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Whereas it is true that no operation has been profoundly affected by the advent of laparoscopy than cholecystectomy has, it is equally true that no procedure has been more instrumental in ushering in the laparoscopic age than laparoscopic cholecystectomy has. Laparoscopic cholecystectomy has rapidly become the procedure of choice for routine gallbladder removal and is currently the most commonly performed major abdominal procedure in Western countries.[1] A National Institutes of Health consensus statement in 1992 stated that laparoscopic cholecystectomy provides a safe and effective treatment for most patients with symptomatic gallstones and has become the treatment of choice for many patients.[2] This procedure has more or less ended attempts at noninvasive management of gallstones. The initial driving force behind the rapid development of laparoscopic cholecystectomy was patient demand. Prospective randomized trials were late and largely irrelevant because advantages were clear. Hence, laparoscopic cholecystectomy was introduced and gained acceptance not through organized and carefully conceived clinical trials but through acclamation. Laparoscopic cholecystectomy decreases postoperative pain, decreases the need for postoperative analgesia, shortens the hospital stay from 1 week to less than 24 hours, and returns the patient to full activity within 1 week (compared with 1 month after open cholecystectomy).[3, 4] Laparoscopic cholecystectomy also provides improved cosmesis and improved patient satisfaction as compared with open cholecystectomy. Although direct operating room and recovery room costs are higher for laparoscopic cholecystectomy, the shortened length of hospital stay leads to a net savings. More rapid return to normal activity may lead to indirect cost savings.[5] Not all such studies have demonstrated a cost savings, however. In fact, with the higher rate of cholecystectomy in the laparoscopic era, the costs in the United States of treating gallstone disease may actually have increased. Trials have shown that laparoscopic cholecystectomy patients in outpatient settings and those in inpatient settings recover equally well, indicating that a greater proportion of patients should be offered the outpatient modality

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Waterhouse–Friderichsen syndrome (WFS), hemorrhagic adrenalitis or fulminant meningococcemia is defined as adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection: Typically the pathogen is the meningococcus Neisseria meningitidis.

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Epididymitis is infection or less frequently, inflammation of the epididymis (the coiled tube on the back of the testicle). The majority of men that develop epididymitis develop it because of a bacterial infection. Although males of any age can develop epididymitis, it occurs most frequently between ages of 20 to 39.

The hepatitis E virus, responsible for major epidemics of viral hepatitis in subtropical and tropical countries, was cloned only 7 years ago.1 Hepatitis E was found to belong to the family of Caliciviridae, which includes the Norwalk virus—a common cause of gastroenteritis in humans—and consists of a single, plus-strand RNA genome of approximately 7.2 kb without an envelope (Fig. 1). The virus contains at least three open reading frames encoding viral proteins against which antibodies are made on exposure. These antibodies, especially those against the capsid protein derived from the second open reading frame2 and a protein of unknown function derived from the third open reading frame, are detected by currently available serologic assays. Retrospective studies on stored sera of past epidemics of viral hepatitis in Mexico, Africa, Afghanistan, Pakistan, India, Bangladesh, Burma, Nepal, and Borneo have revealed that all were caused by strains of hepatitis E. In addition, hepatitis E was found to be responsible for the hepatitis epidemic in the southern part of Xinjiang, China, in which 120,000 persons became infected between September 1986 and April 1988.3 Hepatitis E predominantly affects young adults (15 to 40 years old). The symptoms of hepatitis E are similar to those of hepatitis A. Frequently, a prodrome consisting of anorexia, nausea, low-grade fever, and right upper abdominal pain is present 3 to 7 days before jaundice develops. Aminotransferase levels peak (usually between 1,000 and 2,000 U/L) near the onset of symptoms; bilirubin levels (10 to 20 mg/dL) peak later. Jaundice usually resolves after 1 to 2 weeks. In about 10% of cases, the disease is fulminant—especially in pregnant women, among whom mortality rates as high as 20% due to hemorrhagic and thrombotic complications have been reported. No evidence has suggested that hepatitis E can cause chronic infection. Transmission is by the fecal-oral route, predominantly through fecally contaminated drinking water supplies. In addition, however, preliminary reports have suggested transmission of the hepatitis E virus through blood transfusions. Volunteer studies confirmed the presence of the virus in serum and feces before and during clinical disease.4 The virus is shed into feces approximately 1 week before symptoms develop. The incubation period varies from 2 to 9 weeks (mean duration, approximately 45 days). Until now, a few reports had described symptomatic hepatitis E acquired in Europe;5, 6 all patients with symptomatic hepatitis E in the United States were travelers returning from Mexico, Africa, or the Far East, in whom hepatitis E developed after their return home.7 In this issue of the Mayo Clinic Proceedings (pages 1133 to 1136), Kwo and associates describe a case of hepatitis E in a man who had not left the United States during the previous 10 years. Specific serologic tests for hepatitis E virus IgG (enzyme immunoassays and a fluorescent antibody blocking assay) and IgM8 (US strain-specific enzyme-linked immunosorbent assay with use of synthetic polypeptides deduced from the viral genome, as shown in Figure 1), developed at Abbott Laboratories (IgG and IgM) as well as at the Centers for Disease Control and Prevention (IgG), were used to prove that the patient indeed had acute hepatitis E. Researchers at Abbott Laboratories have prepared a report that describes most of the viral genome in this patient (Fig. I).8 Their results are interesting because this strain from the United States differs considerably from hepatitis E strains isolated in Mexico, Burma, Pakistan, or China. Furthermore, the sequence of the US strain is highly homologous (98% and 94% homology at the amino acid level to the second and third open reading frames, respectively) to a recently isolated hepatitis E strain from American swine.9 This finding suggests that, in the United States, hepatitis E is a zoonosis with the swine population as one of its hosts. This relationship would confirm earlier studies in Asia, where swine were also found to carry variants of the hepatitis E virus.10 Why are these two recent discoveries important for medicine in the United States? First, other sporadic, locally acquired cases of acute hepatitis may be caused by hepatitis E. Second, these back-to-back discoveries strongly suggest that a common natural host for hepatitis E is present in countries with more moderate climates. Because swine do not seem to experience any symptoms associated with infection and because symptoms in humans can be minor or absent, we now may also have an explanation for the 1 to 2% of positive hepatitis E serologic results in blood donors in the United States,11 Netherlands,12 and Italy,6 countries with large swine staples. Clearly, more research needs to be done to confirm this hypothesis. Third, in countries with more moderate climates, hepatitis E may often result in a subclinical infection. Is this variation in manifestation due to less virulent strains, and do sequence variations determine virulence? Fourth, swine may be used as an animal model for study of the disease as well as vaccine development.

Medial medullary syndrome, also known as Dejerine syndrome, represents less than 1% of brainstem stroke syndromes. Thrombotic or embolic occlusion of small perforating branches from vertebral or proximal basilar artery supplying the medial aspect of medulla oblongata cause this rare syndrome. It is characterized by contralateral hemiplegia/hemiparesis as well as hemisensory loss with ipsilateral hypoglossal palsy (ipsilateral tongue weakness and atrophy) from involvement of CN XII nucleus. Other manifestations e.g. vertigo, nausea, ipsilateral limb ataxia are also reported.

Before the angioplasty procedure begins, you will receive some pain medicine. You may also be given medicine that relaxes you, and blood thinning medicines to prevent a blood clot from forming. You will lie on a padded table. Your doctor will insert a flexible tube (catheter) through a surgical cut into an artery. Sometimes the catheter will be placed in your arm or wrist, or in your upper leg or groin area. You will be awake during the procedure. The doctor will use live x-ray pictures to carefully guide the catheter up into your heart and arteries. Dye will be injected into your body to highlight blood flow through the arteries. This helps the doctor see any blockages in the blood vessels that lead to your heart. A guide wire is moved into and across the blockage. A balloon catheter is pushed over the guide wire and into the blockage. The balloon on the end is blown up (inflated). This opens the blocked vessel and restores proper blood flow to the heart. A wire mesh tube (stent) may then be placed in this blocked area. The stent is inserted along with the balloon catheter. It expands when the balloon is inflated. The stent is left there to help keep the artery open

A distal radius fracture almost always occurs about 1 inch from the end of the bone. The break can occur in many different ways, however. One of the most common distal radius fractures is a Colles fracture, in which the broken fragment of the radius tilts upward. This fracture was first described in 1814 by an Irish surgeon and anatomist, Abraham Colles -- hence the name "Colles" fracture.

What is Wallenberg syndrome? Wallenberg syndrome is a rare condition in which an infarction, or stroke, occurs in the lateral medulla. The lateral medulla is a part of the brain stem. Oxygenated blood doesn’t get to this part of the brain when the arteries that lead to it are blocked. A stroke can occur due to this blockage. This condition is also sometimes called lateral medullary infarction. The cause of the syndrome isn’t always clear, however.

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Asthma is a condition in which your airways narrow and swell and produce extra mucus. This can make breathing difficult and trigger coughing, wheezing and shortness of breath. For some people, asthma is a minor nuisance. For others, it can be a major problem that interferes with daily activities and may lead to a life-threatening asthma attack. Asthma can't be cured, but its symptoms can be controlled. Because asthma often changes over time, it's important that you work with your doctor to track your signs and symptoms and adjust treatment as needed.

Breast abscesses are often linked to mastitis – a condition that causes breast pain and swelling (inflammation), and usually affects women who are breastfeeding. Infections can occur during breastfeeding if bacteria enter your breast tissue, or if the milk ducts (tiny tubes) become blocked. This can cause mastitis which, if not treated, can result in an abscess forming. Women who aren't breastfeeding can also develop mastitis if bacteria enter the milk ducts through a sore or cracked nipple, or a nipple piercing. White blood cells are sent to attack the infection, which causes tissue at the site of the infection to die. This creates a small, hollow area that fills with pus (an abscess).

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Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently. Not all conditions that lead to heart failure can be reversed, but treatments can improve the signs and symptoms of heart failure and help you live longer. Lifestyle changes — such as exercising, reducing salt in your diet, managing stress and losing weight — can improve your quality of life. One way to prevent heart failure is to control conditions that cause heart failure, such as coronary artery disease, high blood pressure, diabetes or obesity.

Thoracentesis is a procedure in which a needle is inserted into the pleural space between the lungs and the chest wall. This procedure is done to remove excess fluid, known as a pleural effusion, from the pleural space to help you breathe easier. It may be done to determine the cause of your pleural effusion. Some conditions such as heart failure, lung infections, and tumors can cause pleural effusions.