Lots of things can cause pain and swelling in your leg. But if your symptoms stem from a blood clot deep in your leg, it can be dangerous. Blood clots can happen to anyone, anytime. But some people are at increased risk. Taking steps to reduce your chances of a blood clot forming in your veins can help you avoid potentially serious problems.
Blood clots can arise anywhere in your body. They develop when blood thickens and clumps together. When a clot forms in a vein deep in the body, it’s called deep vein thrombosis. Deep vein blood clots typically occur in the lower leg or thigh.
“Deep vein thrombosis has classic symptoms—for example swelling, pain, warmth, and redness on the leg,” says Dr. Andrei Kindzelski, an NIH blood disease expert. “But about 30–40% of cases go unnoticed, since they don’t have typical symptoms.” In fact, some people don’t realize they have a deep vein clot until it causes a more serious condition.
Deep vein clots—especially those in the thigh—can break off and travel through the bloodstream. If a clot lodges in an artery in the lungs, it can block blood flow and lead to a sometimes-deadly condition called pulmonary embolism. This disorder can damage the lungs and reduce blood oxygen levels, which can harm other organs as well.
Some people are more at risk for deep vein thrombosis than others. “Usually people who develop deep vein thrombosis have some level of thrombophilia, which means their blood clots more rapidly or easily,” Kindzelski says. Getting a blood clot is usually the first sign of this condition because it’s hard to notice otherwise. In these cases, lifestyle can contribute to a blood clot forming—if you don’t move enough, for example. Your risk is higher if you’ve recently had surgery or broken a bone, if you’re ill and in bed for a long time, or if you’re traveling for a long time (such as during long car or airplane rides).
Having other diseases or conditions can also raise your chances of a blood clot. These include a stroke, paralysis (an inability to move), chronic heart disease, high blood pressure, surgical procedure, or having been recently treated for cancer. Women who take hormone therapy pills or birth control pills, are pregnant, or within the first 6 weeks after giving birth are also at higher risk. So are those who smoke or who are older than 60. But deep vein thrombosis can happen at any age.
You can take simple steps to lower your chances for a blood clot. Exercise your lower leg muscles if you’re sitting for a long time while traveling. Get out of bed and move around as soon as you’re able after having surgery or being ill. The more active you are, the better your chance of avoiding a blood clot. Take any medicines your doctor prescribes to prevent clots after some types of surgery.
A prompt diagnosis and proper treatment can help prevent the complications of blood clots. See your doctor immediately if you have any signs or symptoms of deep vein thrombosis or pulmonary embolism (see the Wise Choices box). A physical exam and other tests can help doctors determine whether you’ve got a blood clot.
There are many ways to treat deep vein thrombosis. Therapies aim to stop the blood clot from getting bigger, prevent the clot from breaking off and moving to your lungs, or reduce your chance of having another blood clot. NIH scientists continue to research new medicines and better treatment options.
If you think you may be at risk for deep vein thrombosis, talk with your doctor.
THE POLIO CRUSADE IN AMERICAN EXPERIENCE A GOOD VIDEO
THE STORY OF THE POLIO CRUSADE pays tribute to a time when Americans banded together to conquer a terrible disease. The medical breakthrough saved countless lives and had a pervasive impact on American philanthropy that ...
A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.
On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.
The patient's legs, showing massive enlargement of the right calf and wasting on the left
What is that nature of the acute illness in infancy?
What is the nature of the subsequent deterioration?
What investigations should be performed?
What is the differential diagnosis of the cause of the progressive calf hypertrophy?
An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.
A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3
Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.
Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition
The differential diagnosis of the progressive calf hypertrophy is given in the box.
Causes of calf muscle hypertrophy
Chronic partial denervation
hereditary motor and sensory neuropathy
spinal muscular atrophy
following paralytic poliomyelitis
Neuromyotonia and myokymia
continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis