Congenital hip dysplasia
* Introduction
* Pathogenesis
* Signs and symptoms
* Diagnosis
* Treatment
Treatment
Multiple observational studies show increased rates of spontaneous healing of hip dysplasia in the newborn period. They are due to bone growth and development of the femur and the acetabular cartilage. Indications for surgery depend on the severity of the disease, and the formation bilateralitate or not a false acetabulum. Indications for treatment depend on patient age and the success of previous techniques. Children under 6 months examination instability are treated with a form of limb tijare and harnesses. If this method has no benefit to trying to reduce the traction before closed reduction.
Pavlik harness therapy: Treatment for hip dysplasia begins with a careful examination of the newborn. If there is instability indicate a Pavlik harness. Ultrasound is an excellent way to reduce thigh as technical documentation Pavlik and should be performed during therapy. If the balance is subluxated posterior then Pavlik therapy should be discontinued. Pavlik duration of therapy is not established. If the patient has more than 6 months of therapy success is less than 50%, so should be used for patients under 6 months.
Reduction therapy: When the patient has more than 6 months or if therapy is not successful Pavlik try a closed reduction. Traction is performed frequently for 2-3 weeks before the discount. Traction can be performed at home or hospital. Should be monitored closely to ensure the integrity of the skin. General benefit of traction is still controversial. The reduction is performed using artrografiei inhisa to determine the reduction. To define a cone of stability of balance, which includes: flexion, abduction and internal and external rotation. If the cone is over 30 degrees is considered satisfactory technique. After performing a CT reduction is to determine posterior subluxation. When the child is over two years or failure to consider other methods attempted open reduction. If the patient has more than three years trying to shorten a member. One patient with residual acetabular dysplasia over four years should be treated with an acetabular procedure. Treatment for a patient diagnosed in adult age is considered for residual hip dysplasia.
Open reduction: The treatment of choice for children over 2 years at diagnosis or who failed closed reduction attempts. In children with short teratology dischiza reduction can be effected by medial approach. More common in older children are using the standard-anterolateral. If your child is over 3 years is made shorter limb. Pelvic osteotomy is required for residual hip dysplasia.
Complications of treatment: There may be numerous complications, including redeployment phases, stiffness balance, ineffective, and most devastating hemorrhage, necrosis of femoral head. Necrosis rate varies significantly. Studies show that extreme abduction combined with extension and internal rotation have a higher rate of avascular necrosis.
Prognosis: Early diagnosis is crucial issue of treatment of children with hip dysplasia. Evolution of children treated for hip dysplasia is very good, especially if dysplasia is controlled by closed treatment. If successful techniques have not closed and open reduction is required, the prognosis is less favorable, although short-term prognosis seems favorable. If secondary procedures are needed to achieve reduction worsens prognosis.
Showing posts with label Diseases of bones/ muscles and joints. Show all posts
Showing posts with label Diseases of bones/ muscles and joints. Show all posts
Saturday, January 29, 2011
Congenital hip dysplasia Diagnosis
Congenital hip dysplasia
* Introduction
* Pathogenesis
* Signs and symptoms
* Diagnosis
* Treatment
Diagnosis
Imaging Studies: Echography shows major benefits in the evaluation and treatment of children with hip dysplasia. Even some children with ultrasound may be delayed or fetuses diagnosed with hip dysplasia supradiagnosticati. An ultrasound evaluation is performed by measuring angles or alpha or beta dimanica assessment. The angle alpha is superior to the acetabulum angle of 60 degrees considered normal. Beta angle is 55 degrees below normal, and form components of the acetabulum cartilage.
Standard radiograph of the pelvis includes anterioposterior issue with hips in neutral and false profile of the patient is at an angle of 65 degrees from the X-ray plate so you can see the front of the acetabulum. MRI is useful for identification of bone or soft tissue abnormalities.
Artrogramele dynamic studies are performed by injecting contrast into the patient's hip joint by fluoroscopy and examination under anesthesia. Do the opposite of reduction. It describes the growth of medial joint space by combining the femoral head medial contrast, poor prognostic indicator. After practicing a reduction in the transverse plane tomography to ensure that balance is not subluxated or dislocated posterior. The differential diagnosis is made with the following conditions: septic arthritis, hamartroza traumatic, congenital coxa summer, cerebral palsy, abnormal joint laxity.
* Introduction
* Pathogenesis
* Signs and symptoms
* Diagnosis
* Treatment
Diagnosis
Imaging Studies: Echography shows major benefits in the evaluation and treatment of children with hip dysplasia. Even some children with ultrasound may be delayed or fetuses diagnosed with hip dysplasia supradiagnosticati. An ultrasound evaluation is performed by measuring angles or alpha or beta dimanica assessment. The angle alpha is superior to the acetabulum angle of 60 degrees considered normal. Beta angle is 55 degrees below normal, and form components of the acetabulum cartilage.
Standard radiograph of the pelvis includes anterioposterior issue with hips in neutral and false profile of the patient is at an angle of 65 degrees from the X-ray plate so you can see the front of the acetabulum. MRI is useful for identification of bone or soft tissue abnormalities.
Artrogramele dynamic studies are performed by injecting contrast into the patient's hip joint by fluoroscopy and examination under anesthesia. Do the opposite of reduction. It describes the growth of medial joint space by combining the femoral head medial contrast, poor prognostic indicator. After practicing a reduction in the transverse plane tomography to ensure that balance is not subluxated or dislocated posterior. The differential diagnosis is made with the following conditions: septic arthritis, hamartroza traumatic, congenital coxa summer, cerebral palsy, abnormal joint laxity.
Congenital hip dysplasia Pathogenesis
Congenital hip dysplasia
* Introduction
* Pathogenesis
* Signs and symptoms
* Diagnosis
* Treatment
Pathogenesis
Etiologic factors of hip dysplasia are not known, but the condition seems to be associated with a number of factors such as genetic, racial, sex and intrauterine position of the child, oligohidramonosul, cerebral palsy, myelomeningocele, artrogripoza. Racial differences are an etiological factor for hip dysplasia, so the condition is more common among natives of Lapland, American, black and Chinese populations. Compared to the genetic predisposition seems to exist a 10-fold for children with parents suffering from hip dysplasia to the disease. Other factors incriminated are female, first child. Over 80% of patients are female. Other musculoskeletal disorders of intrauterine or superposition of states malpozitiei as metatarsus adductus and torticollis are reported to be associated with hip dysplasia. Dysplasia is more common on the left side than on the right side due to its location on the child's mother left in front of the sacrum. Children from cultures which wraps your baby close, forcing adductie thighs. Development of hip dysplasia involves abnormal growth of it. Associated ligament laxity.
Anatomy of hip joint development: Develop normal balance dintrun single block of cartilage that separates the acetabular and femoral components at 7-8 weeks of gestation. Shape characteristic of balance is the result of contact between acetabulu and femur during growth. At birth the acetabulum is a small bone and a cartilage component of the sea. In the first 6 weeks postnatally succeptibil acetabulum is modeling. If you are in a position the femoral head in acetabulum abnormal balance is abnormal.
Normal growth depends on increasing the acetabulum of the normal epiphyseal cartilage of the triradiate and three centers of ossification of the acetabular portion of the pubis, iliac and ischiatic. Normal growth depends on increasing the interstitial apozitionala acetabulum from acetabulum normal. This spherical femoral head in acetabulum is critical to stimulate normal development of the acetabulum. Anatomy dislocated hip, especially after a few months include forming a bridge called neolimbus. Closed reduction is not successful in late presentations of multiple secondary barriers to the reduction. These include abductorului and psoas contraction, ligament tears, transverse acetabular ligament, and capsular constriction pulvinara. The long dislocations interpozitia labrum may interfere with the reduction.
* Introduction
* Pathogenesis
* Signs and symptoms
* Diagnosis
* Treatment
Pathogenesis
Etiologic factors of hip dysplasia are not known, but the condition seems to be associated with a number of factors such as genetic, racial, sex and intrauterine position of the child, oligohidramonosul, cerebral palsy, myelomeningocele, artrogripoza. Racial differences are an etiological factor for hip dysplasia, so the condition is more common among natives of Lapland, American, black and Chinese populations. Compared to the genetic predisposition seems to exist a 10-fold for children with parents suffering from hip dysplasia to the disease. Other factors incriminated are female, first child. Over 80% of patients are female. Other musculoskeletal disorders of intrauterine or superposition of states malpozitiei as metatarsus adductus and torticollis are reported to be associated with hip dysplasia. Dysplasia is more common on the left side than on the right side due to its location on the child's mother left in front of the sacrum. Children from cultures which wraps your baby close, forcing adductie thighs. Development of hip dysplasia involves abnormal growth of it. Associated ligament laxity.
Anatomy of hip joint development: Develop normal balance dintrun single block of cartilage that separates the acetabular and femoral components at 7-8 weeks of gestation. Shape characteristic of balance is the result of contact between acetabulu and femur during growth. At birth the acetabulum is a small bone and a cartilage component of the sea. In the first 6 weeks postnatally succeptibil acetabulum is modeling. If you are in a position the femoral head in acetabulum abnormal balance is abnormal.
Normal growth depends on increasing the acetabulum of the normal epiphyseal cartilage of the triradiate and three centers of ossification of the acetabular portion of the pubis, iliac and ischiatic. Normal growth depends on increasing the interstitial apozitionala acetabulum from acetabulum normal. This spherical femoral head in acetabulum is critical to stimulate normal development of the acetabulum. Anatomy dislocated hip, especially after a few months include forming a bridge called neolimbus. Closed reduction is not successful in late presentations of multiple secondary barriers to the reduction. These include abductorului and psoas contraction, ligament tears, transverse acetabular ligament, and capsular constriction pulvinara. The long dislocations interpozitia labrum may interfere with the reduction.
Congenital hip dysplasia
Congenital hip dysplasia
* Introduction
* Pathogenesis
* Signs and symptoms
* Diagnosis
* Treatment
Hip dysplasia can be traumatic or congenital. Development of hip dysplasia definition is still controversial. Typically hip dysplasia is the term used for patients who are born with hip dislocations or instability, which can then lead to dysplasia Solca. A broader definition of hip dysplasia is the abnormal growth of the balance. This includes bone structures as the proximal femur and acetabulum, labrum, capsule and other soft tissues. The annual incidence of congenital hip dysplasia is 2-4 cases per 1000 births and approximately 80% of individuals affected are girls. The condition can occur at any time from conception until skeletal maturity.
Congenital hip dysplasia is the result of interruption of the normal relationship between the acetabulum and femoral head. Without a proper contact between them, none will develop normally. At birth the acetabulum is large, small bones and cartilage content and the percentage of the acetabulum Covers femoral head is smaller, so the first 6 sapatamini child's life are critical for the development of joint. The etiology of hip dysplasia is not clear, but the condition seems to be associated with a number of factors such as genetics, race, child sex, intrauterine position, oligohidramonosul, cerebral palsy, myelomeningocele, artrogripoza. Development of hip dysplasia involves abnormal growth of it. Associate ligementara laxity.
Early clinical manifestations are identified during examination of the newborn and make ortolan maneuver. Other physical signs include asymmetry late dislocations buttock or lateral skin folds, decreased abduction on the affected side, walk or bipedal position with external rotation and inequality between the legs. Unilateral dislocations cause significant inequality of the legs, the imbalance of the weight and pain of the thigh and knee. Developing false acetabulum is associated with adverse prognosis in 75% of patients. Failure to diagnose and treat hip dysplasia in the immediate neonatal period may cause significant morbidity: the need to open and develop osteoarthritis therapies. The possible complications of treatment include recurrent dysplasia, recurrent dislocations and femoral head avascular necrosis.
Indications for surgery depend on the severity of the disease, and the formation bilateralitate or not a false acetabulum. Indications for treatment depend on patient age and the success of previous techniques. Children under 6 months examination instability are treated with a form of limb tijare and harnesses. If this method has no benefit to trying to reduce the traction before closed reduction. When the child is over two years or failure to consider other methods attempted open reduction. If the patient has more than three years trying to shorten a member. One patient with residual acetabular dysplasia over four years should be treated with an acetabular procedure. Treatment for a patient diagnosed in adult age is considered for residual hip dysplasia.
Evolution of children treated for hip dysplasia is very good, especially if dysplasia is controlled by closed treatment. If successful techniques have not closed and open reduction is required, the prognosis is less favorable, although short-term prognosis seems favorable. If secondary procedures are needed to achieve reduction worsens prognosis. Early diagnosis is crucial issue of treatment of children with hip dysplasia. Using ultrasound and other imaging procedures and implementation of specific educational programs decreased the number of children with hip dysplasia and late diagnosis. Less invasive techniques: the endoscopy, imaging-guided surgery is an effort to decrease mortality from surgery and speed recovery.
Although for most patients the problem resolves spontaneously within the first months of life, persitienta dysplasia can cause chronic pain, disorders of growth and weight and degenerative arthritis. In its severe hip dysplasia is one of the most common congenital malformations and a significant cause of disability in childhood.
* Introduction
* Pathogenesis
* Signs and symptoms
* Diagnosis
* Treatment
Hip dysplasia can be traumatic or congenital. Development of hip dysplasia definition is still controversial. Typically hip dysplasia is the term used for patients who are born with hip dislocations or instability, which can then lead to dysplasia Solca. A broader definition of hip dysplasia is the abnormal growth of the balance. This includes bone structures as the proximal femur and acetabulum, labrum, capsule and other soft tissues. The annual incidence of congenital hip dysplasia is 2-4 cases per 1000 births and approximately 80% of individuals affected are girls. The condition can occur at any time from conception until skeletal maturity.
Congenital hip dysplasia is the result of interruption of the normal relationship between the acetabulum and femoral head. Without a proper contact between them, none will develop normally. At birth the acetabulum is large, small bones and cartilage content and the percentage of the acetabulum Covers femoral head is smaller, so the first 6 sapatamini child's life are critical for the development of joint. The etiology of hip dysplasia is not clear, but the condition seems to be associated with a number of factors such as genetics, race, child sex, intrauterine position, oligohidramonosul, cerebral palsy, myelomeningocele, artrogripoza. Development of hip dysplasia involves abnormal growth of it. Associate ligementara laxity.
Early clinical manifestations are identified during examination of the newborn and make ortolan maneuver. Other physical signs include asymmetry late dislocations buttock or lateral skin folds, decreased abduction on the affected side, walk or bipedal position with external rotation and inequality between the legs. Unilateral dislocations cause significant inequality of the legs, the imbalance of the weight and pain of the thigh and knee. Developing false acetabulum is associated with adverse prognosis in 75% of patients. Failure to diagnose and treat hip dysplasia in the immediate neonatal period may cause significant morbidity: the need to open and develop osteoarthritis therapies. The possible complications of treatment include recurrent dysplasia, recurrent dislocations and femoral head avascular necrosis.
Indications for surgery depend on the severity of the disease, and the formation bilateralitate or not a false acetabulum. Indications for treatment depend on patient age and the success of previous techniques. Children under 6 months examination instability are treated with a form of limb tijare and harnesses. If this method has no benefit to trying to reduce the traction before closed reduction. When the child is over two years or failure to consider other methods attempted open reduction. If the patient has more than three years trying to shorten a member. One patient with residual acetabular dysplasia over four years should be treated with an acetabular procedure. Treatment for a patient diagnosed in adult age is considered for residual hip dysplasia.
Evolution of children treated for hip dysplasia is very good, especially if dysplasia is controlled by closed treatment. If successful techniques have not closed and open reduction is required, the prognosis is less favorable, although short-term prognosis seems favorable. If secondary procedures are needed to achieve reduction worsens prognosis. Early diagnosis is crucial issue of treatment of children with hip dysplasia. Using ultrasound and other imaging procedures and implementation of specific educational programs decreased the number of children with hip dysplasia and late diagnosis. Less invasive techniques: the endoscopy, imaging-guided surgery is an effort to decrease mortality from surgery and speed recovery.
Although for most patients the problem resolves spontaneously within the first months of life, persitienta dysplasia can cause chronic pain, disorders of growth and weight and degenerative arthritis. In its severe hip dysplasia is one of the most common congenital malformations and a significant cause of disability in childhood.
Muscle cramps
Muscle cramps
Muscle cramps are involuntary contractions of a muscle or muscle group. Cramps cause intense pain and inability to use muscles affected.
Muscle cramps
Cramps are unpleasant, often painful muscle caused by contraction or shortening. Can be caused by cold, low physical or overutilization of calcium in the blood (especially teenagers when they need Pein blood calcium and bone maturation). However, most commonly found to cause muscle cramps is low levels of blood sodium and potassium, along with excessive dehydration. Febrile illness or poisoning can also cause cramps, particularly in stomach-called muscle cramps. These muscles contract or relax spasms mu. Cramps are involuntary, can be very painful and are maintained from several seconds up to several minutes. Occasionally may take up to 15 minutes. Upon triggering spasm, the muscle is hard and visible. Spasm is due to spontaneous contractions and affect individual muscle groups.
Muscle cramps are common in athletes and older people who perform strenuous activities. Athletes are prone to leg cramps when the body is tired or is not properly trained effort. Develop cramps at the end of intense exercise and 4 hours later. Older persons are more succeptibile the normal cramps muscle atrophy beginning at age 40 and accelerates time with inactivity. Paramiotonie People with congenital myotonic severe defects or by glycolysis metabolic myopathies (McArdle's disease, Cori disease or Forbes disease Bulls deficit defidrogenaza lactate) can cause muscle pain and muscle spasms nonneurale.
Most cramps can be stopped evolving when muscle stretches. To recommend outpatient leg cramps. For gastrocnemius muscle cramp (thigh leg) may make the person can stretch the affected limb to support the hands on the wall. Gentle massage helps relax the muscles, also aplicxarea local heat. An unusual and unexplained therapeutic method is represented by firm pinching of the tissue overlying the lip, under nose and keep up to stop cramp ciupiturii (15 min). Botulinum toxin injections are used successfully for some dystonic muscle disorders localized to a limited group of muscles. A favorable response can be maintained for several months. Treatment of cramps associated with specific diseases requires treatment.
Muscle cramps
Causes of muscle cramps There are many causes of cramping: hiperflexia, hypoxia, exposure to sudden changes in temperature, dehydration, low sodium in the blood, or hypocalcemia. Muscle cramps can be a symptom or complication of pregnancy, kidney disease, thyroid disease, or hypocalcemia hipopotasemiei, restless legs syndrome, varicose veins and multiple sclerosis. Electrolyte imbalances can cause muscle cramps and tetany, especially low levels of potassium and calcium. This disorder derives from the large losses of interstitial fluid through sweat. Interstitial fluid contains a majority amount of water and salt from the body. The loss of osmotically active particles in muscle cells leads to disruption of osmotic balance and swelling of muscles. Edema cause impaired muscle calcium pump of sarcoplasmic reticulum lumen and muscle, troponin and calcium remains trapped in the muscle contraction is continued. Association was noted with restless legs syndrome muscle cramps, both the result of excess insulin. Avoiding low concentrations of glucose in the blood helps to avoid cramps. External causes: Many medicines can cause cramps. Strong diuretics (furosemide) that eliminates body fluids can cause cramping. They also cause loss of sodium and potassium, calcium, magnesium. Statins are known to cause myalgia and cramps among other adverse effects, including lowering blood glucose. Other risk factors are vigorous physical exercise, age, female sex, history of cramping in history and hypothyroidism. Up to 80% of the athletes who use statins suffer significant effects come true muscle. Coenzyme Q10 supplementation is useful to avoid some strength by combination with statins. Drugs such as donepezil (Alzheimer's) and neostigmine (for myasthenia gravis), raloxifene (osteoporosis) causes cramps. Tolcapone (Parkinson's) cause cramping in 10% of patients. Nifedipine (for arrhythmia, hypertension), terbutaline (for asthma) and albuterlul cause muscle cramps. Cramps are detected in patients who discontinued medication with a sedative, including alcohol, barbiturates, benzodiazepines. Some vitamin deficiencies can cause muscle cramps, directly or indirectly: thiamine (B1), pantothenic acid (B5), pyridoxine (B6).
Signs and symptoms Muscle cramps
Cramps are extremely common. Almost every person has experienced a muscle cramp at some point in life. Cramps are common in adults and are common along with aging. Characteristic cramps are painful. One has to stop its activities because it can not use the affected muscle. Severe cramps and fever associated with muscle swelling that may persist for several days after cessation of cramp. Affected muscle protruding subcutaneously and is tough. Muscle cramps are common in athletes and older people who perform strenuous activities. Athletes are prone to leg cramps when the body is tired or is not properly trained effort. Develop cramps at the end of intense exercise and 4 hours later. Older persons are more succeptibile the normal cramps muscle atrophy beginning at age 40 and accelerates time with inactivity.
Types of Muscle cramps: Skeletal muscle cramps - Chassis: Skeletal muscles can be controlled voluntarily to other muscle groups. Of these the most commonly affected are those of leg cramps, thigh and sole. These cramps are associated with vigorous activity and can be extremely painful. Nocturnal leg cramps: Nocturnal cramps are involuntary muscle contractions that occur at night, sleep or less at rest. Duration of night cramps is very variable, from several seconds up to several minutes. Muscle pain may remain for a period after the cessation of cramps. These cramps are more common in the elderly, but may be encountered at any age. Are common in teens and some people who exercise at night. They can be very painful, especially if the person is dehydrated. Usually the application of pressure on the affected leg cramps outpatient determine disappearance. Precise cause of these cramps is unclear. Potential contributing factors are dehydration, low levels of certain minerals in the body (magnesium, potassium, calcium and sodium) and decreased blood flow through the muscles, if prolonged rest. These cramps are relieved by stretching exercises of the affected leg and great toe flexion. Outpatient shortens cramps. Nocturnal cramps are considered normal in the advanced stages of pregnancy. Smooth muscle cramps - colicele: Underlying smooth muscle contractions cramps (colicelor) internal organs: intestine, uterus, ureter (renal lithiasis colic). Menstrual cramps (dysmenorrhea) Menstruation is also a different intensity because of cramps in the abdomen, low back and groin irradiation. Menstrual cramps can be treated with ibuprofen, acetaminophen, stretching exercises or the application of local heat. Menstrual cramps that do not respond to these treatments may be symptomatic of endometriosis. Cramps in pregnancy: Some women may experience cramping at 7 days after ovulation. If you are pregnant the cramps are called, hears implantation, and they occur when the zygote attaches itself to the uterus. Not all women feel them. Another type of cramp during pregnancy is round ligament Äúdurerea have. This is a cramp that occurs as the muscles under your uterus expand to support the weight of the uterus. These cramps are not normal and bring medical problems. Cramps by dehydration and exposure to high temperatures: Exposure to heat cramps occur when the body's core temperature exceeds the safe internal organs. Heat cramps are the first signs of disturbances caused by heat. Loss of body salt through sweat musculrare cause painful spasms. Dyspnoea: In tetany all nerve cells in the body stimulating the muscles are activated. This reaction cause spasms or cramps throughout the body. The name is derived from tetanus toxin tetanus effect on the nerves. Today the name is used for muscles cramps and other etiology. Decreased calcium and magnesium also produces muscle tetany. Often they are accompanied by hyperactivity of other functions outside of the muscle nerve. For example, hypocalcemia can cause muscle spasms not only the hand and wrist, and perioral tingling sensation. Dystonic cramps: In this category are not required for the muscles that enable movement are stimulated to contract. The muscles that are affected by this type of cramping include those working in the opposite direction of the motion made and those who exaggerate the movement. Some dystonic cramps affect small groups of muscles (eyelids, perioral, neck, larynx). Hands and arms are affected while performing some repetitive motion (cramps writer, the musician). Each of these gates produces repetitive muscle cramps by fatigue.
Treatment of muscle cramps Muscle cramps can be treated by applying a gentle massage on the affected muscles, stretching hands above his head, inhaling deeply through your mouth and applying heat or cold. Heat improves blood flow to peripheral muscles and increases flexibility. Application of excessive heat or cold may aggravate the exhausted muscles cramping. Mechanical loading of the muscles are already exhausted or disability cause muscle cramps installation. Treatment for leg cramps is the fastest MEMBER lifting and stretching it by grasping fingers.
In case of inadequate oxygenation, excess lactic acid produced by anaerobic respiration determine the onset of cramps. Oxygenation is improved by rapid deep breaths.
Muscle cramps
Cramps by dehydration and lack of salt in the body are treated with water and salt consumption. Caused by excessive heat cramps contitii requires the following therapeutic Intro-fasting person affected by the cold breeze, a cool room -This will take a drink electrolytes (Gatorade, Pedialyte) or salt water Spray water over the patient's skin Wrap the patient in cool clothes, wet, wet compresses applied Will mass-to-painful muscles and relax.
Eating foods rich in potassium helps prevent muscle cramps.
If the affected vein treatment for varicose veins with sclerotherapy, endovenous laser or surgery without relief of symptoms.
Quinina is prescribed to treat leg cramps. Commercial products containing mixtures of calcium gluconate, vitamin B3 and D3 are most suitable for treating these cramps. Botulinum toxin injections are used successfully for some dystonic muscle disorders localized to a limited group of muscles. A favorable response can be maintained for several months. Prevention of muscle cramps: Doctors recommend exercise before and after heat cramps are caused by physical activity. Proper hydration before, during and after activity is important, especially if the duration exceeds one hour effort. Excessive fatigue in hot environment should be avoided. The task will be to add calcium and potassium. Dystonic cramps caused by repetitive activities can be prevented by ergonomizarea easy job: support for the wrist, avoiding high heels, adjusting seat positions flosirea breaks and comfortable. Avoid excessive pressure making activities. Nocturnal cramps can be avoided by stretching exercises before bedtime. Muscle cramps
Muscle cramps are involuntary contractions of a muscle or muscle group. Cramps cause intense pain and inability to use muscles affected.
Muscle cramps
Cramps are unpleasant, often painful muscle caused by contraction or shortening. Can be caused by cold, low physical or overutilization of calcium in the blood (especially teenagers when they need Pein blood calcium and bone maturation). However, most commonly found to cause muscle cramps is low levels of blood sodium and potassium, along with excessive dehydration. Febrile illness or poisoning can also cause cramps, particularly in stomach-called muscle cramps. These muscles contract or relax spasms mu. Cramps are involuntary, can be very painful and are maintained from several seconds up to several minutes. Occasionally may take up to 15 minutes. Upon triggering spasm, the muscle is hard and visible. Spasm is due to spontaneous contractions and affect individual muscle groups.
Muscle cramps are common in athletes and older people who perform strenuous activities. Athletes are prone to leg cramps when the body is tired or is not properly trained effort. Develop cramps at the end of intense exercise and 4 hours later. Older persons are more succeptibile the normal cramps muscle atrophy beginning at age 40 and accelerates time with inactivity. Paramiotonie People with congenital myotonic severe defects or by glycolysis metabolic myopathies (McArdle's disease, Cori disease or Forbes disease Bulls deficit defidrogenaza lactate) can cause muscle pain and muscle spasms nonneurale.
Most cramps can be stopped evolving when muscle stretches. To recommend outpatient leg cramps. For gastrocnemius muscle cramp (thigh leg) may make the person can stretch the affected limb to support the hands on the wall. Gentle massage helps relax the muscles, also aplicxarea local heat. An unusual and unexplained therapeutic method is represented by firm pinching of the tissue overlying the lip, under nose and keep up to stop cramp ciupiturii (15 min). Botulinum toxin injections are used successfully for some dystonic muscle disorders localized to a limited group of muscles. A favorable response can be maintained for several months. Treatment of cramps associated with specific diseases requires treatment.
Muscle cramps
Causes of muscle cramps There are many causes of cramping: hiperflexia, hypoxia, exposure to sudden changes in temperature, dehydration, low sodium in the blood, or hypocalcemia. Muscle cramps can be a symptom or complication of pregnancy, kidney disease, thyroid disease, or hypocalcemia hipopotasemiei, restless legs syndrome, varicose veins and multiple sclerosis. Electrolyte imbalances can cause muscle cramps and tetany, especially low levels of potassium and calcium. This disorder derives from the large losses of interstitial fluid through sweat. Interstitial fluid contains a majority amount of water and salt from the body. The loss of osmotically active particles in muscle cells leads to disruption of osmotic balance and swelling of muscles. Edema cause impaired muscle calcium pump of sarcoplasmic reticulum lumen and muscle, troponin and calcium remains trapped in the muscle contraction is continued. Association was noted with restless legs syndrome muscle cramps, both the result of excess insulin. Avoiding low concentrations of glucose in the blood helps to avoid cramps. External causes: Many medicines can cause cramps. Strong diuretics (furosemide) that eliminates body fluids can cause cramping. They also cause loss of sodium and potassium, calcium, magnesium. Statins are known to cause myalgia and cramps among other adverse effects, including lowering blood glucose. Other risk factors are vigorous physical exercise, age, female sex, history of cramping in history and hypothyroidism. Up to 80% of the athletes who use statins suffer significant effects come true muscle. Coenzyme Q10 supplementation is useful to avoid some strength by combination with statins. Drugs such as donepezil (Alzheimer's) and neostigmine (for myasthenia gravis), raloxifene (osteoporosis) causes cramps. Tolcapone (Parkinson's) cause cramping in 10% of patients. Nifedipine (for arrhythmia, hypertension), terbutaline (for asthma) and albuterlul cause muscle cramps. Cramps are detected in patients who discontinued medication with a sedative, including alcohol, barbiturates, benzodiazepines. Some vitamin deficiencies can cause muscle cramps, directly or indirectly: thiamine (B1), pantothenic acid (B5), pyridoxine (B6).
Signs and symptoms Muscle cramps
Cramps are extremely common. Almost every person has experienced a muscle cramp at some point in life. Cramps are common in adults and are common along with aging. Characteristic cramps are painful. One has to stop its activities because it can not use the affected muscle. Severe cramps and fever associated with muscle swelling that may persist for several days after cessation of cramp. Affected muscle protruding subcutaneously and is tough. Muscle cramps are common in athletes and older people who perform strenuous activities. Athletes are prone to leg cramps when the body is tired or is not properly trained effort. Develop cramps at the end of intense exercise and 4 hours later. Older persons are more succeptibile the normal cramps muscle atrophy beginning at age 40 and accelerates time with inactivity.
Types of Muscle cramps: Skeletal muscle cramps - Chassis: Skeletal muscles can be controlled voluntarily to other muscle groups. Of these the most commonly affected are those of leg cramps, thigh and sole. These cramps are associated with vigorous activity and can be extremely painful. Nocturnal leg cramps: Nocturnal cramps are involuntary muscle contractions that occur at night, sleep or less at rest. Duration of night cramps is very variable, from several seconds up to several minutes. Muscle pain may remain for a period after the cessation of cramps. These cramps are more common in the elderly, but may be encountered at any age. Are common in teens and some people who exercise at night. They can be very painful, especially if the person is dehydrated. Usually the application of pressure on the affected leg cramps outpatient determine disappearance. Precise cause of these cramps is unclear. Potential contributing factors are dehydration, low levels of certain minerals in the body (magnesium, potassium, calcium and sodium) and decreased blood flow through the muscles, if prolonged rest. These cramps are relieved by stretching exercises of the affected leg and great toe flexion. Outpatient shortens cramps. Nocturnal cramps are considered normal in the advanced stages of pregnancy. Smooth muscle cramps - colicele: Underlying smooth muscle contractions cramps (colicelor) internal organs: intestine, uterus, ureter (renal lithiasis colic). Menstrual cramps (dysmenorrhea) Menstruation is also a different intensity because of cramps in the abdomen, low back and groin irradiation. Menstrual cramps can be treated with ibuprofen, acetaminophen, stretching exercises or the application of local heat. Menstrual cramps that do not respond to these treatments may be symptomatic of endometriosis. Cramps in pregnancy: Some women may experience cramping at 7 days after ovulation. If you are pregnant the cramps are called, hears implantation, and they occur when the zygote attaches itself to the uterus. Not all women feel them. Another type of cramp during pregnancy is round ligament Äúdurerea have. This is a cramp that occurs as the muscles under your uterus expand to support the weight of the uterus. These cramps are not normal and bring medical problems. Cramps by dehydration and exposure to high temperatures: Exposure to heat cramps occur when the body's core temperature exceeds the safe internal organs. Heat cramps are the first signs of disturbances caused by heat. Loss of body salt through sweat musculrare cause painful spasms. Dyspnoea: In tetany all nerve cells in the body stimulating the muscles are activated. This reaction cause spasms or cramps throughout the body. The name is derived from tetanus toxin tetanus effect on the nerves. Today the name is used for muscles cramps and other etiology. Decreased calcium and magnesium also produces muscle tetany. Often they are accompanied by hyperactivity of other functions outside of the muscle nerve. For example, hypocalcemia can cause muscle spasms not only the hand and wrist, and perioral tingling sensation. Dystonic cramps: In this category are not required for the muscles that enable movement are stimulated to contract. The muscles that are affected by this type of cramping include those working in the opposite direction of the motion made and those who exaggerate the movement. Some dystonic cramps affect small groups of muscles (eyelids, perioral, neck, larynx). Hands and arms are affected while performing some repetitive motion (cramps writer, the musician). Each of these gates produces repetitive muscle cramps by fatigue.
Treatment of muscle cramps Muscle cramps can be treated by applying a gentle massage on the affected muscles, stretching hands above his head, inhaling deeply through your mouth and applying heat or cold. Heat improves blood flow to peripheral muscles and increases flexibility. Application of excessive heat or cold may aggravate the exhausted muscles cramping. Mechanical loading of the muscles are already exhausted or disability cause muscle cramps installation. Treatment for leg cramps is the fastest MEMBER lifting and stretching it by grasping fingers.
In case of inadequate oxygenation, excess lactic acid produced by anaerobic respiration determine the onset of cramps. Oxygenation is improved by rapid deep breaths.
Muscle cramps
Cramps by dehydration and lack of salt in the body are treated with water and salt consumption. Caused by excessive heat cramps contitii requires the following therapeutic Intro-fasting person affected by the cold breeze, a cool room -This will take a drink electrolytes (Gatorade, Pedialyte) or salt water Spray water over the patient's skin Wrap the patient in cool clothes, wet, wet compresses applied Will mass-to-painful muscles and relax.
Eating foods rich in potassium helps prevent muscle cramps.
If the affected vein treatment for varicose veins with sclerotherapy, endovenous laser or surgery without relief of symptoms.
Quinina is prescribed to treat leg cramps. Commercial products containing mixtures of calcium gluconate, vitamin B3 and D3 are most suitable for treating these cramps. Botulinum toxin injections are used successfully for some dystonic muscle disorders localized to a limited group of muscles. A favorable response can be maintained for several months. Prevention of muscle cramps: Doctors recommend exercise before and after heat cramps are caused by physical activity. Proper hydration before, during and after activity is important, especially if the duration exceeds one hour effort. Excessive fatigue in hot environment should be avoided. The task will be to add calcium and potassium. Dystonic cramps caused by repetitive activities can be prevented by ergonomizarea easy job: support for the wrist, avoiding high heels, adjusting seat positions flosirea breaks and comfortable. Avoid excessive pressure making activities. Nocturnal cramps can be avoided by stretching exercises before bedtime. Muscle cramps
Chondrosarcoma Treatment
Chondrosarcoma
* Introduction
* Diagnosis
* Treatment
Chondrosarcoma Treatment
Treatment
Extended surgical curettage and bone graft or artificial plastic. Skeletally immature patients is recommended to fill the bone defect with polymethylmethacrylate, this skeletal growth while allowing the tumor cells are destroyed. In older patients where skeletal development is not a problem bone grafting is recommended for small lesions. For large lesions and cement reconstruction is necessary. Filling the defect with polymethylmethacrylate is recommended after removal of recurrent lesions.
Block or wide excision is reserved for advanced tumors that can not be treated by intralesional excision. The rate of recurrence after en bloc excision is 7%. Options include reconstruction after wide excision and reconstruction with structural allogrefarea endoprosthesis or allograft prosthetic.
Chondrosarcoma Treatment Prognosis: The prognosis is generally correlated with lesion size, anatomical location and histological grading of the site. Patients with axial lesions were most negative prognosis from those with lesions of the appendicular skeleton. 5-year survival rate for patients with grade 1 lesions is 90%, the rate dropped to 29% for those with grade 3 tumors. Grade 1 lesions do not metastasize. Metastatic extension typically is most frequently associated pulmonary lesions of grade 3. Extending through the lymph nodes is more frequent in chondrosarcoma than in other bone neoplasms. Tumor Recurrence after surgery occurs in 5-10 years. Recurrent chondrosarcoma is more aggressive than the primary, and the histological grading is increased.
* Introduction
* Diagnosis
* Treatment
Chondrosarcoma Treatment
Treatment
Extended surgical curettage and bone graft or artificial plastic. Skeletally immature patients is recommended to fill the bone defect with polymethylmethacrylate, this skeletal growth while allowing the tumor cells are destroyed. In older patients where skeletal development is not a problem bone grafting is recommended for small lesions. For large lesions and cement reconstruction is necessary. Filling the defect with polymethylmethacrylate is recommended after removal of recurrent lesions.
Block or wide excision is reserved for advanced tumors that can not be treated by intralesional excision. The rate of recurrence after en bloc excision is 7%. Options include reconstruction after wide excision and reconstruction with structural allogrefarea endoprosthesis or allograft prosthetic.
Chondrosarcoma Treatment Prognosis: The prognosis is generally correlated with lesion size, anatomical location and histological grading of the site. Patients with axial lesions were most negative prognosis from those with lesions of the appendicular skeleton. 5-year survival rate for patients with grade 1 lesions is 90%, the rate dropped to 29% for those with grade 3 tumors. Grade 1 lesions do not metastasize. Metastatic extension typically is most frequently associated pulmonary lesions of grade 3. Extending through the lymph nodes is more frequent in chondrosarcoma than in other bone neoplasms. Tumor Recurrence after surgery occurs in 5-10 years. Recurrent chondrosarcoma is more aggressive than the primary, and the histological grading is increased.
Chondrosarcoma Diagnosis
Chondrosarcoma
* Introduction
* Diagnosis
* Treatment
Diagnosis
Studi imaging: Radiograph is essential for initial diagnosis of chondrosarcoma. Radiograph is sometimes supplemented with CT scan, which is more sensitive in detecting calcifications in the matrix and confirm intramedullary tumors endostiale cortical damage. Radiography typically shows a lesion radiolucenta, which often contains calcifications matrix. The degree of organization may be correlated with tumor grade matrix calcification. Aggressive tumors contain irregular calcifications. Typical appearance of rings and arcs. Intramedullary lesion edge is determined by the degree of tumor aggression. It is bad defined. The presence of cortical destruction and a soft tissue mass indicates malignancy.
Radionuclide scan showed increased intake of radioisotopes in areas of bone scans, but the difference between chondrosarcoma and encondrom not argue. Capturing the isotope can show metabolic activity osteocondrom or malignant transformation. In the absence of malignancy is unusual capture.
Magnetic resonance imaging is the preferred method for evaluating tumor extension extraosoase intramedullary extension and demonstration. MRI is useful in evaluating the thinning carticajului osteocondrom meet to develop a secondary chondrosarcoma. It is the most sensitive for identifying small amounts of calcified matrix intro tumor.
Chondrosarcoma Diagnosis Histological examination: macroscopic Chondrosarcoma looks gray-white lobe. May show focal calcification, mucoid degeneration or necrosis. It is differentiated from benign cartilaginous lesions by large nuclei, multiple cells in gaps, binucleate cells and nuclei pleomorfismul hyperchrome. The differential diagnosis is made with the following conditions: myocardial bone encondromul, osteosarcoma, osteocondromul, fibrosarcoma.
* Introduction
* Diagnosis
* Treatment
Diagnosis
Studi imaging: Radiograph is essential for initial diagnosis of chondrosarcoma. Radiograph is sometimes supplemented with CT scan, which is more sensitive in detecting calcifications in the matrix and confirm intramedullary tumors endostiale cortical damage. Radiography typically shows a lesion radiolucenta, which often contains calcifications matrix. The degree of organization may be correlated with tumor grade matrix calcification. Aggressive tumors contain irregular calcifications. Typical appearance of rings and arcs. Intramedullary lesion edge is determined by the degree of tumor aggression. It is bad defined. The presence of cortical destruction and a soft tissue mass indicates malignancy.
Radionuclide scan showed increased intake of radioisotopes in areas of bone scans, but the difference between chondrosarcoma and encondrom not argue. Capturing the isotope can show metabolic activity osteocondrom or malignant transformation. In the absence of malignancy is unusual capture.
Magnetic resonance imaging is the preferred method for evaluating tumor extension extraosoase intramedullary extension and demonstration. MRI is useful in evaluating the thinning carticajului osteocondrom meet to develop a secondary chondrosarcoma. It is the most sensitive for identifying small amounts of calcified matrix intro tumor.
Chondrosarcoma Diagnosis Histological examination: macroscopic Chondrosarcoma looks gray-white lobe. May show focal calcification, mucoid degeneration or necrosis. It is differentiated from benign cartilaginous lesions by large nuclei, multiple cells in gaps, binucleate cells and nuclei pleomorfismul hyperchrome. The differential diagnosis is made with the following conditions: myocardial bone encondromul, osteosarcoma, osteocondromul, fibrosarcoma.
Chondrosarcoma
Chondrosarcoma
* Introduction
* Diagnosis
* Treatment
Chondrosarcoma is the second most common malignant bone, representing 25% of primary bone neoplasms. Chondrosarcomas represents a group of tumors with different characteristics, ranging from slow-growing lesions without metastases highly aggressive metastasizing tumors up.
Chondrosarcomas incidence is dependent on patient age. In children the incidence is low. Most tumors occur at ages over 40 years. The risk is increased in patients with chondrosarcoma syndromes encondromatoza: Ollier disease, syndrome Maffuci, metacondromatoza) and those with hereditary multiple exostoza. Patients with these conditions are generally young.
For patients with chondrosarcoma, prognosis is generally correlated with lesion size, anatomical location and histological grading of the site. Patients with axial lesions were most negative prognosis from those with lesions of the appendicular skeleton. 5-year survival rate for patients with grade 1 lesions is 90%, the rate dropped to 29% for those with grade 3 tumors.
Pathogenesis chondrosarcoma Chondrosarcoma is a malignant tumor of origin in the formation of cartilaginous tumor matrix is likely condroida. Chondrosarcomas are classified as central (originating in the intramedullary canal) or peripheral. Juxtacorticale lesions rarely appear. Occur when lesions are primary or secondary de novo occur when a preexisting lesion or as a encondrom osteocondrom. Grade 1 lesions do not metastasize. Metastatic extension typically is most frequently associated pulmonary lesions of grade 3. Extending through the lymph nodes is more frequent in chondrosarcoma than in other bone neoplasms. Tumor Recurrence after surgery occurs in 5-10 years. Recurrent chondrosarcoma is more aggressive than the primary, and the histological grading is increased. Tumors are characterized by the degree of differentiation. Grade 1 is the least aggressive in terms of histology, and grade 3 is the most aggressive tumor. Most condrosarcoame are classified pathologically as conventional clear cell, myxoid, mesenchymal and undifferentiated.
Signs and symptoms Age of occurrence of Chondrosarcomas is over 40 years. Chondrosarcomas side affects patients between 20-40 years. Chondrosarcomas are rare in children, and when everybody is more aggressive. Tumors are predominantly axial location is the most common pelvic bones, femur, humerus, ribs, scapula, sternum or spine. The tubular bones of metaphysics is most affected. Metaphysics is the most frequently affected proximal than distal. Impaired distal humerus is unusual. Chondrosarcomas are rare hand and foot, and if complications are discovered are multiple encondromatozei syndrome.
The most common symptom at presentation is pain, which is present for several months and is of medium intensity. It may worsen at night. Local swelling may be present. When the tumor is adjacent to a joint may be present epansamentele or restrict movement. The average duration of symptoms before presentation is 1-2 years. The tumor occurs occasionally as a pathological fracture.
There are three additional types condrosarcoame: Mesenchymal chondrosarcoma: A rare variant with histological bimorph and undifferentiated cells resembling Ewing's sarcoma. Shows predilection for the spine, ribs and jaw. It is found in the third decade of life. It is more common in women and can grow extremely large. Spread to lungs, lymph nodes and other bones. Clear cell chondrosarcoma: It is a malignant cartilage tumor that may be the adult version of chondrosarcoma. It is a rare tumor with better prognosis and lower grading. It detects the femur and humerus epiphysis. Histologically soft tissue invasion is rare. Shows the clear cell cytoplasm vacuole. Calcified cartilage matrix shows trabeculae and giant cells. Chondrosarcoma didiferentiat: It is the most malignant form of chondrosarcoma. This tumor is a mixture of low-grade Chondrosarcoma and highly fibrous sarcoma, in which an aspect fibrocitele cartilage. Didiferentiate portion of the lesion may be malignant fibrous histiocitom histological data, undifferentiated sarcoma or osteosarcoma. It has a 10% survival rate at 5 years.
* Introduction
* Diagnosis
* Treatment
Chondrosarcoma is the second most common malignant bone, representing 25% of primary bone neoplasms. Chondrosarcomas represents a group of tumors with different characteristics, ranging from slow-growing lesions without metastases highly aggressive metastasizing tumors up.
Chondrosarcomas incidence is dependent on patient age. In children the incidence is low. Most tumors occur at ages over 40 years. The risk is increased in patients with chondrosarcoma syndromes encondromatoza: Ollier disease, syndrome Maffuci, metacondromatoza) and those with hereditary multiple exostoza. Patients with these conditions are generally young.
For patients with chondrosarcoma, prognosis is generally correlated with lesion size, anatomical location and histological grading of the site. Patients with axial lesions were most negative prognosis from those with lesions of the appendicular skeleton. 5-year survival rate for patients with grade 1 lesions is 90%, the rate dropped to 29% for those with grade 3 tumors.
Pathogenesis chondrosarcoma Chondrosarcoma is a malignant tumor of origin in the formation of cartilaginous tumor matrix is likely condroida. Chondrosarcomas are classified as central (originating in the intramedullary canal) or peripheral. Juxtacorticale lesions rarely appear. Occur when lesions are primary or secondary de novo occur when a preexisting lesion or as a encondrom osteocondrom. Grade 1 lesions do not metastasize. Metastatic extension typically is most frequently associated pulmonary lesions of grade 3. Extending through the lymph nodes is more frequent in chondrosarcoma than in other bone neoplasms. Tumor Recurrence after surgery occurs in 5-10 years. Recurrent chondrosarcoma is more aggressive than the primary, and the histological grading is increased. Tumors are characterized by the degree of differentiation. Grade 1 is the least aggressive in terms of histology, and grade 3 is the most aggressive tumor. Most condrosarcoame are classified pathologically as conventional clear cell, myxoid, mesenchymal and undifferentiated.
Signs and symptoms Age of occurrence of Chondrosarcomas is over 40 years. Chondrosarcomas side affects patients between 20-40 years. Chondrosarcomas are rare in children, and when everybody is more aggressive. Tumors are predominantly axial location is the most common pelvic bones, femur, humerus, ribs, scapula, sternum or spine. The tubular bones of metaphysics is most affected. Metaphysics is the most frequently affected proximal than distal. Impaired distal humerus is unusual. Chondrosarcomas are rare hand and foot, and if complications are discovered are multiple encondromatozei syndrome.
The most common symptom at presentation is pain, which is present for several months and is of medium intensity. It may worsen at night. Local swelling may be present. When the tumor is adjacent to a joint may be present epansamentele or restrict movement. The average duration of symptoms before presentation is 1-2 years. The tumor occurs occasionally as a pathological fracture.
There are three additional types condrosarcoame: Mesenchymal chondrosarcoma: A rare variant with histological bimorph and undifferentiated cells resembling Ewing's sarcoma. Shows predilection for the spine, ribs and jaw. It is found in the third decade of life. It is more common in women and can grow extremely large. Spread to lungs, lymph nodes and other bones. Clear cell chondrosarcoma: It is a malignant cartilage tumor that may be the adult version of chondrosarcoma. It is a rare tumor with better prognosis and lower grading. It detects the femur and humerus epiphysis. Histologically soft tissue invasion is rare. Shows the clear cell cytoplasm vacuole. Calcified cartilage matrix shows trabeculae and giant cells. Chondrosarcoma didiferentiat: It is the most malignant form of chondrosarcoma. This tumor is a mixture of low-grade Chondrosarcoma and highly fibrous sarcoma, in which an aspect fibrocitele cartilage. Didiferentiate portion of the lesion may be malignant fibrous histiocitom histological data, undifferentiated sarcoma or osteosarcoma. It has a 10% survival rate at 5 years.
Condrocalcinoza Treatment
Condrocalcinoza
* Introduction
* Diagnosis
* Treatment
Treatment
Treatment depends on the degree of impairment. For patients who demonstrate symptoms following treatment algorithm led to arthritic patients with osteoarthritis: modification of activity, physical therapy and administration of anti-inflammatory drugs. Surgery is indicated when the response to these modalities is unsatisfactory. For people with acute episodes of pain and disability is recommended for symptomatic arthrocentesis with intra-articular corticosteroid administration. NSAIDs and colchicine can be used to prevent recurrent episodes.
There are several studies showing favorable results by reducing calcium deposits acetic acid-EDTA ethylene diamine. It strongly binds divalent cations including calcium and shows the potential to remove the affected area. The role of EDTA in the treatment of extensive investigations because condrocalcinozei still need the agent shows significant adverse effects.
Pulsed ultrasound proved to be an effective treatment for some diseases calcification. Patients have pain relief. In a study carried out 50% of treated subjects showed calcifications halved after 6 weeks of treatment. Methotrexate has been shown effective in patients with severe disease and joint destruction. Recent studies suggest the important role of inflamason complex. Anakira is such an option in patients with this condition.
Surgical therapy: Arthroscopic surgery allows debridement of the superficial deposits of crystals. This procedure does not alter disease progression. Surgical treatment of osteoarthritis with debridement, microfracture chondroplasty by, radiofrequency chondroplasty, osteochondral transfer, osteotomy and partial or total joint reinlocuirea complete regimens. When lesions are present tofacee indicate large surgical excision. Although the impact on the viability of storing crystals and future performance of the articular cartilage and meniscus are not clear, it is considered a fragile tissue induced by precipitates.
* Introduction
* Diagnosis
* Treatment
Treatment
Treatment depends on the degree of impairment. For patients who demonstrate symptoms following treatment algorithm led to arthritic patients with osteoarthritis: modification of activity, physical therapy and administration of anti-inflammatory drugs. Surgery is indicated when the response to these modalities is unsatisfactory. For people with acute episodes of pain and disability is recommended for symptomatic arthrocentesis with intra-articular corticosteroid administration. NSAIDs and colchicine can be used to prevent recurrent episodes.
There are several studies showing favorable results by reducing calcium deposits acetic acid-EDTA ethylene diamine. It strongly binds divalent cations including calcium and shows the potential to remove the affected area. The role of EDTA in the treatment of extensive investigations because condrocalcinozei still need the agent shows significant adverse effects.
Pulsed ultrasound proved to be an effective treatment for some diseases calcification. Patients have pain relief. In a study carried out 50% of treated subjects showed calcifications halved after 6 weeks of treatment. Methotrexate has been shown effective in patients with severe disease and joint destruction. Recent studies suggest the important role of inflamason complex. Anakira is such an option in patients with this condition.
Surgical therapy: Arthroscopic surgery allows debridement of the superficial deposits of crystals. This procedure does not alter disease progression. Surgical treatment of osteoarthritis with debridement, microfracture chondroplasty by, radiofrequency chondroplasty, osteochondral transfer, osteotomy and partial or total joint reinlocuirea complete regimens. When lesions are present tofacee indicate large surgical excision. Although the impact on the viability of storing crystals and future performance of the articular cartilage and meniscus are not clear, it is considered a fragile tissue induced by precipitates.
Condrocalcinoza Diagnosis
Condrocalcinoza
* Introduction
* Diagnosis
* Treatment
Diagnosis
Laboratory studies: Erythrocyte-sedimentation rate is high, leukocytosis observed The young patients will Evel hemochromatosis, hyperparathyroidism, hypothyroidism -Evaluation of serum calcium, phosphorus, magnesium and alkaline phosphatase The measurement of iron, transferrin saturation and ferritin, thyroid hormones -Performing polarized light microscopy after aspiration of fluid from the affected joint, the crystals are rhomboid, weakly positive birefringence and difficult to see.
Imaging Studies: Routine radiograph demonstrates pathology. Calcifications is recognized by hyaline cartilage or fibrous structures that appear dense on X-ray as a line parallel to the surface in articular hyaline cartilage. It is similar to a calcified sheath that reflects the articular surface as a concrete surface white, hard, 3-4 mm thick in the subchondral articular surface. The disease can mimic rheumatoid arthritis and osteoarthritis primary imaging. While radiocarpiene and metacarpal phalange joints are not affected in osteoarthritis, the lesions present in these locations are highly suggestive condrocalcinoza. You notice a large subchondral cysts. Pseudoreumatoida form of the disease is erosive. The condition is suggested by degenerative osteoarthritis with unusual locations such as shoulder and elbow that do not support the weight. Identatiile radiocarpiene joint collapse and joint space with sclerosis indicate disease Calcium pyrophosphate storage.
Computed tomography showed calcified masses with typical lobe configuration in yellow ligament or joint capsule. The observed mass of low density septal areas. Pressure erosions can be seen with disruption of bone cortex. Fine granular calcifications are also seen. Subchondral cysts or erosions and fractures that may be present.
Diagnostic criteria for storage disease Calcium pyrophosphate: Criterion I-show storage of calcium pyrophosphate in synovial tissue or fluid by X-rays, or chemical analysis difractionala Criterion IIa-positive identification of crystals without birefringence with polarized light microscopy Criterion IIb-this typical radiographic calcifications Criterion-IIIa acute arthritis of the knee and other large joints Criterion-IIIb chronic arthritis of the knee, hip, wrist, carpienelor, elbow, shoulder, accompanied by acute exacerbations with unusual locations, subchondral cyst formation, severe degeneration, osteophytes formation, tendon calcifications.
Histological examination: Histological changes described in storage disease calcium pyrophosphate and calcium deposits correspond to Cartilage inflammation. These are nonspecific, but condrocartilaj calcium deposits are the most typical feature in these patients. Pathognomonic feature is seen in polarized microscopy showing rhomboid crystals, intracellular, weakly positive birefringence.
The differential diagnosis is been completed with the following conditions: ankylosing spondylitis, gout, skeletal hiperosteoza broadcast, meniscus cracks, neuropathic arthropathy, Osgood-Schlatter disease, osteoarthritis, osteocondromatoza, osteosarcoma, rheumatoid arthritis, septic arthritis, spinal stenosis, osteochondritis dissecans, synovial osteocondromatoza.
* Introduction
* Diagnosis
* Treatment
Diagnosis
Laboratory studies: Erythrocyte-sedimentation rate is high, leukocytosis observed The young patients will Evel hemochromatosis, hyperparathyroidism, hypothyroidism -Evaluation of serum calcium, phosphorus, magnesium and alkaline phosphatase The measurement of iron, transferrin saturation and ferritin, thyroid hormones -Performing polarized light microscopy after aspiration of fluid from the affected joint, the crystals are rhomboid, weakly positive birefringence and difficult to see.
Imaging Studies: Routine radiograph demonstrates pathology. Calcifications is recognized by hyaline cartilage or fibrous structures that appear dense on X-ray as a line parallel to the surface in articular hyaline cartilage. It is similar to a calcified sheath that reflects the articular surface as a concrete surface white, hard, 3-4 mm thick in the subchondral articular surface. The disease can mimic rheumatoid arthritis and osteoarthritis primary imaging. While radiocarpiene and metacarpal phalange joints are not affected in osteoarthritis, the lesions present in these locations are highly suggestive condrocalcinoza. You notice a large subchondral cysts. Pseudoreumatoida form of the disease is erosive. The condition is suggested by degenerative osteoarthritis with unusual locations such as shoulder and elbow that do not support the weight. Identatiile radiocarpiene joint collapse and joint space with sclerosis indicate disease Calcium pyrophosphate storage.
Computed tomography showed calcified masses with typical lobe configuration in yellow ligament or joint capsule. The observed mass of low density septal areas. Pressure erosions can be seen with disruption of bone cortex. Fine granular calcifications are also seen. Subchondral cysts or erosions and fractures that may be present.
Diagnostic criteria for storage disease Calcium pyrophosphate: Criterion I-show storage of calcium pyrophosphate in synovial tissue or fluid by X-rays, or chemical analysis difractionala Criterion IIa-positive identification of crystals without birefringence with polarized light microscopy Criterion IIb-this typical radiographic calcifications Criterion-IIIa acute arthritis of the knee and other large joints Criterion-IIIb chronic arthritis of the knee, hip, wrist, carpienelor, elbow, shoulder, accompanied by acute exacerbations with unusual locations, subchondral cyst formation, severe degeneration, osteophytes formation, tendon calcifications.
Histological examination: Histological changes described in storage disease calcium pyrophosphate and calcium deposits correspond to Cartilage inflammation. These are nonspecific, but condrocartilaj calcium deposits are the most typical feature in these patients. Pathognomonic feature is seen in polarized microscopy showing rhomboid crystals, intracellular, weakly positive birefringence.
The differential diagnosis is been completed with the following conditions: ankylosing spondylitis, gout, skeletal hiperosteoza broadcast, meniscus cracks, neuropathic arthropathy, Osgood-Schlatter disease, osteoarthritis, osteocondromatoza, osteosarcoma, rheumatoid arthritis, septic arthritis, spinal stenosis, osteochondritis dissecans, synovial osteocondromatoza.
Condrocalcinoza
Condrocalcinoza
* Introduction
* Diagnosis
* Treatment
Condrocalcinoza - storage disease calcium pyrophosphate is a rheumatologic disorder with varied clinical manifestations due to precipitation of calcium pyrophosphate in connective tissues. It's known as alternative names that specify certain clinical or radiographic descriptions, although neither is synonymous with storage disease calcium pyrophosphate. Pseudogout refers to the evidence of acute clinical sinovitei joints red, swollen and sensitive that are similar to arthritis of gout. Condrocalcinoza refers to the radiographic appearance of hyaline cartilage calcifications or fibrocartilajului. Arthropathy with pyrophosphates is a term that refers to both the above conditions. Statistics is the most affected knee joint.
Storage disease calcium pyrophosphate crystals of mineral deposit consists of soft tissues. It is found in high concentrations in hyaline cartilage, synovial tissue, capsule, meniscus, ligament yellow, soft tissues of the hand and rare fibrocartilajul temporomandibular joint. Polyarticular arthritis is monoarticular although initially starts. Although in theory any joint can be affected no preferential localization. In rare cases pseudogout can affect the spinal canal and cause myelopathy.
Condrocalcinozei exact pathology is unknown, although cleavage increased adenosine triphosphate (energy molecule necessary for most anmalelor) may increase the level of pyrophosphate in the joints and is considered a method of crystal growth. There is some research that suggests the involvement of genes with a role in inorganic phosphate transport.
Patients usually present with inflammation in one or more joints with pain. Hyperparathyroidism, hemochromatosis, and hypophosphatemia associated with renal osteodistrophy condrocalcinoza. Other risk factors are condrocalcinoza Wilson's disease and osteochondritis.
Treatment for asymptomatic form of the disease does not prevent joint destruction. Acute pseudogout is recommended for intra-articular corticosteroid injections, systemic corticosteroids, NSAIDs or colchicine. Surgical removal of calcifications still remains an experimental procedure.
Pathogenesis condrocalcinozei The exact physiological dysfunction condrocalcinoza is not clear, but studies involving condrocitul and surrounding matrix as responsible agents. Some chemical and physical events determine the activation of a cascade that evolves into chondrocyte hypertrophy and degeneration. Escape into the surrounding intercellular matrix material and alter the binding of calcium effect of matrix proteoglycans. Calcium pyrophosphate crystals grow from the matrix of hypertrophic chondrocytes adjacent to those affected. Rupture of collagen fibers has been proposed to be the source of inorganic pyrophosphate.
Storage disease calcium pyrophosphate is the result of a cascading inflammatory response to the storage crystal. Enzyme abnormalities or allow the formation of pyrophosphate in excess of saturation, which precipitated especially hyaline or fibrous cartilage. People with this disorder may have more than one type of crystals (hydroxyapatite and pyrophosphate). The disease can be divided into two varieties: primary and secondary. Refers to secondary disease associated with rheumatoid arthritis spondiloartropatia. Distribution of disease in people with secondary form is identical to that seen in primary form. Primary form can be divided in turn into family variants, metabolic and idiopathic. The joint damage is different between them. Variety abolii family tends to begin earlier in life than one idiopathic. Metabolic Causes and associations include: hyperparathyroidism, haemochromatosis, hypomagnesaemia, gout, ochronosis, Wilson disease, acromegaly, Paget's disease and sidnromul Gitelman.
Among varieties metabolic impairment hemochromatosis causes more severe the hand wrist, knee, ankle and metacarpals, while ochronosis affects especially the shoulder, hip, knee and spine. Hemochromatosis is a disorder of iron metabolism that accumulate and destroy body tissues, including joints. Wilson's disease consists of abnormal accumulation of copper. Ochronosis is another storage disease in homogentisinic acid accumulates as a result of the metabolising enzyme deficiency. Gitelman syndrome is a variant of Bartter-sidnromului autosomal recessive renal tubular disease. Varieties of metabolic storage disease is genetic calcium pyrophosphate.
Signs and symptoms of condrocalcinoza Condrocalcinoza or storage disease, a variant of calcium pyrophosphate arthritis. It is a chemical that manifest error by at least four associated clinical entati. Condrocalcinoza is described as soft tissue impregnation with calcium. The term is sometimes used synonymously with storage disease Calcium pyrophosphate, but technically refers to the visible presence of calcification in soft tissue imaging studies.
Condrocalcinozei manifestations include four main distinct entities: Pseudogout: Presentation appears to be similar to acute gout. Technically it is called pseudogout although the term is used synonymously with calcium pyrophosphate storage disease. Gout can be distinguished by shape crystals of pseudogout: gout crystals (sodium ugly) are in the form of needles and not birefringence, while crystals of pseudogout (calcium pyrophosphate) are diamond-shaped and have positive birefringence. Advanced electron microscopy techniques can be used to finalize the diagnosis.
Pseudogout affecting a small percentage of people condrocalcinoza-25%. Onset is usually monoarticular or pauciarticular, and is preceded by injury or surgery in the area. Pseudogout was identified after adenoma excision parotiroidian. Onset is aggressive, reaches a peak within a few hours and is manifested by pain, swelling, local heat and redness. Fever is present in half of patients with pseudogout. The knee is affected most frequently. Shoulder, elbow, ankle and joint first metacarpofalangiana are commonly affected. Evolution includes natural spontaneous resolution within a few days or weeks at most. Treatment speeds recovery.
The disease is characterized by acute oligoarticular arthritis or monoarticulara. Clinical manifestations are similar to gout. Shows acute swelling and pain but not so intense. Pseudogout can be precipitated by medical conditions such as myocardial infarction, congestive heart failure, cerebrovascular accident, or can occur after surgery. Trauma can also be a trigger. Occasionally, pseudogout may present as a syndrome pseudoseptic acute arthritis, fever and leukocytosis. Pseudogout tofacee: Mineral material can be stored in large reservoirs producing a pseudotumor. This can be massive-loaded with consequences. I am discreet painful. Lesions are found in the temporomandibular joint, sternoclaviculara, transverse ligament of C1, metatarsophalangeal joints, spinal facet joints. Impaired spinal nerve is associated with incarceration and symptomatic spinal stenosis requiring surgical decompression. Storage of calcium pyrophosphate family: A family pattern occurs at a young age, usually the third decade of life. Tends to be more aggressive with more negative long-term prognosis. Longevity satisfactory joint function is reduced in these individuals. Genetic studies involving a gene responsible for autosomal dominant inheritance mode. Gene mutation cause high levels of intracellular inorganic pyrophosphate. Low levels of extracellular inorganic pyrophosphate allows storage of hydroxyapatite in articular hyaline cartilage and fibrocartilaj. Osteoarthritis: The most common is osteoarthritis condrocalcinozei presentation. Symptoms are similar to those of the typical patient with osteoarthritis. Note that this condrocalcinozei worsens with age.
Other variants of condrocalcinozei include: Pseudosteoartrita: Often affects metacarpophalangeal joints, wrists, elbows and shoulders, joints affected by osteoarthritis are not primary. Most commonly affects the knee. This variant of the disease include 50% of cases. Approximately 50% of patients and associated with pseudogout. Bone spurs are shaped hook radiological elements common in these patients and found the initial and second metacarpal heads. This condrocalcinozei the radiograph is common. Arthritis pseudoreumatoida: This model of the disease is found in approximately 5% of patients with storage disease and calcium pyrophosphate is associated with inflammation of the metacarpophalangeal joints symmetrically. Clinic patients accuse morning stiffness and swelling. Erythrocyte sedimentation rate is high. Late age of onset, rheumatoid factor, and this lack condrocalcinozei help differentiate from rheumatoid arthritis. Pseudoneuropatica joint: Neuropaticlike arthropathy is seen in less than 5% of patients. Most often affects the knee. It is a severe destructive condition. Unlike true neuropathic arthropathy presents no clear basis of neurological condition. This condrocalcinozei support the implementation of diagnosis.
* Introduction
* Diagnosis
* Treatment
Condrocalcinoza - storage disease calcium pyrophosphate is a rheumatologic disorder with varied clinical manifestations due to precipitation of calcium pyrophosphate in connective tissues. It's known as alternative names that specify certain clinical or radiographic descriptions, although neither is synonymous with storage disease calcium pyrophosphate. Pseudogout refers to the evidence of acute clinical sinovitei joints red, swollen and sensitive that are similar to arthritis of gout. Condrocalcinoza refers to the radiographic appearance of hyaline cartilage calcifications or fibrocartilajului. Arthropathy with pyrophosphates is a term that refers to both the above conditions. Statistics is the most affected knee joint.
Storage disease calcium pyrophosphate crystals of mineral deposit consists of soft tissues. It is found in high concentrations in hyaline cartilage, synovial tissue, capsule, meniscus, ligament yellow, soft tissues of the hand and rare fibrocartilajul temporomandibular joint. Polyarticular arthritis is monoarticular although initially starts. Although in theory any joint can be affected no preferential localization. In rare cases pseudogout can affect the spinal canal and cause myelopathy.
Condrocalcinozei exact pathology is unknown, although cleavage increased adenosine triphosphate (energy molecule necessary for most anmalelor) may increase the level of pyrophosphate in the joints and is considered a method of crystal growth. There is some research that suggests the involvement of genes with a role in inorganic phosphate transport.
Patients usually present with inflammation in one or more joints with pain. Hyperparathyroidism, hemochromatosis, and hypophosphatemia associated with renal osteodistrophy condrocalcinoza. Other risk factors are condrocalcinoza Wilson's disease and osteochondritis.
Treatment for asymptomatic form of the disease does not prevent joint destruction. Acute pseudogout is recommended for intra-articular corticosteroid injections, systemic corticosteroids, NSAIDs or colchicine. Surgical removal of calcifications still remains an experimental procedure.
Pathogenesis condrocalcinozei The exact physiological dysfunction condrocalcinoza is not clear, but studies involving condrocitul and surrounding matrix as responsible agents. Some chemical and physical events determine the activation of a cascade that evolves into chondrocyte hypertrophy and degeneration. Escape into the surrounding intercellular matrix material and alter the binding of calcium effect of matrix proteoglycans. Calcium pyrophosphate crystals grow from the matrix of hypertrophic chondrocytes adjacent to those affected. Rupture of collagen fibers has been proposed to be the source of inorganic pyrophosphate.
Storage disease calcium pyrophosphate is the result of a cascading inflammatory response to the storage crystal. Enzyme abnormalities or allow the formation of pyrophosphate in excess of saturation, which precipitated especially hyaline or fibrous cartilage. People with this disorder may have more than one type of crystals (hydroxyapatite and pyrophosphate). The disease can be divided into two varieties: primary and secondary. Refers to secondary disease associated with rheumatoid arthritis spondiloartropatia. Distribution of disease in people with secondary form is identical to that seen in primary form. Primary form can be divided in turn into family variants, metabolic and idiopathic. The joint damage is different between them. Variety abolii family tends to begin earlier in life than one idiopathic. Metabolic Causes and associations include: hyperparathyroidism, haemochromatosis, hypomagnesaemia, gout, ochronosis, Wilson disease, acromegaly, Paget's disease and sidnromul Gitelman.
Among varieties metabolic impairment hemochromatosis causes more severe the hand wrist, knee, ankle and metacarpals, while ochronosis affects especially the shoulder, hip, knee and spine. Hemochromatosis is a disorder of iron metabolism that accumulate and destroy body tissues, including joints. Wilson's disease consists of abnormal accumulation of copper. Ochronosis is another storage disease in homogentisinic acid accumulates as a result of the metabolising enzyme deficiency. Gitelman syndrome is a variant of Bartter-sidnromului autosomal recessive renal tubular disease. Varieties of metabolic storage disease is genetic calcium pyrophosphate.
Signs and symptoms of condrocalcinoza Condrocalcinoza or storage disease, a variant of calcium pyrophosphate arthritis. It is a chemical that manifest error by at least four associated clinical entati. Condrocalcinoza is described as soft tissue impregnation with calcium. The term is sometimes used synonymously with storage disease Calcium pyrophosphate, but technically refers to the visible presence of calcification in soft tissue imaging studies.
Condrocalcinozei manifestations include four main distinct entities: Pseudogout: Presentation appears to be similar to acute gout. Technically it is called pseudogout although the term is used synonymously with calcium pyrophosphate storage disease. Gout can be distinguished by shape crystals of pseudogout: gout crystals (sodium ugly) are in the form of needles and not birefringence, while crystals of pseudogout (calcium pyrophosphate) are diamond-shaped and have positive birefringence. Advanced electron microscopy techniques can be used to finalize the diagnosis.
Pseudogout affecting a small percentage of people condrocalcinoza-25%. Onset is usually monoarticular or pauciarticular, and is preceded by injury or surgery in the area. Pseudogout was identified after adenoma excision parotiroidian. Onset is aggressive, reaches a peak within a few hours and is manifested by pain, swelling, local heat and redness. Fever is present in half of patients with pseudogout. The knee is affected most frequently. Shoulder, elbow, ankle and joint first metacarpofalangiana are commonly affected. Evolution includes natural spontaneous resolution within a few days or weeks at most. Treatment speeds recovery.
The disease is characterized by acute oligoarticular arthritis or monoarticulara. Clinical manifestations are similar to gout. Shows acute swelling and pain but not so intense. Pseudogout can be precipitated by medical conditions such as myocardial infarction, congestive heart failure, cerebrovascular accident, or can occur after surgery. Trauma can also be a trigger. Occasionally, pseudogout may present as a syndrome pseudoseptic acute arthritis, fever and leukocytosis. Pseudogout tofacee: Mineral material can be stored in large reservoirs producing a pseudotumor. This can be massive-loaded with consequences. I am discreet painful. Lesions are found in the temporomandibular joint, sternoclaviculara, transverse ligament of C1, metatarsophalangeal joints, spinal facet joints. Impaired spinal nerve is associated with incarceration and symptomatic spinal stenosis requiring surgical decompression. Storage of calcium pyrophosphate family: A family pattern occurs at a young age, usually the third decade of life. Tends to be more aggressive with more negative long-term prognosis. Longevity satisfactory joint function is reduced in these individuals. Genetic studies involving a gene responsible for autosomal dominant inheritance mode. Gene mutation cause high levels of intracellular inorganic pyrophosphate. Low levels of extracellular inorganic pyrophosphate allows storage of hydroxyapatite in articular hyaline cartilage and fibrocartilaj. Osteoarthritis: The most common is osteoarthritis condrocalcinozei presentation. Symptoms are similar to those of the typical patient with osteoarthritis. Note that this condrocalcinozei worsens with age.
Other variants of condrocalcinozei include: Pseudosteoartrita: Often affects metacarpophalangeal joints, wrists, elbows and shoulders, joints affected by osteoarthritis are not primary. Most commonly affects the knee. This variant of the disease include 50% of cases. Approximately 50% of patients and associated with pseudogout. Bone spurs are shaped hook radiological elements common in these patients and found the initial and second metacarpal heads. This condrocalcinozei the radiograph is common. Arthritis pseudoreumatoida: This model of the disease is found in approximately 5% of patients with storage disease and calcium pyrophosphate is associated with inflammation of the metacarpophalangeal joints symmetrically. Clinic patients accuse morning stiffness and swelling. Erythrocyte sedimentation rate is high. Late age of onset, rheumatoid factor, and this lack condrocalcinozei help differentiate from rheumatoid arthritis. Pseudoneuropatica joint: Neuropaticlike arthropathy is seen in less than 5% of patients. Most often affects the knee. It is a severe destructive condition. Unlike true neuropathic arthropathy presents no clear basis of neurological condition. This condrocalcinozei support the implementation of diagnosis.
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