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.

The objective of carotid endarterectomy (CEA) is to prevent strokes. In the United States, stroke is the third leading cause of death overall and the second leading cause of death for women.[1] Among patients suffering a stroke, 50-75% had carotid artery disease that would have been amenable to surgical treatment. Several prospective randomized trials have compared the safety and efficacy of CEA with those of medical therapy in symptomatic and asymptomatic patients. Data from these prospective trials have confirmed that CEA offers better protection from ipsilateral strokes than medical therapy alone in patients presenting with either symptomatic or asymptomatic carotid artery disease.

What is an Aneurysm? A cerebral or intracranial aneurysm is an abnormal focal dilation of an artery in the brain that results from a weakening of the inner muscular layer (the intima) of a blood vessel wall. The vessel develops a "blister-like" dilation that can become thin and rupture without warning. The resultant bleeding into the space around the brain is called a subarachnoid hemorrhage (SAH). This kind of hemorrhage can lead to a stroke, coma, and/or death. Aneurysms are usually found at the base of the brain just inside the skull, in an area called the subarachnoid space. In fact, 90 percent of SAHs are attributed to ruptured cerebral aneurysms and the two terms are often used synonymously.

Vesicoureteral (ves-ih-koe-yoo-REE-tur-ul) reflux is the abnormal flow of urine from your bladder back up the tubes (ureters) that connect your kidneys to your bladder. Normally, urine flows only down from your kidneys to your bladder. Vesicoureteral reflux is usually diagnosed in infants and children. The disorder increases the risk of urinary tract infections, which, if left untreated, can lead to kidney damage. Vesicoureteral reflux can be primary or secondary. Children with primary vesicoureteral reflux are born with a defect in the valve that normally prevents urine from flowing backward from the bladder into the ureters. Secondary vesicoureteral reflux is due to a urinary tract malfunction, often caused by infection. Children may outgrow primary vesicoureteral reflux. Treatment, which includes medication or surgery, aims at preventing kidney damage.

Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma. Most cases of COPD are the result of exposure to noxious stimuli, most often cigarette smoke. The normal inflammatory response is amplified in persons prone to COPD development. The pathogenic mechanisms are not clear but are most likely diverse. Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction. The primary offender has been found to be human leukocyte elastase, with synergistic roles suggested for proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells. Accelerated aging and autoimmune mechanisms have also been proposed as having roles in the pathogenesis of COPD.[5, 6] Cigarette smoke causes neutrophil influx, which is required for the secretion of MMPs; this suggests, therefore, that neutrophils and macrophages are required for the development of emphysema. Studies have also shown that in addition to macrophages, T lymphocytes, particularly CD8+, play an important role in the pathogenesis of smoking-induced airflow limitation. To support the inflammation hypothesis further, a stepwise increase in alveolar inflammation has been found in surgical specimens from patients without COPD versus patients with mild or severe emphysema. Indeed, mounting evidence supports the concept that dysregulation of apoptosis and defective clearance of apoptotic cells by macrophages play a prominent role in airway inflammation, particularly in emphysema.[7] Azithromycin (Zithromax) has been shown to improve this macrophage clearance function, providing a possible future treatment modality.[8] In patients with stable COPD without known cardiovascular disease, there is a high prevalence of microalbuminuria, which is associated with hypoxemia independent of other risk factors.[9] Chronic bronchitis Mucous gland hyperplasia (as seen in the images below) is the histologic hallmark of chronic bronchitis. Airway structural changes include atrophy, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening.

Migraine treatments can help stop symptoms and prevent future attacks. Many medications have been designed to treat migraines. Some drugs often used to treat other conditions also may help relieve or prevent migraines. Medications used to combat migraines fall into two broad categories: Pain-relieving medications. Also known as acute or abortive treatment, these types of drugs are taken during migraine attacks and are designed to stop symptoms. Preventive medications. These types of drugs are taken regularly, often on a daily basis, to reduce the severity or frequency of migraines. Your treatment strategy depends on the frequency and severity of your headaches, the degree of disability your headaches cause, and your other medical conditions. Some medications aren't recommended if you're pregnant or breast-feeding. Some medications aren't given to children. Your doctor can help find the right medication for you

Most of the time, treatment for hemorrhoids involves steps that you can take on your own, such as lifestyle modifications. But sometimes medications or surgical procedures are necessary. Medications If your hemorrhoids produce only mild discomfort, your doctor may suggest over-the-counter creams, ointments, suppositories or pads. These products contain ingredients, such as witch hazel or hydrocortisone, that can relieve pain and itching, at least temporarily. Don't use an over-the-counter cream or other product for more than a week unless directed by your doctor. These products can cause side effects, such as skin rash, inflammation and skin thinning. Minimally invasive procedures If a blood clot has formed within an external hemorrhoid, your doctor can remove the clot with a simple incision, which may provide prompt relief. For persistent bleeding or painful hemorrhoids, your doctor may recommend another minimally invasive procedure. These treatments can be done in your doctor's office or other outpatient setting. Rubber band ligation. Your doctor places one or two tiny rubber bands around the base of an internal hemorrhoid to cut off its circulation. The hemorrhoid withers and falls off within a week. This procedure — called rubber band ligation — is effective for many people. Hemorrhoid banding can be uncomfortable and may cause bleeding, which might begin two to four days after the procedure but is rarely severe. Injection (sclerotherapy). In this procedure, your doctor injects a chemical solution into the hemorrhoid tissue to shrink it. While the injection causes little or no pain, it may be less effective than rubber band ligation. Coagulation (infrared, laser or bipolar). Coagulation techniques use laser or infrared light or heat. They cause small, bleeding, internal hemorrhoids to harden and shrivel. While coagulation has few side effects, it's associated with a higher rate of hemorrhoids coming back (recurrence) than is the rubber band treatment. Surgical procedures If other procedures haven't been successful or you have large hemorrhoids, your doctor may recommend a surgical procedure. Surgery can be performed on an outpatient basis or you may need to stay in the hospital overnight. Hemorrhoid removal. During a hemorrhoidectomy, your surgeon removes excessive tissue that causes bleeding. Various techniques may be used. The surgery may be done with a local anesthetic combined with sedation, a spinal anesthetic or a general anesthetic. Hemorrhoidectomy is the most effective and complete way to treat severe or recurring hemorrhoids. Complications may include temporary difficulty emptying your bladder and urinary tract infections associated with this problem. Most people experience some pain after the procedure. Medications can relieve your pain. Soaking in a warm bath also may help. Hemorrhoid stapling. This procedure, called stapled hemorrhoidectomy or stapled hemorrhoidopexy, blocks blood flow to hemorrhoidal tissue. Stapling generally involves less pain than hemorrhoidectomy and allows an earlier return to regular activities. Compared with hemorrhoidectomy, however, stapling has been associated with a greater risk of recurrence and rectal prolapse, in which part of the rectum protrudes from the anus. Talk with your doctor about what might be the best option for you.

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DiGeorge syndrome, also called 22q11.2 deletion syndrome, is a disorder caused by a defect in chromosome 22. It results in the poor development of several body systems. Medical problems commonly associated with DiGeorge syndrome include heart defects, poor immune system function, a cleft palate, complications related to low levels of calcium in the blood, and delayed development with behavioral and emotional problems. The number and severity of symptoms associated with DiGeorge syndrome vary greatly. However, almost everyone with DiGeorge syndrome needs treatment from specialists in a variety of fields. Before the discovery of the chromosome 22 defect, the disorder was known by several names — DiGeorge syndrome, velocardiofacial syndrome, Shprintzen syndrome, CATCH22 and others. Although the term "22q11.2 deletion syndrome" is frequently used today — and is generally a more accurate description — previous names for the disorder are still used.

X-linked agammaglobulinemia (XLA), or Bruton agammaglobulinemia, is an inherited immunodeficiency disease caused by mutations in the gene coding for Bruton tyrosine kinase (BTK). The disease was first elucidated by Bruton in 1952, for whom the gene is named. BTK is critical to the maturation of pre–B cells to differentiating mature B cells. The BTK gene defect has been mapped to the long arm of the X chromosome at band Xq21.3 to Xq22, spanning 37.5kb with 19 exons forming 659 amino acids to complete the BTK cytosolic tyrosine kinase. A database of BTK mutations (BTKbase: Mutation registry for X-linked agammaglobulinemia) lists 544 mutation entries from 471 unrelated families showing 341 unique molecular events. No single mutation accounts for more than 3% of mutations in patients. In addition to mutations, a number of variants or polymorphisms have been found.

Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo

Severe combined immunodeficiency (SCID) is a life-threatening syndrome of recurrent infections, diarrhea, dermatitis, and failure to thrive. It is the prototype of the primary immunodeficiency diseases and is caused by numerous molecular defects that lead to severe compromise in the number and function of T cells, B cells, and occasionally natural killer (NK) cells. Clinically, most patients present before age 3 months. Without intervention, SCID usually results in severe infection and death in children by age 2 years. A committee of experts, initially sponsored by the World Health Organization (WHO), meets every 2 years with the goal to classify the group of primary immunodeficiency diseases according to current understanding of the pathways that become defective in the immune system.[1] Eight classification groups have been determined, with SCID being one of the best studied. Over the past few decades, the diverse molecular genetic causes of SCID have been identified with progress from studies of the immune system.[2] SCID is considered a pediatric emergency because survival depends on expeditious stem cell reconstitution, usually by bone marrow transplantation (BMT). Appropriate diagnosis is essential because instituting proper treatment is lifesaving. Despite the heterogeneity in the pathogenesis of immune defects, common cutaneous manifestations and typical infections can provide clinical clues in diagnosing this pediatric emergency.[3] Skin manifestations were prevalent in primary immunodeficiency disorders studied in 128 pediatric patients in Kuwait; skin infections were the most prevalent findings, seen in 39 patients (30%), followed by dermatitis in 24 (19%).[4] Skin infections were significantly more prevalent in those with congenital defects in phagocyte number, function, or both, as well as in those with well-defined immunodeficiencies. Dermatitis was evident in all patients with hyper–immunoglobulin (Ig) E syndrome and Wiskott-Aldrich syndrome.[4] Erythroderma of infancy with diffuse alopecia was seen exclusively in patients with SCID disorders, and telangiectasia in patients with ataxia telangiectasia; and partial albinism with silvery gray hair was associated with Chediak-Higashi syndrome. With the advances in BMT and gene therapy, patients now have a better likelihood of developing a functional immune system in a previously lethal genetic disease. However, once an infant develops serious infections, intervention is rarely successful.

The term chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been used to identify patients with a chronically progressive or relapsing symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. It can be considered the chronic equivalent of acute inflammatory demyelinating polyradiculoneuropathy, the most common form of Guillain-Barré syndrome. Signs and symptoms CIDP typically starts insidiously and evolves slowly, in either a slowly progressive or a relapsing manner, with partial or complete recovery between recurrences; periods of worsening and improvement usually last weeks or months. Most experts consider the necessary duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made. Symptoms reported include the following: Preceding infection (infrequent) Initial limb weakness, both proximal and distal Sensory symptoms (eg, tingling and numbness of hands and feet) Motor symptoms (usually predominant) In about 16% of patients, a relatively acute or subacute onset of symptoms In children, usually a more precipitous onset of symptoms Symptoms of autonomic system dysfunction (eg, orthostatic dizziness) Pertinent physical findings are limited to the nervous system, except when the condition is associated with other diseases. Such findings may include the following. Signs of cranial nerve (CN) involvement (eg, facial muscle paralysis or diplopia) Gait abnormalities Motor deficits (eg, symmetric weakness of both proximal and distal muscles in upper and lower extremities) Diminished or absent deep tendon reflexes Sensory deficits (typically in stocking-glove distribution) Impaired coordination See Clinical Presentation for more detail. Diagnosis Laboratory studies that may be helpful include the following: Cerebrospinal fluid analysis: Elevated protein levels are common (80% of patients); 10% of patients also have mild lymphocytic pleocytosis and increased gamma globulin Complete blood count (CBC), erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA) level, biochemistry profile, and serum and urine immunoelectrophoresis (to exclude associated systemic disorders) In certain instances, genetic testing Other tests and procedures that may be warranted are as follows: MRI of the spine with gadolinium enhancement Electromyography (EMG) is a critical test to determine whether the disorder is truly a peripheral neuropathy and whether the neuropathy is demyelinating Peripheral (sural) nerve biopsy (see the image below): This is considered when the diagnosis is not completely clear, when other causes cannot be excluded, or when profound axonal involvement is observed on EMG; biopsy was once commonly recommended for most patients before immunosuppressive therapy, but current guidelines no longer recommend it

Hypercalcemia is a condition in which the calcium level in your blood is above normal. Too much calcium in your blood can weaken your bones, create kidney stones, and interfere with the way your heart and brain works. Hypercalcemia most commonly results from overactive parathyroid glands. These four tiny glands are each about the size of a grain of rice and are located on or near the thyroid gland. Other causes of hypercalcemia include cancer, certain other medical disorders, some medications, and excessive use of calcium and vitamin D supplements. Signs and symptoms of hypercalcemia may range from nonexistent to severe. Treatment depends on the underlying cause.

The term dermoid cyst does not appear to be restricted to a single kind of lesion nor is it used in only a single medical discipline. The term dermoid cyst can be found in the vocabulary of dermatologists, dermatopathologists, general pathologists, gynecologists, neurosurgeons, or pediatricians. If asked, all of these clinicians would most probably define and describe dermoid cysts differently. For example, gynecologists and general pathologists might say that a dermoid cyst is a cystic tumor of the ovary. In contrast, neurosurgeons tend to view a dermoid cyst is associated with a congenital cyst of the spine or an intracranial congenital cyst. For pediatricians and dermatologists, dermoid cyst means subcutaneous cysts, which are usually congenital.[1]

Anemia is a condition in which you don't have enough healthy red blood cells to carry adequate oxygen to the body's tissues. Having anemia may make you feel tired and weak. There are many forms of anemia, each with its own cause. Anemia can be temporary or long term, and it can range from mild to severe. See your doctor if you suspect you have anemia because it can be a warning sign of serious illness. Treatments for anemia range from taking supplements to undergoing medical procedures. You may be able to prevent some types of anemia by eating a healthy, varied diet.

Breast cancer usually starts off in the inner lining of milk ducts or the lobules that supply them with milk. A malignant tumor can spread to other parts of the body. A breast cancer that started off in the lobules is known as lobular carcinoma, while one that developed from the ducts is called ductal carcinoma. The vast majority of breast cancer cases occur in females. This article focuses on breast cancer in women. We also have an article about male breast cancer. Breast cancer is the most common invasive cancer in females worldwide. It accounts for 16% of all female cancers and 22.9% of invasive cancers in women. 18.2% of all cancer deaths worldwide, including both males and females, are from breast cancer. Breast cancer rates are much higher in developed nations compared to developing ones. There are several reasons for this, with possibly life-expectancy being one of the key factors - breast cancer is more common in elderly women; women in the richest countries live much longer than those in the poorest nations. The different lifestyles and eating habits of females in rich and poor countries are also contributory factors, experts believe. According to the National Cancer Institute, 232,340 female breast cancers and 2,240 male breast cancers are reported in the USA each year, as well as about 39,620 deaths caused by the disease.

Nipple Sensation After Breast Augmentation

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Choking Infant