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intracranial hematoma occurs when a blood vessel ruptures within your brain or between your skull and your brain. The collection of blood (hematoma) compresses your brain tissue. An intracranial hematoma may occur because the fluid that surrounds your brain can't absorb the force of a sudden blow or a quick stop. Then your brain may slide forcefully against the inner wall of your skull and become bruised. Although some head injuries — such as one that causes only a brief lapse of consciousness (concussion) — can be minor, an intracranial hematoma is potentially life-threatening and often requires immediate treatment. An intracranial hematoma often, but not always, requires surgery to remove the blood.

ECG

Excision of Pilonidal Cyst. Open method.

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.

Inflammatory bowel disease (IBD) involves chronic inflammation of all or part of your digestive tract. IBD primarily includes ulcerative colitis and Crohn's disease. Both usually involve severe diarrhea, pain, fatigue and weight loss. IBD can be debilitating and sometimes leads to life-threatening complications. Ulcerative colitis (UL-sur-uh-tiv koe-LIE-tis) is an inflammatory bowel disease that causes long-lasting inflammation and sores (ulcers) in the innermost lining of your large intestine (colon) and rectum. Crohn's disease is an IBD that cause inflammation of the lining of your digestive tract. In Crohn's disease, inflammation often spreads deep into affected tissues. The inflammation can involve different areas of the digestive tract — the large intestine, small intestine or both. Collagenous (kuh-LAJ-uh-nus) colitis and lymphocytic colitis also are considered inflammatory bowel diseases but are usually regarded separately from classic inflammatory bowel disease.

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.

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.

Bronchiectasis is an abnormal dilation of the proximal and medium-sized bronchi (>2 mm in diameter) caused by weakening or destruction of the muscular and elastic components of the bronchial walls. Affected areas may show a variety of changes, including transmural inflammation, edema, scarring, and ulceration, among other findings. Distal lung parenchyma may also be damaged secondary to persistent microbial infection and frequent postobstructive pneumonia. Bronchiectasis can be congenital but is most often acquired.[9] Congenital bronchiectasis usually affects infants and children. These cases result from developmental arrest of the bronchial tree. Acquired forms occur in adults and older children and require an infectious insult, impairment of drainage, airway obstruction, and/or a defect in host defense. The tissue is also damaged in part by the host response of neutrophilic proteases, inflammatory cytokines, nitric oxide, and oxygen radicals. This results in damage to the muscular and elastic components of the bronchial wall. Additionally, peribronchial alveolar tissue may be damaged, resulting in diffuse peribronchial fibrosis.[12] The result is abnormal bronchial dilatation with bronchial wall destruction and transmural inflammation. The most important functional finding of altered airway anatomy is severely impaired clearance of secretions from the bronchial tree. Impaired clearance of secretions causes colonization and infection with pathogenic organisms, contributing to the purulent expectoration commonly observed in patients with bronchiectasis. The result is further bronchial damage and a vicious cycle of bronchial damage, bronchial dilation, impaired clearance of secretions, recurrent infection, and more bronchial damage

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.

Croup refers to an infection of the upper airway, which obstructs breathing and causes a characteristic barking cough. The cough and other symptoms of croup are the result of swelling around the vocal cords (larynx), windpipe (trachea) and bronchial tubes (bronchi). When a cough forces air through this narrowed passage, the swollen vocal cords produce a noise similar to a seal barking. Likewise, taking a breath often produces a high-pitched whistling sound (stridor). Croup typically occurs in younger children. Croup usually isn't serious and most cases can be treated at home.

Coarctation of the aorta (CoA[1][2] or CoAo), also called aortic narrowing, is a congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts. The word “coarctation” means narrowing. Coarctations are most common in the aortic arch. The arch may be small in babies with coarctations. Other heart defects may also occur when coarctation is present, typically occurring on the left side of the heart. When a patient has a coarctation, the left ventricle has to work harder. Since the aorta is narrowed, the left ventricle must generate a much higher pressure than normal in order to force enough blood through the aorta to deliver blood to the lower part of the body. If the narrowing is severe enough, the left ventricle may not be strong enough to push blood through the coarctation, thus resulting in lack of blood to the lower half of the body. Physiologically its complete form is manifested as interrupted aortic arch

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

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection injury of the spinal cord, often in the cervical cord region. (See Presentation.) Patients with Brown-Séquard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrome. (See Etiology, Presentation, and Workup.) As an incomplete spinal cord syndrome, the clinical presentation of Brown-Séquard syndrome may range from mild to severe neurologic deficit. (See Presentation.) Brown-Séquard–plus syndrome The pure Brown-Séquard syndrome reflecting hemisection of the cord is not often observed. A clinical picture composed of fragments of the syndrome or of the hemisection syndrome plus additional symptoms and signs is more common. These less-pure forms of the disorder are often referred to as Brown-Séquard–plus syndrome.[1] Interruption of the lateral corticospinal tracts, the lateral spinal thalamic tract, and at times the posterior columns produces a picture of a spastic, weak leg with brisk reflexes and a strong leg with loss of pain and temperature sensation. Note that spasticity and hyperactive reflexes may not be present with an acute lesion.

Clopidogrel keeps the platelets in your blood from coagulating (clotting) to prevent unwanted blood clots that can occur with certain heart or blood vessel conditions. Clopidogrel is used to prevent blood clots after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels. Clopidogrel may also be used for other purposes not listed in this medication guide

Cystic fibrosis (CF) is a multisystem disease affecting the digestive system, sweat glands, upper and lower respiratory tracts, and the reproductive tract, but progressive lung disease continues to be the major cause of morbidity and mortality [1]. CF is characterized by abnormal transport of chloride and sodium across the respiratory epithelium, resulting in thickened, viscous airway secretions [2]. Over a highly variable time course ranging from months to decades after birth, individuals eventually develop chronic infection of the respiratory tract with a characteristic array of bacterial flora [3], leading to progressive respiratory insufficiency and eventual respiratory failure. The rate of progression varies widely, depending in part on genotype (including gene modifiers) as well as environmental factors. Registry data from CF Centers in the United States, Canada, and Europe indicate a median survival of about 41 years [4]. Females with CF appear to have higher morbidity and mortality than males [5]. This "gender gap" is modest but consistent across many populations and is hypothesized to be due to the pro-inflammatory effects of estrogens.

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.