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The finding of fever along with a unilateral Babinski’s sign should make one think of a cerebral abscess or an epidural abscess somewhere in the spinal column buy gabapentin discount symptoms zoning out. The finding of fever with bilateral Babinski’s signs should make one think of encephalitis order gabapentin with a visa symptoms gonorrhea, particularly if there are disturbances of consciousness buy genuine gabapentin on line medications gerd. However cheap gabapentin 300 mg on line treatment tennis elbow, fever may be associated with a cerebral vascular accident, so don’t be misled. The diagnostic workup depends on other symptoms and signs that help the physician determine what level the neurologic lesion might be. If there is an acute unilateral Babinski’s sign with hemiplegia and cranial nerve signs, a space- occupying lesion or vascular lesion of the brain must be considered. A spinal tap would not be done if there is any possibility of increased intracranial pressure. If a cerebral vascular disease is suspected, then a source for an embolism should be looked for. The fact that Babinski’s sign is a definite sign of neurologic disease is reason enough to call a neurologic specialist in before undertaking any diagnostic studies. Following the algorithm, you find there is no history of trauma, fever, or chills. The pain radiates down the back of both legs and he has had difficulty with urination for the past month. Your examination shows a suprapubic mass, a small nodule of the right lobe of the prostate, saddle hypesthesia and hypalgesia, and absent Achilles reflexes bilaterally. The suprapubic mass disappears after you catheterize him and remove 625 mL of urine. If it is of acute onset, one must consider the possibility of epidural abscess, pyelonephritis, or other abdominal conditions as the cause of the back pain. If it is of gradual onset, one should consider that it may be a tumor, particularly of the spinal cord or cauda equina, a pelvic tumor, or an aortic aneurysm that is compressing one of the nerve roots. In addition, chronic conditions such as lumbar spondylosis, rheumatoid spondylitis, and prostatitis must be considered. If there is a history of trauma, one should consider a compression fracture of the spine, a sprain or herniated disk, as well as spondylolisthesis. Without a history of trauma, one should consider a tumor, herpes zoster, or dissecting aneurysm. Lumbar spondylosis might be silent for a while only to cause pain after a significant traumatic event. Radiation of the pain would certainly be more likely to signify a space-occupying lesion of the spinal column such as a tumor, an epidural abscess, or a herniated disk. If there is no radiation, one would consider osteoarthritis or lumbar spondylosis and rheumatoid spondylitis. If there are, then one must consider the possibility of a spinal cord tumor, cauda equina tumor, or kidney disease. With the patient standing straight and one of your hands on his shoulder and the other on the opposite hip, rotate his body. At least one-fourth of the patients with back pain have one leg shorter than the other. A sedimentation rate and arthritis panel should be done if rheumatoid arthritis is suspected. It is very important to get anteroposterior (A-P) views, as well as oblique and lateral views. At this point, it is wise to observe the results of conservative therapy before ordering expensive diagnostic tests. If there is doubt about the diagnosis at this point, a neurologic or orthopedic specialist may be consulted. When all these studies are negative, it might be wise to get a bone scan because this will show the increased uptake of the sacroiliac joints in rheumatoid spondylitis. Bone scans are also more likely to show metastatic tumors but can be negative in patients with multiple myeloma. In the event that all of the above studies are negative, the possibility of a non-neurologic condition or nonorthopedic condition causing the back pain should be considered. The gums may be swollen, as in phenytoin use and early scurvy, and bleed on slight pressure, as in pyorrhea or other conditions. The presence of an enlarged spleen should bring to mind Hodgkin’s disease, leukemia, lupus erythematosus, thrombocytopenia purpura, and aplastic anemia. A systemic rash that is because of petechiae is common in any disorder that might cause thrombocytopenia. This would test for capillary fragility, and it may be positive in scurvy, thrombocytopenia purpura, leukemia, and other disorders that depress the platelet count. It will also be positive in disorders of platelet function such as von Willebrand’s disease. If these are negative, referral to a dentist or periodontist would be appropriate. X-rays of the teeth need to be done to look for dental caries, abscesses, and pyorrhea. Your examination shows weakness and hypoactive reflexes in the right extremities but a normal ophthalmoscopic examination. Transient blindness may occur in transient ischemic attacks, epilepsy, migraine, and hypertension. The sudden onset of blindness may occur in optic neuritis, retinal vein thrombosis, central retinal artery occlusion, vitreous hemorrhage, detached retina, carotid artery thrombosis, temporal arteritis, injuries to the optic nerve, retrobulbar neuritis, fracture of the skull, glaucoma, posterior cerebral artery occlusion, multiple sclerosis, and hysteria. Unilateral blindness may occur in glaucoma, vitreous hemorrhage, optic neuritis, retinal vein thrombosis, central retinal artery thrombosis, carotid artery thrombosis, temporal arteritis, injury to the optic nerve, fractured skull, brain tumors, retinoblastomas, and sphenoid ridge meningiomas. Bilateral blindness may occur in posterior cerebral artery occlusion, pituitary tumors, retinitis pigmentosa, hereditary optic atrophy, uveitis, toxic amblyopia, 104 cataracts, glaucoma, multiple sclerosis, and iritis. The presence of papilledema should make one suspect optic neuritis, retinal vein thrombosis, and space-occupying lesions of the brain. Besides papilledema, there may be changes on the ophthalmoscopic examination in iritis, glaucoma, papillitis from optic neuritis, retinal vein thrombosis, central retinal artery occlusion, vitreous hemorrhage, detached retina, and retinoblastoma. If one is not available, a careful eye examination including slit lamp examination, visual acuity evaluation, tonometry, and visual field studies should be done. If these are unrevealing, referral to an ophthalmologist or neurologist should be made without further delay. The presence of unilateral blurred vision should suggest such local ocular conditions as cataract, refractive error, iritis, glaucoma, keratitis, retinal detachment, foreign body, and optic neuritis. Orbital fracture and vitreous hemorrhage may also cause unilateral blurred vision. Bilateral blurred vision may result from cocaine use, methyl alcohol poisoning, tobacco, barbiturates, quinine, and other drugs. However, cataracts, glaucoma, chorioretinitis, retinitis pigmentosa, optic atrophy, papilledema, papillitis, optic neuritis, refractive error, pituitary tumors, posterior cerebral artery occlusion, concussion, migraine, and hysteria must also be considered. If this history is positive, then cocaine, tobacco, barbiturates, methyl alcohol, quinine, and other drugs may be responsible.
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It manifests as an absolutely regular rhythm at a rate 130–220 beats/min (average 160) discount 100mg gabapentin mastercard symptoms 3 days after conception. Generally seen in elderly patients or those with chronic lung disease who are experiencing respiratory failure Use diltiazem buy 300 mg gabapentin with visa treatment 6th nerve palsy, verapamil purchase gabapentin 100 mg visa treatment 7th march, or digoxin; avoid beta blockers because of lung disease Atrial flutter generally presents as an absolutely regular rhythm with a ventricular rate 125–150 beats/min and an atrial rate 250–300 beats/min (i generic gabapentin 100mg overnight delivery medications keppra. It has been associated with: Chronic obstructive lung disease Pulmonary embolism Thyrotoxicosis Mitral valve disease Alcohol Paroxysmal arrhythmia in persons with normal heart Therapy is cardioversion if hemodynamically unstable (e. The goals of initial management are hemodynamic stabilization, ventricular rate control, and prevention of embolic complications. Two approaches are used in management: Ventricular rate control Rhythm control (attempts to convert to and maintain sinus rhythm) There is little difference in outcome between rate control and pharmacologic rhythm control; <25% of patients on an antiarrhythmic regimen remained in sinus rhythm at the end of 1 year. As a general concept, rate control alone is considered for the patient who notices very few of the symptoms of the arrhythmia, while rhythm control is applied to the patient who immediately notices the arrhythmia and is experiencing the consequences (shortness of breath, or development of heart failure), or who is symptomatic on rate control. Cardioversion (rhythm control)—mechanical cardioversion involves an electrical shock synchronized with the intrinsic activity of the heart. The synchronization ensures that electrical stimulation does not occur during the vulnerable phase of the cardiac cycle. It is less effective than electrical cardioversion, but it does not require conscious sedation or anesthesia, as does mechanical cardioversion. Thus, techniques have focused on the identification and elimination of these foci. The initial goal is <100– 110 beats/min, although slower rates are sometimes recommended for severely ill patients. Beta blockers, calcium channel blockers, and digoxin are the drugs most commonly used for rate control. These agents do not convert atrial fibrillation to sinus rhythm and should not be used for that purpose. Digoxin, because of the inotropic effects, is the drug of choice in patients with coexisting systolic heart failure. Factors that should guide drug selection include the patient’s medical condition and the presence of concomitant heart failure. The following drugs are recommended for their demonstrated efficacy in rate control at rest and during exercise: atenolol, metoprolol, verapamil, and diltiazem. Therefore, anticoagulation is beneficial for many patients despite its risk of bleeding. It is used to determine whether treatment is required with anticoagulation or antiplatelet therapy. If the patient is hemodynamically unstable, then immediate synchronized cardioversion is indicated (synchronized cardioversion). Avoid digoxin, beta blockers, and calcium-channel blockers, as they can inhibit conduction in the normal conduction pathway, increasing aberrant conduction. That could increase the likelihood of developing ventricular or supraventricular tachycardia. Independent and asynchronous atrial and ventricular contractions produce the following signs. Variation in systolic blood pressure, as measured peripherally Variation in intensity of the heart sounds Intermittent cannon A waves in jugular venous pulses caused by the simultaneous contraction of the atrium and ventricles Extra heart sounds Because of asynchronous activation of the right and left ventricles, the first and second sounds are widely split. Cardiac pacing or isoproterenol infusion may suppress episodes of tachycardia, useful for emergency treatments. Because it has a long half-life (>50 days), drug interactions are possible for weeks after discontinuation. In medium doses, they increase arteriolar dilatation and subsequently decrease afterload and preload. In high doses, they increase coronary artery dilatation and subsequently increase oxygen supply. Side effects of nitrates include orthostatic hypotension, reflex tachycardia, throbbing headache, and blushing—all caused by vasodilation. There must be a window-free period of >8 hours with nitrate therapy to reduce the incidence of tachyphylaxis. Nonselective beta blockers may mask hypoglycemic symptoms in insulin- dependent diabetics. Beta blockers can cause fatigue/insomnia, mental depression, lipid abnormalities, hallucinations, Raynaud phenomenon, bronchoconstriction, mask signs/symptoms of insulin-induced hypoglycemia, and sexual dysfunction. Nebivolol is a unique beta blocker; it is a beta-1 specific blocker that increases nitric oxide and thus does not cause erectile dysfunction. They may be harmful in the postinfarction period, especially if the patient has left ventricular failure. Four general types of shock syndromes are recognized: distributive, cardiogenic, hypovolemic, and obstructive. Physiologic Characteristics of Various Forms of Shock In shock, cardiac output varies, increasing in the hyperdynamic state of distributive shock (and sometimes in hypovolemic shock depending on how much volume has been lost), but is always decreasing in cardiogenic shock. Maximize arterial oxygen saturation Circulatory support with normal saline or blood is used early. Hypotensive patients who do not respond to saline or blood will need pressor support: dopamine, vasopressin, or epinephrine in distributive shock, and dobutamine in cardiogenic shock. Hypotensive patients with septic shock who do not respond promptly to saline should be given a single dose of hydrocortisone, since adrenal insufficiency is common in severely ill patients. It is most commonly a result of iron deficiency, anemia of chronic disease, thalassemia, sideroblastosis, or lead poisoning. It can be caused by an early form of the conditions described, as well as most forms of hemolysis and aplastic anemia. The symptoms of anemia tend to be based on the severity of the anemia rather than the specific etiology. Eventually, confusion and altered mental status may develop as oxygen delivery to the brain decreases. Death from anemia is most often caused by decreased oxygen delivery to the heart and resulting myocardial ischemia. A healthy young patient may have no symptoms at all with hematocrit 27–29%, whereas an older patient with heart disease may develop dyspnea or anginal symptoms with the same hematocrit. A healthy young patient can have transfusion withheld until hematocrit is in the low 20%. An older patient with coronary artery disease will need to be maintained when hematocrit >30%. If there is even a modest increase in blood loss—occult blood in the stool, heavier menstrual flow, or increased demand such as in pregnancy— the body is poorly equipped to increase its level of absorption to exceed 3–4 mg per day. Other etiologies are increased urinary loss of blood, malabsorption, hemolysis, and poor oral intake. As hematocrit lowers to 25%, tachycardia, palpitations, dyspnea on exertion, and pallor develop. Older patients and those with coronary artery disease may become dyspneic at higher levels of hematocrit. More severe anemia results in lightheadedness, confusion, syncope, and chest pain. A systolic ejection murmur (“flow” murmur) may develop in any patient with moderately severe anemia.
Phrenic nerve paralysis Unilateral or bilateral diaphragmatic elevation (Fig C 46-3) with characteristic paradoxical motion of the diaphragm (tends to ascend rather than descend with inspiration) purchase gabapentin 400mg line medicine dispenser. Results from any process interfering with the normal function of the phrenic nerve (inadvertent surgical transection purchase gabapentin on line amex treatment 4s syndrome, primary bronchogenic carcinoma generic 100mg gabapentin fast delivery medicine hollywood undead, or mediastinal metas- tases); intrinsic neurologic disease (poliomyelitis buy gabapentin mastercard symptoms quitting tobacco, Erb’s palsy, peripheral neuritis, hemiplegia); injury to the phrenic nerve, thoracic cage, cervical spine, or brachial plexus; pressure from a substernal thyroid or aneurysm; or lung or mediastinal infection (paralysis may be temporary). Also perinephric, hepatic, or splenic abscess; pancre- atitis; cholecystitis; and perforated ulcer. Intra-abdominal mass Unilateral or bilateral diaphragmatic elevation (Fig C 46-4) caused by enlargement of the liver or spleen; abdominal tumor or cyst of the liver, spleen, kidneys, adrenals, or pancreas; or distended stomach or splenic flexure (left hemidiaphragm). Primary bronchogenic carcinoma (arrow) involving the phrenic nerve causes paralysis of the right hemidiaphragm. Tumor or cyst of diaphragm Very rare lesion that simulates unilateral dia- phragmatic elevation. On (Fig C 46-6) frontal views, the peak of the pseudodiaphragmatic contour is lateral to that of a normal hemi- diaphragm (situated near the junction of the middle and lateral thirds rather than near the center). Altered pulmonary volume Unilateral or bilateral diaphragmatic elevation due to atelectasis (associated pulmonary opacity); postoperative lobectomy or pneumonectomy (rib defects, sutures, shift of the heart and mediastinum); hypoplastic lung (crowded ribs, mediastinal shift, absent or small pulmonary artery, sometimes the scimitar syndrome). Diaphragmatic hernia Mimics unilateral diaphragmatic elevation on (Figs C 46-7 and C 46-8) frontal views. Lateral views show the characteristic anterior location of Morgagni’s hernia or the posterior position of Bochdalek’s hernia. Injury diaphragm to the right side causes herniation of the soft-tissue (Figs C 46-9 and C 46-10) density of the liver into the right hemithorax. On the left, air-containing stomach and bowel herniate into the chest (may mimic diaphragmatic elevation if the bowel loops are filled with fluid). The peak of the pseudodiaphrag- due to splinting secondary to a right lower lung infiltrate. Herniation of a portion of the splenic flexure (arrow), with obstruction to Fig C 46-8 the retrograde flow of barium. Also (Fig C 47-1) pleural, vascular, and bronchial interfaces with occurs in patients with asbestosis and colla- normal parenchyma. The predominant pattern of ground-glass (rather than reticular) opacities is seen in nearly all patients, reflecting the presence of intra-alveolar macrophages and interstitial inflammation. Typical litis, chronic eosinophilic pneumonia, and collagen peribronchial thickening. In most patients, however, no cause is found and the condition is referred to as idiopathic or cryptogenic. Scan at the level of the right upper lobe bronchus in a woman with id- iopathic pulmonary fibrosis shows a reticular pattern and irregular in- terfaces predominantly in the sub- pleural lung regions. Scan at the carinal level shows patchy areas of air- space opacification (“ground-glass” density). Air-space consolidation in the subpleural regions associated with peribronchial thickening (arrows). Usually most evident in the lung periphery, where (Fig C 47-5) the septa appear as lines running perpendicular to the pleura. Sarcoidosis Irregular nodules or interstitial thickening along In late stages, fibrosis typically radiates from the (Fig C 47-6) the bronchovascular bundles. Scan through the septa (small arrows) and ill-defined centrilobular opac- right lower lung shows extensive abnormalities with ities (large arrows). Note also the thickening of the thickening of the interlobular septa (straight arrows), peribronchovascular interstitium, with peribronchial major fissure, and bronchovascular bundles (curved 88 87 cuffing. Nodu- lar thickening of the interlobular septa (curved arrow) and subpleural granulomas (white arrows) are also identified. Supine scan shows moderate thickening of interlobular septal (arrows) and peribronchial (arrow- heads) structures in the nondependent subpleural Fig C 47-8 parenchyma. Scan through the right middle lobe shows an irregu- pleural honeycombing (curved arrow). The interlobar fis- lar mass with aerated lung interposed between it and the adjacent sures are thickened, and there is serration of the pleural thickening. A focal band of soft tissue can be seen in con- lung-pleural interface at sites of interstitial fibrosis, tact with the pleura. The mass was stable on serial radiographs and changes indicative of visceral pleural fibrosis. Scattered calcifications are visible in the right anterior costal plaque (arrows). Extrinsic allergic alveolitis Fine nodular or reticulonodular pattern in the Hypersensitivity disease of the lungs caused by (Fig C 47-11) subacute stage. Bilateral areas of hazy increased inhalation of antigens contained in certain organic density (ground-glass opacification) with dusts. In the acute stage, there is diffuse air-space preservation of underlying vascular markings consolidation that resolves to an interstitial pattern may occur. Repeated exposure to the antigen may lead to acute and subacute changes superimposed on chronic fibrosis. Pulmonary Langerhans cell Small irregular nodules and cystic air spaces Histologically an infiltrative lung disease of histiocytosis that diffusely involve the upper two-thirds of the Langerhans cells. Scan at the level of the right hemidiaphragm shows patchy areas of hazy interstitial density (“ground-glass” density; arrows) that typically do not obscure the underlying vascular markings. Often associated with volume Late stage of radiation-induced lung injury, which (Fig C 47-14) loss, traction bronchiectasis, and pleural thick- develops gradually in patients with radiation ening that results in a sharp demarcation pneumonitis when complete resolution does not between normal and irradiated lung. It evolves within the previously irradiated field, 6–12 months after radiation therapy, and usually becomes stable within 2 years after treatment. Scan through the right upper lobe shows numerous thin-walled cystic air spaces of vari- ous sizes. Note the traction bronchiectasis due to fibrosis and the sharp demarca- tion between normal and irradiated lung. This (Figs C 48-1 and C 48-2) appearance suggests active and contagious disease, especially when associated with adjacent cavitary nodules within the lungs. The terminal tufts of the “tree-in-bud” pattern may represent lesions in the bronchioles and alveolar ducts, whereas the stalk may reflect a lesion affecting the last-order bronchus in the secondary pulmonary lobule. Thick-walled cav- image shows larger nodular opacities (arrows), repre- ity and multiple peripheral small nodules and branch- senting extension of the granulomatous infection into ing linear structures (arrows). Multiple peripheral small nodules connected to branching linear Fig C 48-5 opacities and a thick-walled cavity in the superior segment of Blastomycosis. Note the thickening of the bronchial walls, with endobronchial spread of fungus (“tree-in-bud,” arrow- bronchial dilatation, and mucus impaction. Invasive pulmonary Should be suggested when this pattern occurs in aspergillosis combination with a “halo” of ground-glass opacity (Fig C 48-7) in a patient with leukemia. Viral infection Cytomegalovirus infection, which typically occurs (Figs C 48-8 and C 48-9) in immunocompromised individuals, can cause thickening of the bronchovascular bundles and the “tree-in-bud” pattern.
During relaxation of the calf muscles blood is aspirated from the superficial into the deep veins discount 300 mg gabapentin mastercard medicine 81. The upper two enter the posterior tibial vein where an unvalved soleal venous sinus also enters it purchase gabapentin cheap online symptoms for diabetes. Moreover the clot arising in the soleal veins may extend into the posterior tibial vein and then into the perforating veins thus destroying the valves of the perforators order gabapentin amex treatment kitty colds. The lowest perforator has a short course connecting long saphenous with the posterior tibial vein order gabapentin amex medicine wheel teachings. Whereas one enters the muscle on the medial side close to its junction with the tendo Achilles, the other is situated further up in the calf. These pass at the levels of 2 inches (5 cm), 5 inches (12 cm) and 7 inches (17 cm) above the lateral malleolus. If an individual stands motionless for a long period of time, venous pressure at the ankle may rise to 80 to 100 mm. Even with modest activity of the calf muscles and with competent venous valves, this pressure is reduced to 20 or 30 mm. The superficial veins have loose fatty tissue to support them and thus suffer from varicosity. There are three types of varicosity — primary varicose veins, secondary varicose veins and congenital varicose veins. The defects may be congenital or acquired (either due to thrombosis or due to inflammation in the veins. These cases are mostly due to either congenital arteriovenous fistula or cavernous (venous) haemangioma. This causes failure of the valves quickly giving rise to varicosity of the long or short saphenous vein. During prolonged standing the calf muscles also do not work quite often so the calf pump mechanism also cannot push the venous blood upwards. Pregnancy acts in various ways — (i) Progesterone causes dilatation and relaxation of the veins of the lower limb. This hormonal effect is maximum in the first trimester of pregnancy, (ii) Pregnant uterus causes pressure on the inferior vena cava, thus causing obstruction to the venous flow. After each pregnancy both hormonal and mechanical effects are removed and there is improvement of varicosity. During the subsequent pregnancy these factors again cause the varicosities to develop in a bigger way. Forcible contraction of the calf muscles may force blood through the perforating veins in reverse direction. Such cramp is usually due to sudden change in the calibre of communicating veins which stimulates the muscles through which they pass. These dilated veins may or may not be associated with the following complications. When this varix is tapped with a finger, a fluid thrill may be obtained in the long saphenous vein lower down in the limb. One must assess in inspection whether varicosity has affected the long saphenous vein or the short saphenous vein or the both. The skin of the lower part of the leg should be particularly inspected to exclude oedema, pigmentation, eczema or ulceration. In both the methods, the patient is first placed in the recumbent position and his legs are raised to empty the veins. The sapheno-femoral junction is now compressed with the thumb of the clinician and the patient is asked to stand up quickly, (i) In first method, the pressure is released. If the varices fill very quickly by a column of blood from above, it indicates incompetency of the sapheno-femoral valve. This is called a positive Trendelenburg test, (ii) To test the communicating system, the pressure is not released but maintained for about 1 minute. Gradual filling of the veins during the period indicates incompetency of the communicating veins, mostly situated on the medial side of the lower half of the leg allowing the blood to flow from the deep to the superficial veins. This is also considered as a positive Trendelenburg test and the positive tests are indications for operation. In this test the tourniquet is tied around the thigh or the leg at different levels after the superficial veins have been made empty by raising the leg in recumbent position. Firstly the varicosed- below it remain collapsed, it indicates presence of leg is to be raised to empty the veins. Now the sapheno-femoral junction is Similarly if the veins below the tourniquet fill rapidly compressed as in this figure with the whereas veins above the tourniquet remain empty, the thumb of the clinician and the patient is incompetent communicating veins must be below the asked to stand up. Thus by moving the tourniquet down the leg continued for about 1 minute gradual in steps one can determine the position of the incompetent filling of the veins during this period communicating vein. Firstly an Esmarch it indicates incompetency of the sapheno elastic bandage is applied from toes to the groin. The students are referred tourniquet is then applied at the groin at the upper end of to Figs. A tourniquet is tied round the upper part of the thigh tight enough to prevent any reflux down the vein. If the communicating and the deep veins are normal the varicose veins will shrink whereas if they are blocked the varicose veins will be more distended. An expansile impulse if felt in the long saphenous varicose vein, it may be presumed that the sapheno-femoral valve is incompetent. Similarly if the patient coughs and the sapheno-femoral junction is incompetent a bruit may be heard on auscultation. The examiner palpates along the line of the marked varicosities carefully, so that he can find gap or small pit in the deep fascia which transmits the incompetent perforator. These veins develop due to inferior vena caval obstruction particularly thrombosis. Such veins are more often seen in the flanks communicating with the veins of the chest wall, tributaries of the superior vena cava. Ulcers in the lower limb with presence of varicose veins may not necessarily be the venous ulcers. In these cases varicose vein is the second pathology and not the cause of the ulcer. Of the above-mentioned methods ascending phlebography is the most practical and valuable in the average hospitals. A narrow tourniquet is applied just above the malleoli to direct blood flow into the deep veins. It is a useful investigating procedure for suspected deep vein thrombosis when ultrasonography is not available. Descending venography is performed by inserting a cannula in the femoral vein and the contrast material is injected with the patient standing. The contrast material is heavier than blood, so flows down the limb through incompetent valves. Doppler ultrasound is a valuable non-invasive tool, which can be used to demonstrate saphenofemoral or saphenopopliteal reflux, perforator incompetence and patency of deep veins.
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