Barbed sutures first received US Food and Drug Administration approval for soft tissue approximation in 2005 and early adopters readily embraced this device to develop new techniques. It has become apparent that the advantages are more than just "skin deep." Superficial and deep fascia, cartilage, tendon, joint capsule, and fibrous periprosthetic capsules can also be manipulated. Barbed sutures have revolutionized our approach to facial rejuvenation and body contouring by enhancing our ability to quilt and powerfully lift tissue. The elimination of surgical drains and shorter surgical times has made this a true boon for plastic surgeons as well as many other surgical specialists. This article summarizes some of the current and evolving applications of this exciting new tool.

Proper placement of sutures enhances the precise approximation of the wound edges, which helps minimize and redistribute skin tension. Wound eversion is essential to maximize the likelihood of good epidermal approximation. Eversion is desirable to minimize the risk of scar depression secondary to tissue contraction during healing. Usually, inversion is not desirable, and it probably does not decrease the risk of hypertrophic scarring in an individual with a propensity for hypertrophic scars. The elimination of dead space, the restoration of natural anatomic contours, and the minimization of suture marks are also important to optimize the cosmetic and functional results.

Liposuction procedure under local anesthesia.

Excision of Pilonidal Cyst. Open method.

Interstitial cystitis is a clinical syndrome characterized by daytime and nighttime urinary frequency, urgency, and pelvic pain of unknown etiology. Interstitial cystitis has no clear etiology or pathophysiology, and diagnostic criteria for the syndrome remain undefined. Despite considerable research, universally effective treatments do not exist; therapy usually consists of various supportive, behavioral, and pharmacologic measures. Surgical intervention is rarely indicated. The International Continence Society has coined the term painful bladder syndrome (suprapubic pain with bladder filling associated with increased daytime and nighttime frequency, in the absence of proven urinary infection or other obvious pathology) and reserves the diagnosis of interstitial cystitis for patients with characteristic cystoscopic and histologic features of the condition.[1] An international consensus panel was able to generally agree on the following definition of interstitial cystitis/bladder pain syndrome (IC/BPS): unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder and associated with lower urinary tract symptoms of more than 6 weeks duration, in the absence of infection or other identifiable causes. American Urological Association (AUA) guidelines published in 2011 and amended in 2014 use an evidence-based approach to provide a clinical framework for the diagnosis and management of this condition.[2, 3, 4] In 1887, Skene initially described a condition characterized by inflammation that destroyed the urinary bladder "mucous membrane partly or wholly and extended to the muscular parietes." Guy Hunner popularized the disease with the description of characteristic bladder wall ulcers in association with a symptom complex of chronic bladder inflammation.[5] The first comprehensive epidemiologic description of interstitial cystitis is credited to Hand, who in 1949 described the widespread, small, submucosal bladder hemorrhages and the significant variation in bladder capacity characteristic of the condition. Despite years of intensive research, there are no specific clinical or urinary markers currently clinically available; no absolutely specific radiographic, laboratory, or serologic findings; and no biopsy patterns that are pathognomonic for interstitial cystitis. Some research suggests that the following may all play a role in the disease pathophysiology: (1) pelvic floor dyfunction, (2) dysregulated immune or inflammatory signals, (3) neural hypersensitivity, and (4) disruption of the proteoglycan/glycosaminoglycan (GAG) layer.[6] Interstitial cystitis, howerver, remains a diagnosis of exclusion (see Presentation, DDx, and Workup.) Intensive study has been done to attempt to identify biomarkers for IC/BPS. Some interesting studies have shown that bladder nitric oxide is an accurate marker for Hunner lesions, but these are not present in all patients, and the test requires specific equipment, which has limited widespread clinical use.[7] Differences in levels of cytokines and chemokines, specifically CXCL-10, have shown some ability to differentiate patients with and without Hunner lesions.[8] Other studies of ulcerative IC/BPS have shown that numerous other cytokines and chemokines are up-regulated as well, heralding a possible urinary test to identify patients.[9] An additional substance shown to be up-regulated in IC/BPS patients is antiproliferative factor (APF). This small 8–amino-acid peptide has been associated with suppression of cell growth, increases in transcellular permeability, and lowering of levels of proteins that form intercellular junctional complexes. It is synthesized and secreted from bladder epithelial cells from patients with IC/BPS and may play a key role in pathophysiology.[10] In vitro studies have shown that removal of APF from cell culture media restored cell proliferation and membrane integrity.[11] Studies have also suggested APF in the therapeutic effect of hydrodistension in patients with IC/BPS, although further confirmatory studies are necessary.[12] The most important element in treating patients with interstitial cystitis is education and emotional support. Periodic exacerbations are managed as they occur because no long-term therapy has been shown to prevent or delay recurrent episodes. Therefore, the purpose of treatment is to palliate and alleviate symptoms. Because no discrete pathognomonic pathologic criteria exist for assessing and monitoring disease severity, indications and goals for treatment are based on the degree of patient symptoms. Assessing patient response to treatment is also complicated because of the subjective nature of symptoms; the waxing and waning nature of symptoms without treatment; and the lack of objective serologic, physical, or histopathologic findings. Conservative measures and oral or intravesical treatments are considered first-line treatment. (See Treatment.)

What is polycystic kidney disease? Polycystic kidney disease (also called PKD) causes numerous cysts to grow in the kidneys. These cysts are filled with fluid. If too many cysts grow or if they get too big, the kidneys can become damaged. PKD cysts can slowly replace much of the kidneys, reducing kidney function and leading to kidney failure. How common is PKD? In the United States about 600,000 people have PKD. It is the fourth leading cause of kidney failure. It is found in all races and occurs equally in men and women. It causes about 5% of all kidney failure. What other organs besides the kidney are affected by PKD? PKD can affect other organs besides the kidney. People with PKD may have cysts in their liver, pancreas, spleen, ovaries, and large bowel. Cysts in these organs usually do not cause serious problems, but can in some people. PKD can also affect the brain or heart. If PKD affects the brain, it can cause an aneurysm. An aneurysm is a bulging blood vessel that can burst, resulting in a stroke or even death. If PKD affects the heart, the valves can become floppy, resulting in a heart murmur in some patients. What are the clues that someone has PKD? Most people do not develop symptoms until they are 30 to 40 years old. The first noticeable signs and symptoms may include: Back or side pain An increase in the size of the abdomen Blood in the urine Frequent bladder or kidney infections High blood pressure High blood pressure is the most common sign of PKD. Occasionally, patients may develop headaches related to high blood pressure or their doctors may detect high blood pressure during a routine physical exam. Because high blood pressure can cause kidney damage, it is very important to treat it. In fact, treatment of high blood pressure can help slow or even prevent kidney failure. Fluttering or pounding in the chest About 25% of PKD patients have a so-called floppy valve in the heart, and may experience a fluttering or pounding in the chest as well as chest pain. These symptoms almost always disappear on their own but may be the first hint that someone has PKD. How is PKD diagnosed? Ultrasound is the most reliable, inexpensive and non-invasive way to diagnose PKD. If someone at risk for PKD is older than 40 years and has a normal ultrasound of the kidneys, he or she probably does not have PKD. Occasionally, a CT scan (computed tomography scan) and MRI (magnetic resonance imaging) may detect smaller cysts that cannot be found by an ultrasound. MRI is used to measure and monitor volume and growth of kidneys and cysts. In some situations, genetic testing might also be done. This involves a blood test that checks for abnormal genes that cause the disease. Genetic testing is not recommended for everyone. The test is costly, and it also fails to detect PKD in about 15% of people who have it. However, genetic testing can be useful when a person: has an uncertain diagnosis based on imaging tests has a family history of PKD and wants to donate a kidney is younger than 30-years old with a family history of PKD and a negative ultrasound, and is planning to start a family

10 Animals Found Living Inside Humans

10 Diseases That Will Kill You In A Day

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.

An aortic dissection is a serious condition in which the inner layer of the aorta, the large blood vessel branching off the heart, tears. Blood surges through the tear, causing the inner and middle layers of the aorta to separate (dissect). If the blood-filled channel ruptures through the outside aortic wall, aortic dissection is often fatal. Aortic dissection is relatively uncommon. The condition most frequently occurs in men in their 60s and 70s. Symptoms of aortic dissection may mimic those of other diseases, often leading to delays in diagnosis. However, when an aortic dissection is detected early and treated promptly, the chance of survival greatly improves.

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

Ultrasound of Heart

ECG Learn it

EKG Interpretation Part 3

ECG

EKG Interpretation Part 1

What Causes Ulcers? No single cause has been found for ulcers. However, it is now clear that an ulcer is the end result of an imbalance between digestive fluids in the stomach and duodenum. Most ulcers are caused by an infection with a type of bacteria called Helicobacter pylori (H. pylori). Factors that can increase your risk for ulcers include: Use of painkillers called nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, naproxen (Aleve, Anaprox, Naprosyn, and others), ibuprofen (Motrin, Advil, some types of Midol, and others), and many others available by prescription; even safety-coated aspirin and aspirin in powered form can frequently cause ulcers. Excess acid production from gastrinomas, tumors of the acid producing cells of the stomach that increases acid output (seen in Zollinger-Ellison syndrome) Excessive drinking of alcohol Smoking or chewing tobacco Serious illness Radiation treatment to the area What Are the Symptoms of an Ulcer? An ulcer may or may not have symptoms. When symptoms occur, they may include: A gnawing or burning pain in the middle or upper stomach between meals or at night Bloating Heartburn Nausea or vomiting In severe cases, symptoms can include: Dark or black stool (due to bleeding) Vomiting blood (that can look like "coffee-grounds") Weight loss Severe pain in the mid to upper abdomen

Esophageal varices are abnormal, enlarged veins in the tube that connects the throat and stomach (esophagus). This condition occurs most often in people with serious liver diseases. Esophageal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren't designed to carry large volumes of blood. The vessels can leak blood or even rupture, causing life-threatening bleeding. A number of drugs and medical procedures can help prevent and stop bleeding from esophageal varices.

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.

Hepatitis is an inflammation of the liver. The condition can be self-limiting or can progress to fibrosis (scarring), cirrhosis or liver cancer. Hepatitis viruses are the most common cause of hepatitis in the world but other infections, toxic substances (e.g. alcohol, certain drugs), and autoimmune diseases can also cause hepatitis. There are 5 main hepatitis viruses, referred to as types A, B, C, D and E. These 5 types are of greatest concern because of the burden of illness and death they cause and the potential for outbreaks and epidemic spread. In particular, types B and C lead to chronic disease in hundreds of millions of people and, together, are the most common cause of liver cirrhosis and cancer. Hepatitis A and E are typically caused by ingestion of contaminated food or water. Hepatitis B, C and D usually occur as a result of parenteral contact with infected body fluids. Common modes of transmission for these viruses include receipt of contaminated blood or blood products, invasive medical procedures using contaminated equipment and for hepatitis B transmission from mother to baby at birth, from family member to child, and also by sexual contact. Acute infection may occur with limited or no symptoms, or may include symptoms such as jaundice (yellowing of the skin and eyes), dark urine, extreme fatigue, nausea, vomiting and abdominal pain.