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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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Findings of tenderness, induration, pain and/or erythema along the course of a superficial vein usually establish a clinical diagnosis, especially in patients with known risk factors. In addition, there is often a palpable, sometimes nodular cord, due to thrombus within the affected vein. Persistence of this cord when the extremity is raised suggests the presence of thrombus.
The following symptoms or signs are often associated with thrombophlebitis, although thrombophlebitis is not restricted to the veins of the legs.
Superficial thrombophlebitis is a thrombosis and inflammation of superficial veins which presents as a painful induration with erythema, often in a linear or branching configuration forming cords.
Superficial thrombophlebitis is due to inflammation and/or thrombosis, and less commonly infection of the vein. It is generally a benign, self-limited disorder, however, it can be complicated by deep vein thrombosis (DVT) and even pulmonary embolism (PE). Migratory superficial thrombophlebitis is known as Trousseau's syndrome.
Phlebitis or venitis is the inflammation of a vein, usually in the legs. It most commonly occurs in superficial veins. Phlebitis often occurs in conjunction with thrombosis and is then called thrombophlebitis or superficial thrombophlebitis. Unlike deep vein thrombosis, the probability that superficial thrombophlebitis will cause a clot to break up and be transported in pieces to the lung is very low.
In terms of complications, one of the most serious occurs when the superficial blood clot is associated with a deeper venous thrombosis; this can then dislodge, traveling through the heart and occluding the dense capillary network of the lungs This is a pulmonary embolism which can be life-threatening to the affected individual.
Phlebitis is typically caused by local trauma to a vein, usually from the insertion of an intravenous catheter. However, it can also occur due to a complication of connective tissue disorders such as lupus, or of pancreatic, breast, or ovarian cancers. Phlebitis can also result from certain medications and drugs that irritate the veins, such as desomorphine.
Superficial phlebitis often presents as an early sign in thromboangiitis obliterans (Buerger's disease), a vasculitis that affects small and medium-sized arteries and veins in distal extremities often associated with cigarette smoking.
Most varicose veins are reasonably benign, but severe varicosities can lead to major complications, due to the poor circulation through the affected limb.
- Pain, tenderness, heaviness, inability to walk or stand for long hours, thus hindering work
- Skin conditions / dermatitis which could predispose skin loss
- Skin ulcers especially near the ankle, usually referred to as venous ulcers.
- Development of carcinoma or sarcoma in longstanding venous ulcers. Over 100 reported cases of malignant transformation have been reported at a rate reported as 0.4% to 1%.
- Severe bleeding from minor trauma, of particular concern in the elderly.
- Blood clotting within affected veins, termed superficial thrombophlebitis. These are frequently isolated to the superficial veins, but can extend into deep veins, becoming a more serious problem.
- Acute fat necrosis can occur, especially at the ankle of overweight people with varicose veins. Females are more frequently affected than males.
Signs and symptoms of CVI in the leg include the following:
- Varicose veins
- Itching (pruritus)
- Hyperpigmentation
- Phlebetic lymphedema
- Chronic swelling of the legs and ankles
- Venous ulceration
CVI in the leg may cause the following:
- Venous stasis
- Ulcers.
- Stasis dermatitis, also known as varicose eczema
- Contact dermatitis. Patients with venous insufficiency have a disrupted epidermal barrier, making them more susceptible than the general population to contact sensitization and subsequent dermatitis.
- Atrophie blanche. This is an end point of a variety of conditions, appears as atrophic plaques of ivory white skin with telangiectasias. It represents late sequelae of lipodermatosclerosis where the skin has lost its nutrient blood flow.
- Lipodermatosclerosis. This is an indurated plaque in the medial malleolus.
- Malignancy. Malignant degeneration is a rare but important complication of venous disease since tumors which develop in the setting of an ulcer tend to be more aggressive.
- Pain. Pain is a feature of venous disease often overlooked and commonly undertreated.
- Anxiety.
- Depression.
- Inflammation
- Discoloration
- Skin thickening
- Cellulitis
Varicose veins are veins that have become enlarged and twisted. The term commonly refers to the veins on the leg, although varicose veins can occur elsewhere. Veins have pairs of leaflet valves to prevent blood from flowing backwards (retrograde flow or venous reflux). Leg muscles pump the veins to return blood to the heart (the skeletal-muscle pump), against the effects of gravity. When veins become varicose, the leaflets of the valves no longer meet properly, and the valves do not work (valvular incompetence). This allows blood to flow backwards and they enlarge even more. Varicose veins are most common in the superficial veins of the legs, which are subject to high pressure when standing. Besides being a cosmetic problem, varicose veins can be painful, especially when standing. Severe long-standing varicose veins can lead to leg swelling, venous eczema, skin thickening (lipodermatosclerosis) and ulceration. Although life-threatening complications are uncommon, varicose veins may be confused with deep vein thrombosis, which may be life-threatening.
Non-surgical treatments include sclerotherapy, elastic stockings, leg elevation and exercise. The traditional surgical treatment has been vein stripping to remove the affected veins. Newer, less invasive treatments which seal the main leaking vein are available. Alternative techniques, such as ultrasound-guided foam sclerotherapy, radiofrequency ablation and endovenous laser treatment, are available as well. Because most of the blood in the legs is returned by the deep veins, the superficial veins, which return only about 10% of the total blood of the legs, can usually be removed or ablated without serious harm.
Secondary varicose veins are those developing as collateral pathways, typically after stenosis or occlusion of the deep veins, a common sequel of extensive deep venous thrombosis (DVT). Treatment options are usually support stockings, occasionally sclerotherapy and rarely, limited surgery.
Varicose veins are distinguished from reticular veins (blue veins) and telangiectasias (spider veins), which also involve valvular insufficiency, by the size and location of the veins. Many patients who suffer with varicose veins seek out the assistance of physicians who specialize in vein care or peripheral vascular disease. These physicians include vascular surgeons, phlebologists or interventional radiologists.
Chronic venous insufficiency (CVI) is a medical condition in which blood pools in the veins, straining the walls of the vein. The most common cause of CVI is superficial venous reflux which is a treatable condition. As functional venous valves are required to provide for efficient blood return from the lower extremities, this condition typically affects the legs. If the impaired vein function causes significant symptoms, such as swelling and ulcer formation, it is referred to as chronic venous disease. It is sometimes called "chronic peripheral venous insufficiency" and should not be confused with post-thrombotic syndrome in which the deep veins have been damaged by previous deep vein thrombosis.
Most cases of CVI can be improved with treatments to the superficial venous system or stenting the deep system. Varicose veins for example can now be treated by local anesthetic endovenous surgery.
The prevalence of CVI is far higher in women than in men. The Tampere study, which examined the epidemiology of varicose veins in a large cohort of 3284 men and 3590 women, demonstrated that the prevalence of varicose veins in men and women was 18% and 42%, respectively. The condition has been known since ancient times and Hippocrates used bandaging to treat it.
Possible symptoms include:
- General symptoms: Fever, weight loss
- Skin: Palpable purpura, livedo reticularis
- Muscles and joints: Myalgia or myositis, arthralgia or arthritis
- Nervous system: Mononeuritis multiplex, headache, stroke, tinnitus, reduced visual acuity, acute visual loss
- Heart and arteries: Myocardial infarction, hypertension, gangrene
- Respiratory tract: Nose bleeds, bloody cough, lung infiltrates
- GI tract: Abdominal pain, bloody stool, perforations
- Kidneys: Glomerulonephritis
Vasculitis is a group of disorders that destroy blood vessels by inflammation. Both arteries and veins are affected. Lymphangitis is sometimes considered a type of vasculitis. Vasculitis is primarily caused by leukocyte migration and resultant damage.
Although both occur in vasculitis, inflammation of veins (phlebitis) or arteries (arteritis) are their own are separate entities.
A Zahn infarct is a pseudo-infarction of the liver, consisting of an area of congestion with parenchymal atrophy but no necrosis, and usually due to obstruction of a branch of the portal vein. Zahn infarcts are unique in that there is collateral congestion of liver sinusoids that do not include areas of anoxia seen in most infarcts. Fibrotic tissue may develop in the area of the infarct and it could be caused by an occlusive phlebitis in portal vein radicles. Non ischemic infarct of liver with lines of Zahn.
Temporal arteritis, the second type of giant cell arteritis, is also a chronic, inflammatory disease involving mid- to large-sized arteries. Temporal arteritis has a higher incidence in people of Scandinavian descent. However, the incidence rate differs based on population, region and races. Temporal arteritis is not uncommon in North America. The incidence rate is around 0.017% for individuals over 50 years of age.
Symptoms of temporal arteritis are classified as specific and nonspecific.
Nonspecific symptoms:
- Headache
- Low grade fever
- Sweating
- Anorexia (loss of appetite)
- Weight loss
- General malaise
Specific symptoms:
- Claudication of the jaw
- Engorged, tender vessels
Specific symptoms usually develop in the advanced stages of temporal arteritis.
Polyarteritis nodosa of unknown mechanism can cause testiscular pain. It is often associated with aneurysms and Hepatitis B.
Symptoms of general arteritis may include:
- Inflammation
- Fever
- Increased production of red blood cells (erythrocytes)
- Limping
- Reduced pulse
Lupus anticoagulant (also known as lupus antibody, LA, LAC, or lupus inhibitors) is an immunoglobulin that binds to phospholipids and proteins associated with the cell membrane. Lupus anticoagulant is a misnomer, as it is actually a prothrombotic agent. Lupus anticoagulant antibodies in living systems cause an increase in inappropriate blood clotting. The name derives from their properties in vitro, since in laboratory tests, these antibodies increase aPTT. Investigators speculate that the antibodies interfere with phospholipids used to induce in vitro coagulation. In vivo, the antibodies are thought to interact with platelet membrane phospholipids, increasing adhesion and aggregation of platelets, which accounts for the in vivo prothrombotic characteristics.
The condition was first described by hematologist C. Lockard Conley.
Both words in the term "lupus anticoagulant" can be misleading:
- Most patients with a lupus anticoagulant do not actually have lupus erythematosus, and only a small proportion will proceed to develop this disease (which causes joint pains, skin problems and renal failure, amongst other complications). Patients with lupus erythematosus are more likely to develop a lupus anticoagulant than the general population.
- The term "anticoagulant" accurately describes its function in vitro. However in vivo, it functions as a "procoagulant".
Several case studies on IgG4-related prostatitis have been reported. Patients have been noted to commonly present with lower urinary tract symptoms such as dysuria, pollakisuria, urinary urgency, and a feeling of incomplete emptying. The clinical presentation is similar to that in benign prostatic hyperplasia or chronic prostatitis, although pain, as occurs in CP/CPPS, does not usually appear to be significant.
There are several paired paranasal sinuses, including the frontal, ethmoidal, maxillary and sphenoidal sinuses. The ethmoidal sinuses are further subdivided into anterior and posterior ethmoid sinuses, the division of which is defined as the basal of the middle turbinate. In addition to the severity of disease, discussed below, sinusitis can be classified by the sinus cavity which it affects:
- Maxillary – can cause pain or pressure in the maxillary (cheek) area ("e.g.," toothache, or headache) (J01.0/J32.0)
- Frontal – can cause pain or pressure in the frontal sinus cavity (located above eyes), headache, particularly in the forehead (J01.1/J32.1)
- Ethmoidal – can cause pain or pressure pain between/behind the eyes, the sides of the upper part of the nose (the medial canthi), and headaches (J01.2/J32.2)
- Sphenoidal – can cause pain or pressure behind the eyes, but often refers to the skull vertex (top of the head), over the mastoid processes, or the back of the head.
Men with IgG4-related prostatitis may have similar findings to those that are frequently, but not always, seen in other organ manifestations of IgG4-related disease, such as elevated blood levels of IgG4, IgE and eosinophils.
FDG-PET scans have been reported to be useful as a diagnostic modality for detecting IgG4-related prostatitis in men with IgG4-RD.
IgG4-related disease has been described as an indolent condition. Although possibly based on opinion rather than on objective assessments, symptoms, if any, are commonly described as mild in the medical literature. This can be in spite of considerable underlying organ destruction. People are often described as being generally well at the time of diagnosis, although some may give a history of weight loss.
Pain is generally not a feature of the inflammation. However it may occur as a secondary effect, for example due to either obstruction or compression.
Often diagnosis is made due to the presence of painless swellings or mass lesions, or due to complications of masses, e.g. jaundice due to involvement of the pancreas, biliary tree or liver. Symptoms are commonly attributed to other conditions and other diagnoses may have been made years before diagnosis, e.g. urinary symptoms in men attributed to common prostate conditions. Lesions may also be detected incidentally on radiological images, but can be easily misdiagnosed as malignancies.
Reported cases do include some significant symptoms or findings however:
Headache/facial pain or pressure of a dull, constant, or aching sort over the affected sinuses is common with both acute and chronic stages of sinusitis. This pain is typically localized to the involved sinus and may worsen when the affected person bends over or when lying down. Pain often starts on one side of the head and progresses to both sides.
Acute sinusitis may be accompanied by thick nasal discharge that is usually green in color and may contain pus (purulent) and/or blood. Often a localized headache or toothache is present, and it is these symptoms that distinguish a sinus-related headache from other types of headaches, such as tension and migraine headaches. Another way to distinguish between toothache and sinusitis is that the pain in sinusitis is usually worsened by tilting the head forwards and with valsalva maneuvers.
Infection of the eye socket is possible, which may result in the loss of sight and is accompanied by fever and severe illness. Another possible complication is the infection of the bones (osteomyelitis) of the forehead and other facial bones – Pott's puffy tumor.
Sinus infections can also cause middle ear problems due to the congestion of the nasal passages. This can be demonstrated by dizziness, "a pressurized or heavy head", or vibrating sensations in the head. Post-nasal drip is also a symptom of chronic rhinosinusitis.
Halitosis (bad breath) is often stated to be a symptom of chronic rhinosinusitis; however, gold standard breath analysis techniques have not been applied. Theoretically, there are several possible mechanisms of both objective and subjective halitosis that may be involved.
A 2004 study suggested that up to 90% of "sinus headaches" are actually migraines. The confusion occurs in part because migraine involves activation of the trigeminal nerves, which innervate both the sinus region and the meninges surrounding the brain. As a result, it is difficult to accurately determine the site from which the pain originates. People with migraines do not typically have the thick nasal discharge that is a common symptom of a sinus infection.
IgG4-related disease (IgG4-RD), formerly known as IgG4-related systemic disease, is a chronic inflammatory condition characterized by tissue infiltration with lymphocytes and IgG4-secreting plasma cells, various degrees of fibrosis (scarring) and a usually prompt response to oral steroids. In approximately 51–70% of people with this disease, "serum" IgG4 concentrations are elevated during an acute phase.
It is a relapsing–remitting disease associated with a tendency to mass forming, tissue-destructive lesions in multiple sites, with a characteristic histopathological appearance in whichever site is involved. Inflammation and the deposition of connective tissue in affected anatomical sites can lead to organ dysfunction, or even organ failure, if not treated.
Early detection is important to avoid organ damage and potentially serious complications. Treatment is recommended in all symptomatic cases of IgG4-RD and also in asymptomatic IgG4-RD involving certain anatomical sites.
The main symptoms of hypoparathyroidism are the result of the low blood calcium level, which interferes with normal muscle contraction and nerve conduction. As a result, people with hypoparathyroidism can experience paresthesia, an unpleasant tingling sensation around the mouth and in the hands and feet, as well as muscle cramps and severe spasms known as "tetany" that affect the hands and feet. Many also report a number of subjective symptoms such as fatigue, headaches, bone pain and insomnia. Crampy abdominal pain may occur. Physical examination of someone with hypocalcemia may show tetany, but it is also possible to provoke tetany of the facial muscles by tapping on the facial nerve (a phenomenon known as Chvostek's sign) or by using the cuff of a sphygmomanometer to temporarily obstruct the blood flow to the arm (a phenomenon known as Trousseau's sign of latent tetany).
A number of medical emergencies can arise in people with low calcium levels. These are seizures, severe irregularities in the normal heart beat, as well as spasm of the upper part of the airways or the smaller airways known as the bronchi (both potentially causing respiratory failure).
Hypoparathyroidism can have the following causes:
- Removal of, or trauma to, the parathyroid glands due to thyroid surgery (thyroidectomy), parathyroid surgery (parathyroidectomy) or other surgical interventions in the central part of the neck (such as operations on the larynx and/or pharynx) is a recognized cause. It is the most common cause of hypoparathyroidism. Although surgeons generally make attempts to spare normal parathyroid glands at surgery, inadvertent injury to the glands or their blood supply is still common. When this happens, the parathyroids may cease functioning. This is usually temporary but occasionally long term (permanent).
- Kenny-Caffey Syndrome
- Autoimmune invasion and destruction is the most common non-surgical cause. It can occur as part of autoimmune polyendocrine syndromes.
- Hemochromatosis can lead to iron accumulation and consequent dysfunction of a number of endocrine organs, including the parathyroids.
- Absence or dysfunction of the parathyroid glands is one of the components of chromosome 22q11 microdeletion syndrome (other names: DiGeorge syndrome, Schprintzen syndrome, velocardiofacial syndrome).
- Magnesium deficiency
- A defect in the calcium receptor leads to a rare congenital form of the disease
- Idiopathic (of unknown cause), occasionally familial (e.g. Barakat syndrome (HDR syndrome) a genetic development disorder resulting in hypoparathyroidism, sensorineural deafness and renal disease)