deformity, although the foot appears to lie against the anterior tibia, the hindfoot is actually plantar flexed because of contracture of the posterior calf muscles. To accommodate plantarflexion of the hindfoot and dorsiflexion of the forefoot, the midfoot joints (talonavicular and calcaneocuboid joints) must subluxate or dislocate dorsally.

Congenital vertical talus often accompanies genetic disorders, syndromes such as arthrogryposis, or neuromuscular disorders such as spina bifida. It is occasionally found in otherwise normal infants, however. Treatment is usually surgical, and casting does not resolve the disorder.

Cavus Foot

Cavus foot is a foot with an abnormally high arch. Although it is difficult to ascribe a particular threshold of arching beyond which treatment is necessary, most deformities are dramatic enough to make diagnosis straightforward

Cavus foot frequently accompanies hindfoot varus deformity (cavovarus foot), and there may be clawing of the toes and demonstrable weakness of ankle or foot muscles. In addition, calluses beneath the metatarsal heads and heel skin are common.

Clinical Findings

One of the most common symptoms of cavus foot is anterior ankle pain, sometimes associated with toe walking. This paradoxical situation occurs because of the pathologic anatomy of the cavus foot. The forefoot is severely plantar flexed on the hindfoot, requiring marked ankle dorsiflexion to compensate. When the cavus becomes too severe, ankle dorsiflexion is blocked, leading to anterior ankle impingement and pain. The inability to dorsiflex further compromises forefoot clearance, and, eventually, only the metatarsals can contact the floor. This can be misinterpreted as ankle plantarflexion contracture, leading to unnecessary (and possibly harmful) heel cord release.

The cause of cavus foot is usually muscle imbalance in a growing foot. Thus, cavus is rarely found in early childhood but is fairly frequent after 8–10 years of age. Although intrinsic muscle weakness is a major cause of cavus foot, weakness of the peroneal or anterior tibialis muscles is also implicated. Cavus foot is rarely found in the absence of an underlying neuromuscular condition.

Cavus foot is a marker for neuromuscular disease. Diagnosis requires a thorough search for the underlying cause and may require neurologic consultation, spinal MRI, and electromyographic (EMG) studies. Table 11–6 lists common neuromuscular causes of cavus foot.

Table 11–6. Common Neuromuscular Causes of Cavus Foot.

Cerebral palsy
Charcot-Marie-Tooth disease
Compartment syndrome
Friedrich ataxia
Muscular dystrophy
Spinal cord tumor
Spinal dysraphism (spina bifida)


Conservative treatment of cavus foot includes accommodation by shoe modifications or inserts. These modalities do not actually correct the condition; severe deformity requires surgical correction by tendon transfers to restore muscle balance, by midfoot osteotomy to correct bony deformity, or by triple arthrodesis (hindfoot fusion in a corrected position).

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Osteomyelitis, especially bacterial, may occur as an acute disease. Common symptoms include chills followed by fever, with acute pain and swelling above the site of inflammation. The inflammation begins in the marrow cavity and causes softening and erosion of the long bones, often with the formation of pus-containing abscesses, and soon spreads over the entire bone, with consequent death of the hard portions of the bone.

Chronic osteomyelitis, as is often seen in tuberculosis, fungus infections, or in patients with bacterial infections from other organisms, tends to run a slower and less dramatic course, with less severe pain and less fever, often resulting in bone destruction.

Acute osteomyelitis is treated by injections of antibiotics such as nafcillin, and by concurrent surgery to open the affected bone and drain the pus and dead tissue. Because of antibiotics, severe acute osteomyelitis is rare.

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