FDA prescribing information, side effects and uses. Coumadin has no direct effect on an established thrombus, nor does it reverse ischemic tissue damage. Once a thrombus has occurred, however, the goals of anticoagulant treatment are to prevent further extension of the formed clot and to prevent secondary thromboembolic complications that may result in serious and possibly fatal sequelae. Chief complaint of easy bruising and bleeding. Hemarthrosis Hematuria Menorrhagia. The dosage and administration of Coumadin must be individualized for each patient according to the patient’s INR response to the drug. Adjust the dose based on the patient’s INR and the condition being treated. Consult the latest evidence- based clinical practice guidelines regarding the duration and intensity of anticoagulation for the indicated conditions. An INR of greater than 4. Adjust the warfarin dose to maintain a target INR of 2. INR range, 2. 0- 3. The duration of treatment is based on the indication as follows: In patients with non- valvular AF, anticoagulate with warfarin to target INR of 2. Lose weight without dieting! Live better and be healthier with these quick nutritional tips from the experts. Diet & Weight Management. Coagulation - Algorithm for workup of hereditary bleeding disorders. The optimal dose and regimen to control acute hemarthrosis and to prevent arthropathy in patients with hemophilia. Management of Joint Bleeding in Hemophilia. Hemarthrosis - Bleeding into a Joint. Diet Advice; Exercise. Spontaneous Hemarthrosis in Osteoarthritis of the Knee Treated by. Oral anticoagulation therapy with warfarin has not been fully evaluated by clinical trials in patients with valvular disease associated with AF, patients with mitral stenosis, and patients with recurrent systemic embolism of unknown etiology. However, a moderate dose regimen (INR 2. The appropriate initial dosing of Coumadin varies widely for different patients. Not all factors responsible for warfarin dose variability are known, and the initial dose is influenced by: Select the initial dose based on the expected maintenance dose, taking into account the above factors. Find patient medical information for warfarin oral on WebMD including its uses, side effects and safety, interactions, pictures, warnings and user ratings. Warfarin Interactions. Ginseng Reports of spontaneous bleeding in patients using Ginseng. Spontaneous subdural hematoma is an interesting condition, because it occurs without any cause. While subdural hematoma is caused by head injuries, spontaneous. Bleeding and Bruising: A Diagnostic Work-up. She had no history of trauma or spontaneous bleeding and had tolerated minor. Modify this dose based on consideration of patient- specific clinical factors. Consider lower initial and maintenance doses for elderly and/or debilitated patients and in Asian patients . Routine use of loading doses is not recommended as this practice may increase hemorrhagic and other complications and does not offer more rapid protection against clot formation. Individualize the duration of therapy for each patient. In general, anticoagulant therapy should be continued until the danger of thrombosis and embolism has passed . Determine each patient’s dosing needs by close monitoring of the INR response and consideration of the indication being treated. Typical maintenance doses are 2 to 1. Table 1 displays three ranges of expected maintenance Coumadin doses observed in subgroups of patients having different combinations of CYP2. C9 and VKORC1 gene variants . If the patient’s CYP2. C9 and/or VKORC1 genotype are known, consider these ranges in choosing the initial dose. Patients with CYP2. C9 *1/*3, *2/*2, *2/*3, and *3/*3 may require more prolonged time (> 2 to 4 weeks) to achieve maximum INR effect for a given dosage regimen than patients without these CYP variants. Coumadin has a narrow therapeutic range (index), and its action may be affected by factors such as other drugs and dietary vitamin K. Therefore, anticoagulation must be carefully monitored during Coumadin therapy. Determine the INR daily after the administration of the initial dose until INR results stabilize in the therapeutic range. After stabilization, maintain dosing within the therapeutic range by performing periodic INRs. The frequency of performing INR should be based on the clinical situation but generally acceptable intervals for INR determinations are 1 to 4 weeks. Perform additional INR tests when other warfarin products are interchanged with Coumadin, as well as whenever other medications are initiated, discontinued, or taken irregularly. Heparin, a common concomitant drug, increases the INR . If a patient misses a dose of Coumadin at the intended time of day, the patient should take the dose as soon as possible on the same day. The patient should not double the dose the next day to make up for a missed dose. The intravenous dose of Coumadin is the same as the oral dose. After reconstitution, administer Coumadin for injection as a slow bolus injection into a peripheral vein over 1 to 2 minutes. Coumadin for injection is not recommended for intramuscular administration. Reconstitute the vial with 2. L of Sterile Water for Injection. The resulting yield is 2. L of a 2 mg per m. L solution (5 mg total). Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. Do not use if particulate matter or discoloration is noted. After reconstitution, Coumadin for injection is stable for 4 hours at room temperature. It does not contain any antimicrobial preservative and, thus, care must be taken to assure the sterility of the prepared solution. The vial is for single use only, discard any unused solution. Some dental or surgical procedures may necessitate the interruption or change in the dose of Coumadin therapy. Consider the benefits and risks when discontinuing Coumadin even for a short period of time. Determine the INR immediately prior to any dental or surgical procedure. In patients undergoing minimally invasive procedures who must be anticoagulated prior to, during, or immediately following these procedures, adjusting the dosage of Coumadin to maintain the INR at the low end of the therapeutic range may safely allow for continued anticoagulation. Since the full anticoagulant effect of Coumadin is not achieved for several days, heparin is preferred for initial rapid anticoagulation. During initial therapy with Coumadin, the interference with heparin anticoagulation is of minimal clinical significance. Conversion to Coumadin may begin concomitantly with heparin therapy or may be delayed 3 to 6 days. To ensure therapeutic anticoagulation, continue full dose heparin therapy and overlap Coumadin therapy with heparin for 4 to 5 days and until Coumadin has produced the desired therapeutic response as determined by INR, at which point heparin may be discontinued. As heparin may affect the INR, patients receiving both heparin and Coumadin should have INR monitoring at least: Coumadin may increase the activated partial thromboplastin time (a. PTT) test, even in the absence of heparin. A severe elevation (> 5. PTT with an INR in the desired range has been identified as an indication of increased risk of postoperative hemorrhage. Consult the labeling of other anticoagulants for instructions on conversion to Coumadin. For injection: 5 mg, lyophilized powder in a single- dose vial. Coumadin is contraindicated in women who are pregnant except in pregnant women with mechanical heart valves, who are at high risk of thromboembolism . Coumadin can cause fetal harm when administered to a pregnant woman. Coumadin exposure during pregnancy causes a recognized pattern of major congenital malformations (warfarin embryopathy and fetotoxicity), fatal fetal hemorrhage, and an increased risk of spontaneous abortion and fetal mortality. If Coumadin is used during pregnancy or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to a fetus . Bleeding is more likely to occur within the first month. Risk factors for bleeding include high intensity of anticoagulation (INR > 4. INRs, history of gastrointestinal bleeding, hypertension, cerebrovascular disease, anemia, malignancy, trauma, renal impairment, certain genetic factors . Those at high risk of bleeding may benefit from more frequent INR monitoring, careful dose adjustment to desired INR, and a shortest duration of therapy appropriate for the clinical condition. However, maintenance of INR in the therapeutic range does not eliminate the risk of bleeding. Drugs, dietary changes, and other factors affect INR levels achieved with Coumadin therapy. Perform more frequent INR monitoring when starting or stopping other drugs, including botanicals, or when changing dosages of other drugs . Necrosis may be associated with local thrombosis and usually appears within a few days of the start of Coumadin therapy. In severe cases of necrosis, treatment through debridement or amputation of the affected tissue, limb, breast, or penis has been reported. Careful clinical evaluation is required to determine whether necrosis is caused by an underlying disease. Although various treatments have been attempted, no treatment for necrosis has been considered uniformly effective. Discontinue Coumadin therapy if necrosis occurs. Consider alternative drugs if continued anticoagulation therapy is necessary. Fatal and serious calciphylaxis or calcium uremic arteriolopathy has been reported in patients with and without end- stage renal disease. When calciphylaxis is diagnosed in these patients, discontinue Coumadin and treat calciphylaxis as appropriate. Consider alternative anticoagulation therapy. Anticoagulation therapy with Coumadin may enhance the release of atheromatous plaque emboli. Systemic atheroemboli and cholesterol microemboli can present with a variety of signs and symptoms depending on the site of embolization. The most commonly involved visceral organs are the kidneys followed by the pancreas, spleen, and liver. Some cases have progressed to necrosis or death. A distinct syndrome resulting from microemboli to the feet is known as “purple toes syndrome.” Discontinue Coumadin therapy if such phenomena are observed. Consider alternative drugs if continued anticoagulation therapy is necessary. Do not use Coumadin as initial therapy in patients with heparin- induced thrombocytopenia (HIT) and with heparin- induced thrombocytopenia with thrombosis syndrome (HITTS). Cases of limb ischemia, necrosis, and gangrene have occurred in patients with HIT and HITTS when heparin treatment was discontinued and warfarin therapy was started or continued. In some patients, sequelae have included amputation of the involved area and/or death. Treatment with Coumadin may be considered after the platelet count has normalized. Coumadin can cause fetal harm when administered to a pregnant woman. Spontaneous ICH in Patients Taking Warfarin : Emergency Medicine News. Learning Objectives: After reading this article, the physician should be able to: 1. Identify the incidence of spontaneous intracranial hemorrhage in patients anticoagulated with warfarin. Describe the risk factors for spontaneous intracranial hemorrhage in patients anticoagulated with warfarin. Summarize the symptoms of spontaneous intracranial hemorrhage in patients anticoagulated with warfarin. Release Date: March 2. It would be an unusual shift when an emergency physician did not encounter a patient taking warfarin. The drug is omnipresent — a life saver and a killer. The clinical indications are many, but the complications are gargantuan. Warfarin has been implicated as the one medication associated with the highest incidence of outpatient morbidity, and up to 1. Most emergency physicians have a limited knowledge of warfarin, and primarily understand bleeding complications. The literature on warfarin drug- drug interactions, initiation and reversal of coagulopathy, and a plethora of related issues comprise vast literature that no physician can possibly read or totally remember. Although we rarely start the drug, we frequently must deal with its therapeutic and untoward sequelae. I recently discussed the issue of head trauma in patients anticoagulated with warfarin, and concluded that banging your head and taking warfarin is a bad combination. Seemingly minor head trauma, especially in the elderly anticoagulated patient, is a minefield over which one must tread quite carefully. Although we may not prescribe the drug in the ED, we do prescribe many drugs and offer advice on medical issues that may interfere with the proper use of this anticoagulant. Following patients on warfarin is a huge hassle and chasing the wandering INR consumes a lot of the internist's and cardiologist's time. I noted that the FDA recently mandated that coagulated patients receive specific written instructions from the pharmacy about the clinical issues and dangers of warfarin therapy. Transparency in medicine has now arrived, not only for physicians but also for our prescriptions. This information is well known to any individual with a computer. The sagacious clinician realizes that his patient and his family can quickly check on the doctor's proper or improper use of this drug, so let the clinician beware. This month's discussion reviews the clinical approach to the asymptomatic patient who has an elevated INR discovered during an ED encounter. Last month I discussed the approach to the asymptomatic patient who is serendipitously found to have an elevated INR. A very conservative approach has been promulgated, using either watchful waiting or small doses of oral vitamin K for those not bleeding and an INR less than 9. Simply withholding warfarin for three to five days is considered a reasonable clinical approach in the vast majority of such asymptomatic patients. This month, I discuss a more dramatic and often fatal warfarin- related issue — intracranial hemorrhage, either spontaneous or associated with other risk factors. Watchful waiting is clearly not the norm for these individuals. Oral Anticoagulants and Intracranial Hemorrhage: Facts and Hypotheses. Hart R, et al Stroke 1. This article discusses the nuances and clinical significance of intracranial hemorrhage in patients anticoagulated with warfarin. The authors begin by observing that ICH is the most feared and most lethal complication of all types of outpatient oral anticoagulation. The report reviews the frequency, predictors, and prognosis of this complication, termed a “common” event. Anyone will concede that an anticoagulated patient with head trauma will more likely bleed, but the most scary caveat with warfarin is that such bleeding can be spontaneous. The frequency of ICH in the general population is likely on the increase, probably because of increasing use of warfarin in the elderly. Although the benefits of anticoagulation are well accepted for patients at risk for ischemic stroke, the risk of bleeding from warfarin in some patients may be so great that it negates that benefit. ICH can be divided into three general categories: intraparenchymal (intracerebral), subdural/epidural, and subrachnoid hemorrhage. Of these, intracerebral hemorrhage is the most common, comprising about 7. Subdural hematoma is the least common category of ICH from warfarin, comprising about 3. Unfortunately, although ICH is the most common neurological complication of anticoagulation, especially in the elderly, it is the least treatable. The overall risk of ICH in patients with an INR of 2. Cerebellar hemorrhage is one particularly common type of ICH. Fortunately, ICH is readily visible on a non- enhanced CT scan when it is relatively fresh. Within minutes of a CNS bleed, the CT scan will be diagnostic. Symptoms of ICH in anticoagulated patients are not remarkably different from those who experience this catastrophe from other causes, such as arteriovenous malformation, aneurysm, trauma, or tumor, but there is one major caveat. In about half of those affected, the bleeding is slow, evolving over 1. The symptoms may be atypical when compared with other forms of ICH, such as subarachnoid hemorrhage secondary to an aneurysm. Because the ICH associated with warfarin evolves slowly, the initial symptoms can be subtle, not like the thunderclap headache of a subrachnoid hemorrhage. Symptoms include headache, nausea, and vomiting, confusion, ataxia, or dizziness. Because warfarin- associated hemorrhage continues unabated if anticoagulation is not reversed, a casual approach to even mild hemorrhage cannot be taken. Once the coagulation parameters are remedied, surgical evacuation of the hematoma is often considered. Bleeding issues are relatively straightforward if the patient has a tumor, trauma, or an aneurysm, but the actual mechanism by which warfarin causes a spontaneous ICH is somewhat puzzling. It is unlikely that these anticoagulants induce direct vascular injury or inhibit the normal vascular repair processes. More likely some yet to be identified pathology or vasculopathies are involved. One theory is that otherwise miniscule and self- limited bleeding is accentuated by the anticoagulation. Small vessels that are successfully stanched by the body's normal hemostatic mechanisms are altered by warfarin, making this an attractive theory. This article contains a fascinating micrograph of the brain of an elderly hypertensive patient demonstrating multiple prior asymptomatic microscopic hemorrhages that could lead to frank hemorrhage in the presence of warfarin. At the current time there are few prognostic indicators for patients at risk for spontaneous ICH, although there are some CT or MRI findings of diffuse white matter changes that may be further clarified in the future to stratify risk. Suffice it to say, it is unclear what immediately precipitates so- called spontaneous warfarin- induced ICH in the vast majority of patients. Trivial events, such as a hypertensive flair or a minor mechanical stretch (vigorously shaking the head), have been postulated. It is known that the elderly and those with systolic hypertension have an inherent elevated risk of ICH even in the non- anticoagulated state, and these underlying risks are multiplied as the intensity of anticoagulation increases. In general, the higher the INR, the greater the risk for ICH. The risk of ICH is not always related to the intensity of the anticoagulation. There appears to be no absolutely safe level of anticoagulation or safe INR elevation in some patients. Unfortunately, many patients experience ICH with their INR well within the conventional therapeutic range. Patient factors and anticoagulant intensity appear to be a double insult that determines the absolute risk of ICH. It is generally considered that aspirin administered concomitantly with warfarin probably increases the risk of ICH if that is the only parameter that has changed. Although warfarin- induced subdural hematoma is less frequent than ICH, this is no less life- threatening or critical to the recipient. Warfarin increases the risk of subdural hematoma four- to 1. Hypertension does not seem to be a risk factor for warfarin- associated subdural hematoma to the extent it is with intraparenchymal bleeding. The precipitation of bleeding by minor head trauma, especially in the anticoagulated elderly, is well known. The mortality rate of warfarin- associated subdural hematoma is up to 2. There is a tenuous balance between the benefit of anticoagulation and the risk of ICH in patients who have had or are at risk to have an ischemic stroke. Whether the risks and benefits are positive is up for debate. In some patients, the risk is simply too great. The Risk of Hemorrhage among Patients with Warfarin- Associated Coagulopathy. Garcia D, et al J Am Coll Cardiol 2. Although they do not directly address spontaneous ICH in patients with a warfarin- induced coagulopathy, these authors aimed to determine the risk of major bleeding within 3. INR greater than 5. Most had an INR between 5. Thirteen (1. 3%) patients experienced major hemorrhage during a 3. The highest INR was 1. INR was between 5. None of the events were fatal, and treatment of the elevated INR generally consisted only of withholding warfarin. Of the 1. 3 individuals with hemorrhage, the site was gastrointestinal in 1. GI bleed the most common site of major hemorrhage. Interestingly, there were no cases of spontaneous intracranial hemorrhage even though about half of the patients were over 7. These authors concluded that the risk of major hemorrhage in asymptomatic patients with an INR greater than 5. More than 9. 0 percent of the patients in the cohort were managed without vitamin K reversal. These data seem to suggest that spontaneous ICH is not simply related to the degree of warfarin- induced anticoagulation.
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