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brother support manualsPlease try again.Please try again.Please try again. Please try your request again later. A blood clot from deep vein thrombosis travels up to lungs against gravity Deep vein clots are not like clots in the superficial veins Blood clots form in the deep veins of the legs most often Blood clots form during a long trip in a car or airplane Blood clots are more likely to develop in surgically damaged veins The lung is damaged because of a lack of blood flow to the lung tissue. Unexplained shortness of breath, problems breathing become an issue There may be fast heart rate and light-headedness or fainting There may be sweating, chest pain and severe coughing Diagnosis is by CT scans in lungs and legs to look for blood clots. Anticoagulants or blood thinners decrease the blood's ability to clot Heparin is given as an injection followed by oral warfarin Rarely a catheter is used to help in the blood clot fragmenting. -An original poem by Kenneth Kee Interesting Tips about the Pulmonary Embolism A Healthy Lifestyle 1. Take a well Balanced Diet 2. Pulmonary embolism (PE) is treated with medicines, procedures and other therapies. The main goals of treating PE are to stop the blood clot from getting bigger and keep new clots from forming. Treatment may include medicines to thin the blood and slow its ability to clot. If the symptoms are life threatening, the doctor may give medicine to quickly dissolve the clot. A. Anticoagulants or blood thinners decrease the blood's ability to clot. a. Heparin is given as an injection or through an IV tube. b. Warfarin given as a pill takes 2 to 3 days before it starts to work. Pregnant women usually are treated with heparin only because warfarin is dangerous for the pregnancy. If there is deep vein thrombosis, treatment with blood thinners usually lasts for 3 to 6 months. Sometimes the bleeding is internal which is why people treated with blood thinners usually have routine blood tests.http://www.oecbtb.org/userfiles/adt-alarm-manual-south-africa.xml

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These tests, called PT and PTT tests measure the blood's ability to clot. B. Thrombin inhibitors are a newer type of blood-thinning medicine. They are used to treat some types of blood clots in people who cannot take heparin. C. Thrombolytics are medicines that can quickly dissolve a blood clot. D. When PE is life threatening, a doctor may use treatments that remove or break up blood clots E. Sometimes a doctor may use a catheter (a flexible tube) to break the blood clot. 3. Keep bones and body strong Bone marrow produces our blood Eat foods rich in calcium like yogurt, cheese, milk, and dark green vegetables. Eat foods rich in Vitamin D, like eggs, fatty fish, cereal, and fortified milk. Eat food rich in Vitamins B and C such as green vegetables and fruits Zinc and other minerals are important to the body 4. Get enough rest and Sleep Avoid stress and tension 5. Exercise and stay active. One way to do this is to be active 30 minutes a day at least 5 days a week. Begin slowly especially if a person has not been active. 6. Do not drink more than 2 alcohol drinks a day for a man or 1 alcohol drink a day for a woman. Alcohol use also increases the chance of falling and breaking a bone. Alcohol can affect the neurons and brain cells. 7. Stop or do not begin smoking. It also interferes with blood supply and healing. Chapter 1 Pulmonary Embolism Pulmonary embolism or PE is a serious potentially life-threatening condition due to sudden blockage in a lung artery. CONTENTS Introduction Chapter 1 Pulmonary Embolism Chapter 2 More Facts of Pulmonary Embolism Chapter 3 Treatment of Pulmonary Embolism Chapter 4 DVT Then you can start reading Kindle books on your smartphone, tablet, or computer - no Kindle device required. Full content visible, double tap to read brief content. Videos Help others learn more about this product by uploading a video. Upload video To calculate the overall star rating and percentage breakdown by star, we don’t use a simple average.http://popconsensus.com/admin/image/adt-alarm-panel-manuals.xml Instead, our system considers things like how recent a review is and if the reviewer bought the item on Amazon. It also analyzes reviews to verify trustworthiness. Please try again later. MGoncalves 2.0 out of 5 stars It could have been much better was not for the repeated information it contained, over and over throughout he book.Thank you, Dr.Kee, for making it understandable. By continuing to browse this site you are agreeing to our use of cookies. Death can occur when the venous thrombi break off and form pulmonary emboli, which pass to and obstruct the arteries of the lungs. DVT and pulmonary embolism (PE) most often complicate the course of sick, hospitalized patients but may also affect ambulatory and otherwise healthy persons. 1 2 3 4 It is estimated that each year 600 000 patients develop PE and that 60 000 die of this complication. 5 6 7 This number exceeds the number of American women who die each year from breast cancer. PE is now the most frequent cause of death associated with childbirth. 8 Women are a prime target for PE, being affected more often than men. Deep vein thrombosis is a major complication in orthopedic surgical patients and patients with cancer and other chronic illnesses. DVT can be a chronic disease. Patients who survive the initial episode of DVT are prone to chronic swelling of the leg and pain because the valves in the veins can be damaged by the thrombotic process, leading to venous hypertension. In some instances skin ulceration and impaired mobility prevent patients from leading normal, active lives. In addition, patients with DVT are prone to recurrent episodes. In those instances in which DVT and PE develop as complications of a surgical or medical illness, in addition to the mortality risk, hospitalization is prolonged and healthcare costs are increased. Purpose Over the past 20 years results of clinical trials have provided information that has revolutionized the approach to management of venous thromboembolic disease. New diagnostic modalities and therapeutic agents have been developed that are more effective, less expensive, and more convenient. Patients with venous thromboembolic disease (VTE) are seen by a variety of medical specialists, including general physicians, surgeons, obstetricians, hematologists, radiologists, and chest physicians. Because thromboembolic disease forms only a small part of the practice of most of these clinicians, it is difficult for them to keep abreast of advances that are important for optimal patient care. The purpose of this report is to provide medical trainees and clinicians with the information required to manage venous thromboembolic problems that they are likely to encounter in daily practice. Pathogenesis of Venous Thromboembolism Venous thrombi are intravascular deposits composed of fibrin and red cells with a variable platelet and leukocyte component. 9 They usually form in regions of slow or disturbed flow in large venous sinuses and in valve cusp pockets in the deep veins of the calf (Fig 1 ) or in venous segments that have been exposed to direct trauma. 10 11 12 Venous thrombi often break off to form PE. The formation, growth, and dissolution of venous thrombi and PE reflect a balance between the effects of thrombogenic stimuli and a variety of protective mechanisms. 13 14 15 The factors traditionally implicated in the pathogenesis of venous thrombosis are activation of blood coagulation, venous stasis, and vascular injury. 13 14 15 Vascular damage contributes to the genesis of venous thrombosis through either direct trauma 9 12 13 15 or activation of endothelial cells by cytokines (interleukin-1 and tumor necrosis factor) released as a result of tissue injury and inflammation. Blood coagulation can be activated by intravascular stimuli released at a remote site (eg, products of injured or infarcted tissue) or it can be activated locally by vessel wall damage (eg, damage to the femoral vein during hip surgery) or by cytokine-induced nondenuding endothelial stimulation. 12 15 16 17 18 These cytokines stimulate endothelial cells to synthesize tissue factor and plasminogen activator inhibitor-1 and lead to a reduction in thrombomodulin, thereby reversing the protective properties of normal endothelium. The thrombogenic effects of activation of blood coagulation are amplified by stasis and counteracted by rapid flow. Venous stasis predisposes the patient to local thrombosis by impairing the clearance of activated coagulation factors and limiting the accessibility of thrombin formed in veins to endothelial protein thrombomodulin, which is present in greatest density in the capillaries. The mechanisms that protect against thrombosis are inactivation of activated coagulation factors by circulating inhibitors, dilution and clearance of activated coagulation factors by flowing blood, inhibition of the coagulant activity of thrombin by thrombomodulin, enhancement of the anticoagulant activity of thrombin by thrombomodulin through activation of protein C, and dissolution of fibrin by the fibrinolytic system. 19 20 21 22 23 24 25 Natural History Venous thrombosis in the lower limb can involve the superficial leg veins, the deep veins of the calf (calf vein thrombosis), the more proximal veins, including popliteal veins, the superficial femoral, common femoral, and iliac veins. Less commonly, thrombosis involves other veins in the body. Thrombosis of the superficial veins of the legs usually occurs in varicosities and is benign and self-limiting. Occasionally, however, the thrombi in superficial veins extend into the deep veins and give rise to major PE. Deep calf vein thrombosis is a less serious disorder than proximal vein thrombosis because thrombi in calf veins are generally small and are therefore not usually associated with clinical disability or major complications. Most calf vein thrombi are asymptomatic, 10 but these thrombi can extend proximally and become dangerous. Venous thrombi produce symptoms because they obstruct venous outflow, cause inflammation of the vein wall or perivascular tissue, or embolize into the pulmonary circulation. Extension of thrombosis is more likely if the original thrombogenic stimulus persists. Complete spontaneous lysis of large venous thrombi is uncommon, and even when patients with venous thrombosis are treated with heparin, complete lysis occurs in fewer than 10 of cases. 26 In contrast, complete dissolution of small, asymptomatic calf vein thrombi occurs quite frequently. 10 There is a strong association between DVT and PE. Pulmonary emboli are detected by perfusion lung scanning in ?50 of patients with documented DVT, 3 27 28 29 30 and asymptomatic venous thrombosis is found in ?70 of patients with confirmed clinically symptomatic PE. If the thrombus that embolizes is small (which is frequently the case when it is located in the calf), the embolus is usually asymptomatic and clinically insignificant, although the cumulative effect, if there are repeated showers of small emboli, can cause cor pulmonale. If the thrombus is large and involves the proximal veins, it often produces clinical manifestations; if it is very large or if the patient has a compromised cardiorespiratory system, it can be fatal. Most clinically significant and virtually all fatal emboli arise from thrombi in the proximal veins. 1 Venous thrombi usually organize slowly and can be complicated by the postthrombotic syndrome. 31 The residual abnormality can also act as a nidus for recurrent thrombosis, 32 which occurs in approximately one third of patients over an 8-year follow-up period. 33 Prognosis Studies done before the introduction of anticoagulant therapy reported that the mortality rate for PE was ?20 in hospitalized patients with clinically obvious venous thrombosis. 34 In a small study, Kakkar and colleagues 10 reported that without treatment, ?20 of silent calf vein thrombi extended into the popliteal vein and that extension was associated with a 40 to 50 risk of clinically detectable PE. In a study of patients with clinically suspected DVT, Huisman and associates 35 reported that 6.5 (20 of 307) who had negative impedance plethysmography at presentation developed evidence of extension over the next 10 days. Others have reported a lower frequency of impedance plethysmography (IPG) conversion during serial testing. The estimated frequency of extension rate of untreated symptomatic calf vein thrombosis is ?30, based on the results of these serial IPG studies. In contrast to untreated thrombosis, the short-term prognosis of patients with proximal DVT treated with adequate doses of anticoagulants for 3 months is good. 36 37 38 Clinically significant recurrent events take place in ?5 of patients with proximal vein thrombosis treated with an initial course of heparin followed by oral anticoagulants or intermediate doses of subcutaneous heparin for 3 months. 37 38 39 40 41 42 Thereafter, DVT recurs in 5 to 10 of patients the year after anticoagulant therapy is discontinued 36 37 38 and in ?30 of patients after 8 years. 33 Clinical Course in Symptomatic Patients A comprehensive prospective follow-up study examining long-term prognosis in consecutive patients with a first episode of documented symptomatic DVT of the leg was recently completed by Prandoni and associates. 33 The study assessed the long-term incidence of recurrent venous thromboembolism and postthrombotic syndrome. They were seen at 3 and 6 months after presentation and every 6 months thereafter for follow-up assessments. Patients were asked to return immediately if they developed symptoms suggestive of recurrent venous thromboembolism. Follow-up continued for up to 8 years. A total of 355 consecutive patients with a first episode of DVT confirmed by venography were included in the study. Seventy-eight patients experienced one or more episodes of objectively confirmed recurrent venous thromboembolic events. The risk of recurrent VTE was increased by the presence of malignancy and coagulation abnormalities and reduced in patients who had a reversible risk factor (eg, surgery and trauma or fracture). Of the 355 patients, 83 developed postthrombotic syndrome and 24 developed severe postthrombotic manifestations. The cumulative incidence of postthrombotic syndrome was 17.3 after 1 year and 22.8 after 2 years. Thereafter, the incidence of postthrombotic syndrome rose very gradually to 28.0 after 5 years and 29.1 at 8 years. Thus, in more than 80 of patients manifestations of postthrombotic syndrome became apparent in the first 2 years after acute thrombosis. The cumulative incidence of severe postthrombotic manifestations increased gradually from 2.6 after 1 year to 9.3 after 5 years. Thereafter, the cumulative incidence of severe postthrombotic manifestations did not increase further. It is likely that the use of compression stockings contributed to this low incidence of postthrombotic syndrome, as indicated by a recent controlled study. 43 Ipsilateral recurrent DVT was associated with a strong increase in risk for postthrombotic syndrome (risk ratio 6:4). Surprisingly, there were no significant associations between occurrence of postthrombotic syndrome and size or location of the thrombus. Twenty-six of the 297 patients without a malignancy at baseline developed cancer. This occurred mainly in patients with idiopathic DVT at presentation. 44 Of the 355 patients, 90 died during follow-up. In 6 patients who died suddenly, a definite cause of death was not established. Other studies have also reported that most recurrences take place in patients who have idiopathic venous thrombosis or who are exposed to a continuing risk factor (such as cancer). In these groups, the rate of recurrence is ?15 in the 12 months after treatment is stopped. In contrast, the long-term prognosis in patients who develop venous thrombosis following exposure to a predisposing cause such as surgery or trauma is very good. 45 Thus, provided they are treated with anticoagulants for 3 months, 36 37 38 fewer than 4 of these patients develop recurrences in the following year. 45 46 47 Acute Recurrent Venous Thrombosis The label of recurrent venous thrombosis carries important prognostic implications. Patients are usually treated with anticoagulants for life and may suffer considerable mental anguish. Therefore, it is important to ensure that the diagnosis of recurrent DVT is correct. In many patients with clinically suspected recurrence, the diagnosis of recurrence is not confirmed by objective tests. For example, in a prospective study of patients with clinically suspected acute DVT, almost two thirds did not have this diagnosis confirmed by objective tests, and these patients did very well without anticoagulant therapy. 48 The diagnosis of recurrent venous thrombosis can be difficult because venography, the diagnostic standard for acute venous thrombosis, is less reliable for diagnosis of recurrent venous thrombosis. 48 However, the accuracy of diagnosis of acute recurrence has been improved by the introduction of noninvasive techniques (see below). Postthrombotic Syndrome In early descriptive studies, postthrombotic syndrome was reported to occur in ?50 of patients with symptomatic venous thrombosis. More recently and possibly as a consequence of better initial anticoagulation and the use of graduated compression stockings, the incidence of postthrombotic syndrome after 8 years of follow-up was reported to be no more than ?25. 33 The postthrombotic syndrome is caused by venous hypertension, which occurs as a consequence of recanalization of major venous thrombi leading to patent but scarred and incompetent valves or, less frequently, persistent outflow obstruction produced by large proximal vein thrombi. 31 49 50 51 Recanalization and valve destruction result in a malfunction of the muscular pump mechanism, which leads to increased pressure in the deep veins of the calf. This high pressure results in progressive incompetence of the valves of the perforating veins of the calf, and when this occurs, flow is directed from the deep vein into the superficial system during muscle contraction, leading to edema and impaired viability of subcutaneous tissues and, in its most severe form, ulceration of venous origin. Follow-up studies of patients with proximal vein thrombosis have demonstrated that outflow obstruction (measured by IPG) is relieved either by recanalization or collateral flow in 30 of patients at 3 weeks and in 70 of patients at 3 months. 52 Valvular incompetence is a more important cause of postthrombotic syndrome than is outflow obstruction. 53 In patients with extensive thrombosis in the iliofemoral veins, swelling may never disappear, while in patients with less severe proximal vein thrombosis, swelling may subside after the initial event but return in the next few years. Other manifestations of postthrombotic syndrome are pain in the calf relieved by rest and elevation of the leg, pigmentation and induration around the ankle and the lower third of the leg, and, less commonly, ulceration and venous claudication, a bursting calf pain that occurs during exercise. Patients with extensive thrombosis involving the iliofemoral vein have a higher frequency of venous claudication and frequently have greater disability than patients with more distal vein thrombosis. 50 However, incompetence of perforating veins may follow thrombosis confined to calf veins and may lead to stasis changes. In a follow-up study of calf vein thrombosis in Sweden, the frequency of postthrombotic syndrome was reported to be 13 of 79 or 16 in 2 years’ follow-up. 54 There is evidence from recent studies that recurrent venous thrombosis is an important risk factor for development of postthrombotic syndrome 33 and that risk of developing postthrombotic syndrome is reduced by the use of graduated compression stockings. 43 The role of thrombolytic therapy in prevention of postthrombotic syndrome is uncertain. Changing Oil Since special procedures, materials and tools are required to change the automatic transaxle oil, it is recommended that you trust this job to your authorized SUZUKI dealer. 9-17 Engine Coolant 56KN049 EXAMPLE. Keep out of the reach of children and animals. INSPECTION AND MAINTENANCE Coolant Replacement Since special procedures are required, we recommend you take your vehicle to your SUZUKI dealer for coolant replacement. 9-18. If the fluid level is near “E” mark, refill it. If you wish to use a brand of spark plug other than the specified plugs, consult your SUZUKI dealer.If the clutch fluid level is near the “MIN” line, fill it up to the “MAX” line with DOT3 brake fluid. WARNING Your SUZUKI is equipped with tires which are all the same type and size. This is important to ensure proper steering and handling of the vehicle. WARNING Your SUZUKI is equipped with tires which are all the same type and size. This is important to ensure proper steering and handling of the vehicle. The compact spare is designed to save space in your storage area, and its lighter weight makes it easier to install if a flat tire occurs. Snow tires must be the same size as the standard tires. Also be sure to use the tires of the same type and brand on all four wheels of. The load capacities of your vehicle are indicated by the Gross Vehicle Weight Rating (GVWR), the Gross Axle Weight Rating (GAWR, front and rear), and the total load capacity, the seating capac- ity, and the cargo load capacity. Keep flames and sparks away from the battery or an explosion may occur. Never smoke when work- ing near the battery. WARNING When checking or servicing the bat- tery, disconnect the negative cable. Always use a genuine SUZUKI replacement. Never use a substitute such as a wire even for a temporary fix, or extensive electrical damage and a fire can result. This should be carried out by your SUZUKI dealer. NOTE: If it is difficult to replace headlight bulbs or parking light bulbs due to under-hood com-. To install it, simply push it back in. The bulb can be removed by simply pulling it out. When replacing the bulb, make sure that the contact springs are holding the bulb securely. To remove and install a full glass type bulb (1), simply pull out or push in the bulb. To remove a glass metal type bulb (2) from a bulb holder, push in the bulb and turn it counterclockwise. If so, consult your SUZUKI dealer for proper replacement method. 9-44. NOTE: When raising both of the front wiper arms, pull the driver’s side wiper arm up first. When returning the wiper arms, lower the passenger’s side wiper arm first. Installation 52D125 (4) Locked end 5) Install the new blade in the reverse order of removal, with the locked end positioned toward the wiper arm. To remove and install some types of rear wiper blade from and to the wiper frame. Removal 52D104 1) Flex the locked end of blade (3) away from retainer (4) to unlock it and slide the blade out as shown. To help maintain opti- mum performance and durability of your air conditioner, it needs to be run periodically. If the reason for failure of the starter is not obvious, there may be a major electrical problem. Have the vehi- inspected your authorized SUZUKI dealer. 10-4. If this happens, press the accelerator pedal all the way to the floor and hold it there while cranking the engine. If any abnormality is found, correct it. 2) Check the coolant level in the reservoir. If it is found to be lower than the “LOW”. This procedure is for emergency use only. Listed below are instructions for how to maintain your vehicle to prevent corrosion. Please read and follow these instructions carefully. Important Information About Corrosion Common causes of corrosion 1) Accumulation of road salt, dirt, moisture. Please check with your autho- rized SUZUKI dealer for information on these guards. Store your vehicle in a dry, well-venti- lated area Do not park your vehicle in a damp, poorly ventilated area. The materials could cause personal injury or damage to the vehicle. This number is used to register the vehicle. It is also used to assist your dealer when ordering parts or refer- ring to special service information. In addition, once SUZUKI collects or. For vehicles registered for use and principally operated in Canada please contact Suzuki Canada Inc.Customer Relations 100 East Beaver Creek Road. Tire cold pressure: See the “Tire Information Label”. It's waiting for you at your local Suzuki dealer showroom.It's waiting for you at your local Suzuki dealer showroom.If your handbook does not show please contact your local Suzuki dealer. We’ve checked the years that the manuals coverYou’ll then be shown the first 10 pages of this specific. Then you can clickSpam free: Maximum of 1 email per monthSpam free: Maximum of 1 email per month. Model line. Model: Pages: 297, PDF Size: 4.51 MB Due to improvements or other changes, there may be discrepancies between informa- tion in this manual and your vehicle. SUZUKI MOTOR CORPORATION reserves the right to make production changes at any time, without notice and without incurring any obligation to make the same or similar changes tovehicles previously built or sold. SUZUKI MOTOR CORPORATION believes in conservation and protection of Earth’s natural resources. To that end, we encourage every vehicle owner to recycle, trade in, or properly dis- pose of, as appropriate, used motor oil, coolant, and other fluids, batteries and tires.IF YOU HAVE ANY PROBLEMS WITH YOUR SUZUKI: Please review the New Vehicle Warranty Information booklet supplied with your SUZUKI. Should you have a question or problem regarding the warranty or service of your vehicle, please take the following action: Consult the Service Manager and the Owner of the Suzuki Automotive Dealer- ship. Explain your problem and ask for their assistance in resolving your problem. The Owner of the dealership is in the very best position to assist you as he or she is vitally concerned with your continued satis- faction. If you are still in need of additional informa- tion, or if you are dissatisfied, request that your dealer arrange a meeting with your District Service Manager. If, after doing so, you still require further assistance, and you purchased your SUZUKI in the continental United States, please contact the American Suzuki Cus- tomer Relations Department by telephone at 1-800-934-0934 or in writing at: American Suzuki Motor Corporation Automotive Customer Relations 3251 East Imperial Highway Brea, CA 92821-6795If you purchased your SUZUKI in Canada please contact the Suzuki Canada Cus- tomer Relations Department by telephone at 1-905-889-2677 extension 2254 or in writing at: Suzuki Canada Inc. Customer Relations 100 East Beaver Creek Road Richmond Hill, On L4B 1J6 In the event you require assistance related to your SUZUKI, while temporarily travel- ling in either the United States or Canada, you may wish to contact the Suzuki Cus- tomer Relations Department directly of the country in which you are temporarily oper- ating your vehicle. Please be certain to provide us with the fol- lowing information: the model, Vehicle Identification Number, mileage, accesso- ries involved, event dates, your concern, and any other comments which you may have. When we receive your correspon- dence, we will be pleased to contact the Owner of your dealership and assist in resolving your concern. For owners outside the continental United States, please refer to the distributor’s address listed in your Warranty Information booklet. Pay special atten- tion to the messages highlighted by these signal words: NOTE: Indicates special infor mation to make maintenance easier or instructions clearer.