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Topical Glucocorticoids Twice-daily application of topical corticosteroids is the mainstay of treatment for all forms of dermatitis (Table 143). After wet dressings are discontinued, topical steroids should be applied only to areas of active disease. Clinical Appearance Primary lesions (first to appear) Macule Papule Plaque Vesicle Bulla Pustule Nodule Wheal Secondary changes Scales Lichenification Erosion and oozing Crusts Fissures Scars Atrophy Color the lesion should be described as red, yellow, brown, tan, or blue. Configuration of lesions Annular (circular) Linear (straight lines) Grouped Discrete Distribution Note whether the eruption is generalized, acral (hands, feet, buttocks, face), or localized to a specific skin region. Annular nodules represent granuloma annulare; annular scaly papules are more apt to be caused by dermatophyte infections. Linear papules represent lichen striatus; linear vesicles, incontinentia pigmenti; linear papules with burrows, scabies. Induration of skin with exaggerated skin lines and a shiny surface resulting from chronic rubbing of the skin. A moist, circumscribed, slightly depressed area representing a blister base with the roof of the blister removed. A flat, raised, or depressed area of fibrotic replacement of dermis or subcutaneous tissue. A solid, elevated area < 1 cm in diameter whose top may be pointed, rounded, or flat. A circumscribed, elevated lesion < 1 cm in diameter and containing clear serous fluid. A circumscribed, elevated lesion > 1 cm in diameter and containing clear serous fluid. If it moves with the skin on palpation, it is intradermal; if the skin moves over the nodule, it is subcutaneous. A circumscribed, flat-topped, firm elevation of skin resulting from tense edema of the papillary dermis. Description and Examples potency steroids (see Table 143) are applied to the face or intertriginous areas. These 1- to 2-mm white papules occur predominantly on the face in 40% of newborns. Their intraoral counterparts are called Epstein pearls and occur in up to 6085% of neonates. Base Foam Liquids Powder Grease and emulsifier; oil in water Excess grease and emulsifier; water in oil Grease Combined With Uses Cosmetically eloquent; increasing number of products available. Wet dressings: relieve pruritus, vasoconstrict Shake lotions, drying pastes: relieve pruritus, vasoconstrict Cream: penetrates quickly (1015 min) and thus allows evaporation Emollient cream: penetrates more slowly and thus retains moisture on skin Ointments: occlusive (hold material on skin for prolonged time) and prevent evaporation of water Transparent, colorless, semisolid emulsion: nongreasy, more drying and irritating than cream Enhances evaporation neonatal cephalic pustulosis. This is a more monomorphic eruption with red papules and pustules on the head and neck that appears in the first month of life. This eruption will resolve spontaneously, but responds to topical antiyeast preparations. Harlequin Color Change A cutaneous vascular phenomenon unique to neonates in the first week of life occurs when the infant (particularly one of low birth weight) is placed on one side. The dependent half develops an erythematous flush with a sharp demarcation at the midline, and the upper half of the body becomes pale. The color changes usually subside within a few seconds after the infant is placed supine but may persist for as long as 20 minutes. Mottling A lacelike pattern of bluish, reticular discoloration representing dilated cutaneous vessels appears over the extremities and often the trunk of neonates exposed to lowered room temperature. Thermolabile, low-residue foam vehicle is more cosmetically acceptable and uses novel permeability pathway for delivery. Ointments (eg, Aquaphor, petrolatum) should not be used in intertriginous areas such as the axillae, between the toes, and in the perineum, because they increase maceration. Oils and ointments hold medication on the skin for long periods and are therefore ideal for barriers or prophylaxis and for dried areas of skin. Creams carry medication into skin and are preferable for intertriginous dermatitis. Glucocorticoid Low potencya = 19 Hydrocortisone Desonide Moderate potency = 1099 Mometasone furoate Hydrocortisone valerate Fluocinolone acetonide Triamcinolone acetonide Amcinonide High potency = 100499 Desoximetasone Fluocinonide Halcinonide Super potency = 5007500 Betamethasone dipropionate Clobetasol propionate a Concentrations 0. Sebaceous Gland Hyperplasia Prominent white to yellow papules at the opening of pilosebaceous follicles without surrounding erythema-especially over the nose-represent overgrowth of sebaceous glands in response to maternal androgens. They occur in more than half of newborns and spontaneously regress in the first few months of life.
- Avoid sudden movements, which may worsen symptoms. You may need help walking during attacks.
- Infant raises up (upper torso, shoulders, and head) with arms when lying face down (on tummy)
- Hormone problems
- Allergic reactions to medicines (anesthesia) used during surgery
- Agitation or fidgeting
- Ankylosing spondylitis
- Rapid, deep breathing
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Proper controls are necessary to eliminate rheumatoid factor, which may give rise to a false-positive result. Serum of patients with disseminated infection caused by Trichosporon beigelii may also test positive for cryptococcal antigen. Pulmonary cryptococcosis is difficult to diagnose in most cases without obtaining lung tissue via bronchoscopy, open lung biopsy, or thorascopy. Wet preparations of sputum are only occasionally helpful, and sputum cultures are positive for C. In patients with pleural effusions, fluid tested for cryptococcal antigen may be positive, thereby obviating a more invasive procedure. Blood cultures and tissue for culture and histopathologic study of any other suspected sites of involvement. The diagnosis of cryptococcal meningitis is easier to establish than the diagnosis of cryptococcal pulmonary disease. Once the diagnosis of meningitis is considered, a lumbar puncture should be performed. Yet in most cases, opening pressures are elevated, cultures are positive, cryptococcal antigen titers are high, and India ink preparations reveal organisms. Approaches to therapy of cryptococcosis vary according to site of involvement and underlying host status. Although specific guidelines are poorly defined, the two commonly used drugs are amphotericin B (total dose, 1. Fluconazole should be reserved for patients with mild to moderate forms of cryptococcal lung disease. As a rule, therapy should be continued until clinical, radiographic, and mycologic resolution of disease is evident. Surgical resection may be an important adjunct to drug therapy in patients with extensive lobar consolidation and large mass lesions. The therapy of cryptococcal meningitis has been more extensively studied than the therapy of any other systemic fungal disease. Both renal function and serum flucytosine levels should be closely monitored, and flucytosine doses should be adjusted to maintain serum concentrations in the range of 50 to 100 mg/mL. Potential toxic effects of flucytosine include bone marrow suppression, hepatitis, diarrhea, and rash. Intrathecal therapy with amphotericin B is rarely used nowadays, usually reserved for patients who experience relapse or whose disease is refractory to prolonged courses of high-dose intravenous amphotericin B. Combination amphotericin and flucytosine may be given for the entire period of primary therapy. In addition, flucytosine for prolonged duration should not be used unless serum levels can be monitored. However, because of unacceptable toxicity of flucytosine administered over a prolonged period, this regimen cannot be recommended over more established treatments. Results obtained from a recent, large (381 patients) multicenter clinical trial argue that induction therapy with combination amphotericin (0. Itraconazole (400 mg/day) may be a suitable 1870 alternative for patients unable to take fluconazole during consolidation therapy. Recent data indicate that passive antibody in the form of murine or humanized monoclonal antibodies has the potential to enhance cellular immunity; trials are ongoing. Mechanical measures to reduce intracranial pressure are more effective than medical measures, such as high-dose dexamethasone or mannitol. Fluconazole (200 mg daily) is more effective in preventing relapse than amphotericin (1 mg/kg weekly) and much better tolerated, resulting in better patient compliance. Pretreatment prognostic factors that adversely affect outcome in patients with cryptococcal meningitis include any underlying condition predisposing to T-cell dysfunction. Among these factors, T-cell dysfunction and abnormal mental status appear to be most important. Because an environmental source of infection cannot be determined in the vast majority of patients who develop cryptococcal disease, attempts at eliminating C. A comprehensive review of the disease, including the virulence factors and biology of the organism, pathogenesis and host defenses, clinical manifestations, laboratory diagnosis, and treatment (529 references). Focuses on clinical and laboratory features as well as different treatment options, including primary therapy for acute disease and maintenance therapy to prevent relapse. Results of this large, double-blind, multicenter trial indicate that the combination of higher-dose amphotericin B and flucytosine is associated with an increased rate of sterilization of cerebrospinal fluid and decreased mortality at 2 weeks as compared with regimens used in previous studies.
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Swenne I: Weight requirements for return of menstruations in teenage girls with eating disorders, weight loss, and secondary amenorrhea. Binge eating is either eating excessive amounts of food during a normal mealtime or having a meal that lasts longer than usual. Bulimic individuals feel out of control while eating, unable or unwilling to recognize satiety signals. Any type of food may be eaten in a binge, although typically it is either carbohydrates or junk food. At some point, either prior to or during a binge, bulimic individuals often decide to purge as a means of preventing weight gain. The most common ways to purge are self-induced vomiting, exercise, and laxative use. Some individuals will vomit multiple times during a purge episode, after using large amounts of water to cleanse their system. This can induce significant electrolyte abnormalities such as hyponatremia and hypokalemia, which may put the patient at acute risk for arrhythmia or seizure. Other methods of purging include diuretics, diet pills, cathartics, and nutritional supplements, including Metabolife. Bulimic patients are usually average or slightly above average in body weight and have no physical abnormalities. These patients can receive treatment as outpatients, employing the same multidisciplinary team approach. Manualized family-based treatment, described earlier under General Approach, is ideal for the outpatient setting, if a trained therapist is available. Appropriate nutrition counseling is vital in guiding a patient and family through the initial stages of recovery. If weight loss persists, careful monitoring of vital signs, including supine heart rate, is important in determining whether an increased level of care is needed. Concomitantly, the patient should be referred to a psychotherapist, and if indicated, assessed by a psychiatrist. LeGrange D et al: Manualized family-based treatment for anorexia nervosa: A case series. An episode of binge eating is characterized by both of the following: (1) eating, in a discrete period of time (eg, within any 2-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances. Reprinted, with permission, from the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. If laxatives are used, then a metabolic acidosis develops with hypokalemia and hypochloremia. Asking whether patients have binged, feel out of control while eating, or whether they cannot stop eating can clarify the diagnosis. Parents may report that significant amounts of food are missing or disappearing more quickly than normal. If the physician is suspicious, direct questioning about all the ways to purge should follow. Indicating first that the behavior is not unusual can make questioning less threatening and more likely to elicit a truthful response. For example, the clinician might say, "Some teenagers who try to lose weight make themselves vomit after eating. Short-Term Complications Complications in normal-weight bulimic patients are related to the mechanisms of purging, and many of these complications are listed under Symptoms and Signs, earlier. If the bulimic patient is significantly malnourished, complications may be the same as those encountered in the anorexic patient. Other complications of bulimia include esophageal rupture, acute or chronic esophagitis, and rarely, Barrett syndrome. Chronic vomiting can lead to metabolic alkalosis, and laxative abuse may cause metabolic acidosis. Diet pill use can cause insomnia, hypertension, tachycardia, palpitations, seizures, and sudden death. Treating constipation can be difficult psychologically, because the practitioner may need to prescribe agents similar to the drugs of abuse used during the eating disorder. This can be due to gastroesophageal reflux, as the lower esophageal sphincter is compromised due to repetitive vomiting. Frequent vomiting may result in esophagitis or gastritis, as the mucosa is irritated from increased acid exposure.
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Ultra-low-volume aerial spraying of organophosphate insecticides (malathion) to reduce the population of adult female mosquitoes has been successful in emergency control of epidemics. Like dengue, West Nile fever is a mosquito-transmitted, acute, self-limited illness that presents chiefly with fever, malaise, lymphadenopathy, and rash. Virus transmission involves mosquitoes and wild birds, with mammals, including humans, as incidental end-stage hosts. In endemic areas, human infections are extremely common, with over 60% of young adults having antibodies; this suggests a high prevalence of inapparent or undifferentiated febrile illness in children. Following an incubation period of 1 to 6 days, the onset is usually abrupt without prodromal symptoms. Symptoms include drowsiness, severe frontal headache, ocular pain, myalgia, and pain in the abdomen and back. Examination shows facial flushing, conjunctival injection, and coating of the tongue. Nodes are of moderate size and nontender and usually include the occipital, axillary, and inguinal chains. In half of patients, a pale roseolar maculopapular rash, predominantly on the trunk and upper arms, appears from the second to fifth day. It may be evanescent (several hours) or persist until defervescence; and it does not desquamate. Infection also may result in aseptic meningitis or meningoencephalitis, especially in the elderly. Convalescence is often prolonged, lasting several weeks with prominent symptoms of fatigue. West Nile virus can be isolated from the blood of three fourths of patients on the first day, with viremia persisting but decreasing over 5 days. Serologic diagnosis is possible using a number of tests; however, cross-reactions with other flaviviruses complicate interpretation. Ribavirin has activity against West Nile fever virus, but since the disease is self-limited and almost never fatal, its use does not seem indicated. Phlebotomus (sandfly, pappataci, or 3-day) fever is an acute, relatively mild, self-limited infection transmitted by Phlebotomus flies. There are at least five immunologically distinct phleboviruses (Naples, Sicilian, Punto Toro, Chagres, and Candiru). The principal vector of Phlebotomus fever viruses in the Mediterranean, Middle East, and northwest India is Phlebotomus paptasii, which breeds in dry sandy areas and feeds in early evening. Although undefined, sandfly fever viruses presumably are maintained in a vector-host wildlife cycle between epidemics. Transovarial transmission probably serves as an alternative mechanism for virus perpetuation. Sandflies are small (2 to 3 mm), which enables them to penetrate screens and mosquito netting. There is no pain or itching after the bite; hence, only about 1% of patients remember being bitten. After an incubation period of 2 to 6 days, symptoms develop abruptly in more than 90% of patients. Headache is nearly always present and often is accompanied by pain on ocular movement 1852 and retro-orbital pain. Myalgia is common and may be localized, for example, to the abdomen; if to the chest, it resembles pleurodynia. Other symptoms include vomiting, photophobia, alteration or loss of taste, and arthralgia. Pulse is proportional to the temperature on the first day, followed by relative bradycardia. Lymphopenia with an increase in band neutrophils early in the illness is followed by a relative lymphocytosis (40 to 65%). The virus multiplies readily in most common cell cultures, is cytopathic, and forms plaques.
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Preventing psittacosis acquired from non-psittacine birds is more problematic and will remain a continuing source for human infection. Danesh J, Collins R, Peto R: Chronic infections and coronary heart disease: Is there a link? A randomized intervention trial demonstrated that treatment with an antibiotic active against C. A randomized clinical trial establishes that screening for cervical chlamydial infection reduced the risk of pelvic inflammatory disease by 56%. Genome sequence of an obligate intracellular pathogen of humans: Chlamydia trachomatis. Hornick the rickettsiae are small obligate intracellular, gram-negative pathogens. They do not have a symbiotic relationship with human host cells, and therefore cause metabolic derangements that result in cell death. Infections with the typhus and spotted fever groups of rickettsiae involve endothelial cells. Ehrlichiosis is a relatively new human disease, and two species have been identified: the first, Ehrlichia chaffeenis invades human monocytes, and the other is identical to strains known to cause disease in dogs and horses-thus E. Each of the rickettsiae is transmitted to humans by ticks, mites, lice, fleas, or aerosols originating from animal products (placentas, Q fever) or from feces of the aforementioned insects. Certain other rickettsial infections are major public health problems in developing countries but are not found in the United States. The potential for tourists to return to the United States with an emerging rickettsial infection is increasing. Because of the rarity of rickettsial infections in this country, diagnosis may be delayed. Delays in diagnosing these illnesses can adversely affect the potential for recovery. In this chapter Tables 371-1 through 371-3 are included that summarize (1) the epidemiologic features of rickettsial infections; (2) the host cells involved in the pathogenesis of the clinical manifestations of the disease; and (3) those clinical features that will assist in differentiating the various forms of rickettsial infections. Additional details on the major rickettsial infections that occur in the United States or that represent potential threats to persons traveling abroad are found under separate sections in this chapter. The first two conditions are induced by Rickettsia prowazekii, a pathogen transferred from person to person by the bite of body lice. Persons who have recovered from epidemic typhus have persistent rickettsiae in various host cells, presumably in the reticuloendothelial cells; stresses that cause a defect in the suppressive lymphocytes will, years later, permit these rickettsiae to be reactivated, resulting in a mild typhus-like illness, called Brill-Zinsser disease. A number of persons acquired typhus fever from squirrels living in their attics and probably harboring infected fleas or lice or both. It has been implicated by serologic means as the cause of acute febrile cerebrovasculitis in one patient. Epidemic Louse-Borne Typhus Synonyms include classic, historic, and European typhus; jail, war, camp, and ship fever; Flichfieber (German); typhus exanthematique (French); and tifus exantematico and tabardillo (Spanish). Many of these names indicate the location of the outbreaks-military and concentration camps, crowded ships with poor and starved immigrants, outbreaks in persons living in occupied countries during wartime, and so forth. Each implies crowded, unsanitary living conditions where bathing and laundry facilities are inadequate. Classic typhus fever is manifested by the sudden onset of headache, fever, rash, and an altered mental state. Dogs Tick bite At least 30 states in United States, Europe, and Africa At least 11 U. Viable rickettsiae stimulate the endothelial cell to act like a phagocyte to engulf the rickettsiae in a phagosome and internalize it. If rickettsiae do not break out of the phagosome promptly they begin to disintegrate, perhaps owing to enzymatic activities. The rickettsiae have an enzyme, phospholipase A, that enables them to lyse the phagosome wall and to multiply freely in the cytoplasm. The necrotic cell stimulates an inflammatory response that leads to the vasculitis and subsequent clotting abnormalities. Rare 4-6 7 (3-11) 7 (3-19) 7 (3-11) Relatively mild Moderate Relatively mild Relatively mild 48 (occasionally slow) 72 10-19 (2-21) Occasionally subacute or chronic infections occur.
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Tissue damage is induced by either toxin production or immune complex reaction with release of proteolytic enzymes. Immune complexes consisting of variant antigens of the organism and complement-fixing antibodies have been demonstrated in both the circulation and the target organs of infected patients. The production of autoantibodies is a prominent feature, and they are frequently directed against antigen components of red cells, brain, and heart. Thus the host-parasite interaction can result in generalized febrile episodes, lymphadenopathy, and myocardial and pericardial inflammation, along with anemia, thrombocytopenia, disseminated intravascular coagulation, and renal disease primarily during the acute stage of the disease. The meninges are thickened and infiltrated with lymphocytes, plasma cells, and morular cells. Morular cells are modified plasma cells (up to 20 mm in diameter) with large granular inclusions that have been shown to consist of immunoglobulin. Edema, hemorrhages, and granulomatous lesions are frequently present, along with thrombosis as a result of endarteritis and with neuronal degeneration. African trypanosomes appear to induce a state of B cell polyclonal activation caused either by interference with host T cell control of antibody production or by a B cell mitogen released by the parasite. Polyclonal hypergammaglobulinemia, with very high levels of IgM, is commonly seen. High levels of nonspecific heterophile antibody, rheumatoid factor, and autoantibodies are also produced. However, this difference is not absolute; in some cases Gambian sleeping sickness can progress rapidly, and occasionally Rhodesian sleeping sickness may follow a more chronic course. Gambian Sleeping Sickness Within several days following the bite by an infected tsetse fly, a trypanosomal nodule or chancre develops, typically on the exposed parts of the body. Within a week the lesion becomes a hard, painful nodule surrounded by erythema and swelling, which persists for 1 to 2 weeks. After this incubation period, clinical features develop after systemic, lymphatic, and circulatory invasion of the trypanosomes. Lymphadenopathy with prominent supraclavicular and posterior cervical enlargement is seen in > 80% of infected individuals. Moderate splenomegaly may occur, and urticaria and erythematous rashes have also been observed. Electrocardiograms are often abnormal, but clinical signs of heart disease are unusual. Six months to several years after symptoms first appear, the clinical features of this early hemolymphatic stage progress to a late meningoencephalitic stage. Later, more florid psychological changes may occur, with hallucinations and delusions. Reversion of sleep rhythm is characteristic, with drowsiness during the day, a feature from which the disease derives its name. Alterations in thermoregulation may lead to hypothermia or hyperthermia, and progressive neurologic alterations lead to convulsions, chorea, and athetosis. Adrenal insufficiency, hypothyroidism, and hypogonadism are frequently observed, and pituitary function tests suggest an unusual combined central (hypothalamic/pituitary) and 1953 peripheral defect in hormone secretion. Rhodesian Sleeping Sickness this disease is more acute than Gambian sleeping sickness, and symptoms usually occur a few days after the victim has been bitten by the tsetse fly. Alternating periods of high fever, malaise, and headache, followed by several days of well-being, are often misinterpreted as acute malaria infection. Anemia, thrombocytopenia, and disseminated intravascular coagulation are usually evident within the first several weeks of infection. Liver enzyme values are often elevated, and electrocardiograms are abnormal, usually reflecting underlying myocarditis. Neurologic features are similar to those described for Gambian sleeping sickness, but they occur much earlier and with more rapid deterioration. Without treatment the disease may result in death within a matter of weeks to months, without clear distinction into an early and late phase, as described for Gambian trypanosomias. Following centrifugation, the buffy coat can be examined and trypanosomes fluoresce greenish yellow, remain motile, and are easily identified. In patients with Gambian sleeping sickness, in which trypanosomes are found less frequently in the blood, concentration methods such as anion exchange chromatography, diethylaminoethyl Figure 422-1 Life cycle of Trypanosoma (Trypanozoon) brucei, T. The dose is 20 mg per kilogram of body weight given intravenously up to a maximum single dose of 1 gram. Suramin binds to plasma proteins and may persist in the circulation at low concentrations for as long as 3 months.
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Figure 8 presents the meta-analysis results, along with study-specific event rates. Studies had varying sample sizes (minimum = 149; maximum = 1354) and reported a total of 228 events. Figure 9 presents the meta-analysis results, along with study-specific event rates. Studies were relatively small (sample sizes were 154 and 294) and reported a small number of outcome events (15 events total). However, the estimate was extremely imprecise, reflecting the small number of patients contributing information to the meta-analysis, the very small number of observed events. Studies had varying sample sizes (minimum = 129; maximum = 1343) and reported a total of 344 events. However, the estimate was somewhat imprecise, reflecting the relatively small number of studies contributing information to the metaanalysis. Studies were small (sample sizes of 153 and 229) and reported a small number of outcome events (59 events total). Figure 10 presents the meta-analysis results, along with study-specific event rates. None of the comparisons were statistically significant, and study-specific estimates of effect were very imprecise. The difference in mean or median length of stay between groups ranged from -5 days to 4. Patient Satisfaction and Quality of Life No studies reported information on patient satisfaction and quality of life using appropriate measurement scales. Other Outcomes No studies provided information on other prespecified effectiveness outcomes for this Key Question (unplanned ostomies, failed attempts to restore bowel continuity, readmissions after surgery, additional interventional procedures (other than surgery); admission to intensive care unit, admission to nursing care). These analyses produced results that were consistent with our main analyses (presented above). We also examined whether our results were robust to the choice of alternative analysis methods. Appendix D presents sensitivity analyses for Bayesian pairwise meta-analyses with respect to the choice of alternative prior distributions for the between-studies variance parameter. Appendix E presents results of frequentist (non-Bayesian) analyses for all outcomes and all comparisons presented in the preceding section. Overall, none of these analyses produced results that were qualitatively different from those our main analyses (presented above). Risk of Bias Assessment for Individual Studies Information on trial design needed to assess the risk of bias of individual studies was not fully reported. In addition, blinding of patients, care providers, and outcome assessors was unclear in 14, 10, and 12 of the studies, respectively. Overall, based on the number of items considered indicative of Low risk, eight studies were considered to be at high risk of bias, nine to be at intermediate risk of bias, and one to be at low risk of bias. As always, aggregated risk of bias assessments need to be interpreted with caution, given our inability to fully distinguish inappropriate study design from poor reporting and lack of context-specific evidence that the risk items we assessed are indeed associated with bias. Anatomic Location Using published data and information obtained though author contact, separate analyses by anatomic location were possible for the outcome of anastomotic leakage (data were insufficient for other outcomes). There was limited evidence of effect modification by anatomic location; however, summary estimates were imprecise and evidence was available only from 10 studies (11 publications) that used heterogeneous subgroup definitions. Thus, definitive conclusions about the presence of temporal trends could not be drawn. However, CrIs were wide, indicating substantial uncertainty regarding differences across studies. Clearly, appropriate (and well-reported) procedures of allocation concealment are preferable in any clinical trial. These findings in conjunction with the wide credible intervals observed in the overall meta-analysis support the need for more research. Other risk of bias items were poorly reported and did not show adequate variation across studies; for this reason they were not considered in meta-regression analyses. Because of heterogeneity in patient selection and outcomes reported, differences in study design, and concerns regarding risk for residual confounding we did not perform metaanalysis. The study found no statistically significant difference between the two groups for the outcomes of all-cause mortality, wound dehiscence, wound infection, anastomotic leakage, thrombophlebitis, or the need for repeat laparotomy. For all outcomes, estimates of effect were very imprecise and no between-group difference was statistically significant.
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None of these treatments, including penicillin, prevents post-streptococcal glomerulonephritis. Group A streptococcus is the most common cause of cellulitis; however, alternative diagnoses may be obvious when associated with a primary focus such as an abscess or boil (S. Clinical clues to diagnosis are important because aspiration of the leading edge or punch biopsy yields a causative organism in only 15 and 40% of cases, respectively. Patients with lymphedema of any cause such as lymphoma, filariasis, or sequelae of regional lymph node dissection (as in mastectomy or carcinoma of the prostate) are predisposed to streptococcal cellulitis, as are patients with chronic venous stasis. Recently, recurrent saphenous vein donor site cellulitis has been attributed to group A, C, or G streptococci. Group A streptococci may invade the epidermis and subcutaneous tissue and cause local swelling, erythema, and pain. The skin becomes indurated and, unlike the brilliant redness of erysipelas, is pinkish. Streptococcal cellulitis responds quickly to penicillin, although when staphylococcus is of concern, nafcillin or oxacillin may be a better choice. If fever, pain, or swelling increases, if bluish or violet bullae or discoloration appears, or if signs of systemic toxicity develop, a deeper infection such as necrotizing fasciitis or myositis should be considered (see Necrotizing Fasciitis). When an elevated serum creatine phosphokinase level suggests deeper infection, prompt surgical inspection and debridement should be performed. Cutaneous infection with bright red streaks ascending proximally is invariably due to group A streptococcus. Prompt parenteral antibiotic treatment is mandatory because bacteremia and systemic toxicity develop rapidly once streptococci reach the blood stream via the thoracic duct. Necrotizing fasciitis, originally called 1622 "streptococcal gangrene," is a deep-seated infection of the subcutaneous tissue that results in progressive destruction of fascia and fat but may spare the skin itself. Subsequently, "necrotizing fasciitis" has become the preferred term because Clostridium perfringens, Clostridium septicum, and S. Within the initial 24 hours, swelling, heat, erythema, and tenderness develop and rapidly spread proximally and distally from the original focus. During the next 24 to 48 hours, the erythema darkens, changing from red to purple and then to blue, and blisters and bullae form that contain clear yellow fluid. From the 7th to the 10th days, the line of demarcation becomes sharply defined, and the dead skin begins to reveal extensive necrosis of the subcutaneous tissue. Patients become increasingly prostrated and emaciated and may become unresponsive, mentally cloudy, or even delirious. Since 1989, the mortality rate of necrotizing fasciitis despite antibiotics, surgical debridement, and intensive care unit treatment is higher than that reported by Meleney in 1924, probably because of the increased virulence of streptococci (see Streptococcal Toxic Shock Syndrome below). Historically, streptococcal myositis has been an extremely uncommon infection, only 21 cases being documented from 1900 to 1985. Recently, the prevalence of streptococcal myositis has increased in the United States, Norway, and Sweden. Translocation of streptococci from the pharynx to the deep site of trauma (muscle) must occur hematogenously. Severe pain may be the only symptom, and swelling and erythema may be the only signs of infection. In some cases a single muscle group is involved; however, because patients are frequently bacteremic, multiple sites of myositis or abscess can occur. Myositis is easily distinguished from necrotizing fasciitis anatomically by surgical exploration or incisional biopsy, although the clinical features of both conditions overlap. In published reports, the case fatality rate of necrotizing fasciitis is between 20 and 50%, whereas that of streptococcal myositis is between 80 and 100%. Aggressive surgical debridement is extremely important because of the poor efficacy of penicillin described in human cases, as well as in experimental models of streptococcal myositis (see the section on antibiotic efficacy). Pneumonia caused by group A streptococcus is most common in women in the 2nd and 3rd decades of life and causes large pleural effusions and empyema that develop rapidly. Chest tube drainage is mandatory even though management is complicated by multiple loculations and fibrinous effusions resulting in restrictive lung disease. Prolonged penicillin therapy, thoracoscopy, and decortication of the pleura may be necessary to prevent adhesive pleuritis, fibrosis, and subsequent restrictive lung disease. In the late 1980s, invasive group A streptococcal infections occurred in North America and Europe in previously healthy individuals aged 20 to 50. This illness is associated with bacteremia, deep soft tissue infection, shock, multiorgan failure, and death in 30% of cases.
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Fibromuscular dysplasia predominates in women and occurs, on the average, in the sixth decade of life. It produces ischemic stroke both by the hemodynamic effects of stenosis and by thromboembolism. The condition is also associated with aneurysm formation and with arterial dissection. A dissecting aortic aneurysm, although uncommon, can occlude major branches of the aorta supplying the cranial circulation and produce ischemic strokes. Chest, back, or abdominal pain accompanying the stroke and differences in palpable pulses or in blood pressure in the limbs suggest the diagnosis. Some are associated with fibromuscular dysplasia, others with a variety of childhood conditions, including Ehlers-Danlos and Marfan syndromes and tuberous sclerosis. Pathologically, intraluminal blood enters the subintimal or medial vascular planes, and the lumen becomes progressively narrowed and thrombosed. Carotid artery dissections can sometimes be recognized clinically by intense ipsilateral pain. Homocystinuria is characterized by dislocated ocular lenses, bone deformities, a marfanoid appearance, mental retardation, accelerated atherosclerosis, and arterial or venous thromboses. Several different genetic defects can cause homocystinuria, but the most frequent is a deficiency of the enzyme cystathionine beta-synthase. Approximately one third of affected individuals have one or more strokes by the age of 15 years. In some studies, heterozygous homocystinuria has been reported in up to one quarter of young persons who have suffered strokes. Moderately elevated plasma homocysteine levels without clinical signs of severe homocysteinemia or homocystinuria is also an independent risk factor for cerebrovascular disease. Vasospasm also presumably explains ischemic strokes seen in a small number of patients with migraine headaches. Migraineurs develop ischemic strokes, either in conjunction with migraine (in which case they appear to result from a prolonged migraine attack) or remote from the attack (in which case more traditional stroke mechanisms, such as atherosclerosis, are likely to be responsible). Although focal ischemic strokes may occur, more typically the condition manifests with seizures and a diffuse encephalopathy consistent with disseminated embolization. Associated findings include petechiae, and fat emboli visible on funduscopic examination. Air emboli can occur with open heart surgery, in patients with pneumothorax, or in divers who ascend too rapidly to the surface. Air emboli cause altered mental status and seizures, but the changes are maximal immediately after the embolization. Segmental areas of pallor may be observed on the tongue, and there may be marbling of the skin and air emboli seen on funduscopic examination. When caused by sudden decompression, the condition is treated in a decompression chamber. Moyamoya is a rare condition that is most common among the Japanese, in whom it has been reported to affect fewer than 0. An abnormal vascular network develops at the base of the brain that is believed to provide collateral circulation. The abnormal collateral channels appear on angiograms as a "smoky haze," hence the Japanese term moyamoya. The cause of the vascular occlusion is unknown, but it occurs most commonly in children (peak incidence at age 6 years), in whom it may be associated with ischemic stroke; in adults, it more commonly causes hemorrhage. A similar angiographic picture occasionally accompanies acute tonsillitis, atherosclerosis, meningitis, cancer, trauma, and radiotherapy. A condition in which the walls of small arteries are thickened and disorganized, referred to by some as lipohyalinosis, was originally believed to underlie small; subcortical brain infarcts called lacunes. Traditional causes of stroke, including diabetes and hyperlipidemia, have appeared in these patients with almost the same frequency as in those with nonlacunar, ischemic stroke. Perhaps as a result, treatment recommendations, which initially differed for lacunar strokes, now parallel those for nonlacunar strokes. The reduction of stroke risk factors, through therapy for hypertension, diabetes mellitus, smoking, atherosclerosis, and cardiac arrhythmias (Table 470-3) is largely responsible for the marked decline in the incidence of stroke during the past 30 to 40 years. Treatable risk factors are emphasized, and the expected outcome of such prophylactic therapy is presented.
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Rattus rattus and Rattus norvegicus are two species of rats that can sustain the R. The rat flea disseminates the infection not through its bite but by placing contaminated feces on the skin. These may be rubbed or scratched into the skin; they can be carried to the conjunctival sac 1771 or mucous membranes on the fingers, where the rickettsiae can invade; or they can be aerosolized after drying and cause infection if inhaled. In the flea, the rickettsiae multiply in the enterocytes in the gut, do not kill the flea, and continue to be shed in the feces for the life of the flea. In the previous 10 years, the number ranged from 28 to 67 annually, with Texas and California having the highest numbers. Descriptions of the pathologic lesions in this disease are few because of the rarity of fatal cases. Because the rickettsiae are known to invade endothelial cells, the pathologic consequences should mimic those seen in other rickettsial infections. The reasons for the differences in virulence of these rickettsiae and the varying severity of illnesses produced are unknown. A faint macular-papular pink-colored rash appears in about 80% of patients after 4 to 5 days of illness. Rarely are there any significant complications of this infection, but because it is an infection of the endothelial cells, a vasculitis can cause widespread organ derangement. This disease has no distinguishing characteristics during the early days of symptoms. The rash appearing on the fourth or fifth day should alert the physician to the possibility of a rickettsial infection. Flea bites, if seen early, are discrete and may have a central hemorrhagic punctum. They occur in covered parts of the body, in irregular groups of several to a dozen or more, in the region of the belt, shoulders, and hips, or on the legs. In murine typhus the lesions are on the skin of the chest and abdomen and rarely on the extremities. This test, however, does not distinguish murine typhus from the spotted fever group of infections. Isolating the organism is possible but should be done only in special laboratories where containment facilities are available. Appropriate antibiotic treatment results in prompt cure, and the mortality rate is reduced almost to zero. Tetracycline and chloramphenicol are effective for treating this rickettsial infection. The usual dosage of 25 mg/kg of tetracycline per day in four doses or chloramphenicol, 50 mg/kg/day in four doses, effects a prompt cure. Relapses do occur when antibiotics are administered early in the course of the illness. When rat control programs are instituted, appropriate insecticides should be simultaneously used to prevent the fleas from seeking humans for feeding as the rat population is decreased. It is a sometimes fatal systemic infection manifested by fever, severe headache, rash, and other organ disease caused by the vasculitis induced by Rickettsia rickettsii. The organism is usually transmitted to humans from animal reservoirs by a tick bite. In human infections the rickettsiae invade and multiply within endothelial cells of arteries and veins. Attempts to correlate virulence with structural components in the polysaccharide portion of the cell wall have been unsuccessful. This disease was named for the geographic site of its original discovery; the causative agent was named for the discoverer, Howard T. By the 1940s the disease had become more common on the East Coast than in the West. Serologic surveys in children and adults in North Carolina, the state with the highest number of reported cases, demonstrate that subclinical infections occur. Ninety per cent of reported cases occur between April 1 and September 30, with two thirds in May, June, and July.