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Biomedical subjects

John R Bartholomew

Publications and source records attributed to John R Bartholomew.

11 recordsLinked to original sources
PubMed2005

Transitioning from argatroban to warfarin in heparin-induced thrombocytopenia: an analysis of outcomes in patients with elevated international normalized ratio (INR).

BACKGROUND: Heparin-induced thrombocytopenia (HIT) can lead to catastrophic thromboembolic complications and requires treatment with an alternative, rapidly active anticoagulant, such as a direct thrombin inhibitor (DTI), either to prevent or treat these complications. Switching to oral warfarin after initial treatment with a DTI is necessary in most patients. Most references related to warfarin suggest that an increased risk for bleeding will occur with elevated international normalized ratios (INRs) > 4.6. In patients receiving argatroban, it is not uncommon to achieve an INR > 4 during this transition. Because the clinical outcomes in patients achieving an INR > 4 during combined argatroban/warfarin therapies for HIT are not well described, we evaluated the clinical outcomes of 111 patients with this phenomenon. METHODS: We identified patients from the prospective studies of argatroban anticoagulation, Argatroban-911 and Argatroban-915. Data collected from these studies included death from all causes, amputation, new thrombosis, major bleeding, INR values, argatroban doses, aPTT values, platelet counts, and duration of therapy. RESULTS: Patients were on argatroban monotherapy for a median of 2.8 (0.1-8.1) days, and on cotherapy for a median of 3.7 (0.9-12.8) days. The median platelet count was 70.9 (18-325) x 10(9)/L at the time of HIT diagnosis and increased to 94 (30-324) x 10(9)/L by the time warfarin was initiated. At a median argatroban dose of 1.4 (0.2-2.0) mcg/kg/min, the maximum INR ranged from 4.1 to 21.2 (median 6.4, n = 111) and the corresponding aPTT ranged from 48.1 to 105 (median 71, n = 93) seconds. After argatroban cessation, the first recorded INR within 4 to 24 hours ranged from 1.5 to 12.5 (median 2.9, n = 58). Adverse clinical outcomes occurred in 9 (8.1%) patients during cotherapy and in 12 (10.8%) patients after argatroban anticoagulation was discontinued. Adverse clinical outcomes included 7 cases of new thrombosis, 3 amputations, 12 deaths and 1 major bleed. Eleven of 12 (91.7%) patients died due to causes other than thrombosis, and most deaths (83%) occurred following cotherapy. Five (4.5%) patients developed new thrombosis during argatroban/warfarin cotherapy despite an INR > 4. In contrast only 1 (0.9%) patient experienced major bleeding. CONCLUSION: In patients receiving argatroban/warfarin cotherapy and with an elevated INR > 4, the risk for thrombosis exceeds the risk of bleeding. Traditional paradigms concerning elevated INRs and warfarin may need to be redesigned for the patient population on cotherapy with direct thrombin inhibitors.Abbreviated Abstract. The clinical outcomes of 111 patients with INRs > 4 while on combined argatroban (dose < or = 2 mcg/kg/min) and warfarin were evaluated. Adverse clinical outcomes (7 new thrombosis, 3 amputations, 12 deaths and 1 major bleed) occurred in 21 patients. Eleven deaths were due to causes other than thrombosis. Five patients developed new thrombosis while only 1 had major bleeding. The risk for thrombosis exceeds the risk of bleeding in patients with HIT despite an INR > 4.

Adult↗
PubMed2005

The incidence and clinical features of heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is an important adverse reaction of heparin therapy that can have catastrophic consequences if overlooked or misdiagnosed. Treatment with either unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) can trigger this complication. Orthopedic, cardiac, and vascular surgery patients exposed to prophylactic or therapeutic doses of heparin are at particular risk. Awareness of the clinical features and different presentations of HIT are essential for preventing severe morbidity and mortality associated with this disease.

Anticoagulants↗
PubMed2005

Atheromatous embolization.

Atheromatous embolization is a multisystem disease complicating advanced atherosclerosis. It occurs most often as a complication of angiography, an endovascular procedure or cardiovascular surgery. Atheromatous embolization can present in a subtle manner where it is often under-recognized, or with catastrophic results including myocardial infarction, strake or acute renal failure. It may mimic other disease processes and often goes underdiagnosed and undertreated. A high clinical suspicion is the key to diagnosis. Atheromatous embolization results in significant morbidity and mortality; therefore, early recognition followed by aggressive management may help to prevent end-organ damage and improve overall clinical outcomes. Management strategies should include risk factor modification, prevention of further insults by discontinuing or avoiding predisposing factors, supportive treatment and interventional or surgical approaches to remove the atheroembolic source. Atheromatous embolization is expected to increase as our population ages and the epidemics of diabetes mellitus and obesity increase.

Adrenal Cortex Hormones↗
PubMed2005

Transition to an oral anticoagulant in patients with heparin-induced thrombocytopenia.

Recommendations for transitioning from therapy with heparin or a low-molecular-weight heparin preparation to therapy with an oral anticoagulant in patients with acute venous or arterial thromboembolism have undergone several changes during the last two decades. Physicians are now comfortable with beginning treatment with an oral anticoagulant once the diagnosis is confirmed, and loading doses are no longer considered to be necessary. Exceptions to early transition may be necessary in patients with an extensive iliofemoral or axillary-subclavian vein thrombosis or pulmonary embolism where thrombolytic agents may be indicated, or in individuals who require surgery or other invasive procedures, or if there are concerns about bleeding. The avoidance of early transition to oral anticoagulants in patients with acute heparin-induced thrombocytopenia also has been advised because of the potential for further thrombotic complications, including venous limb gangrene and warfarin-induced skin necrosis.

Administration, Oral↗
PubMed2005

Varicose veins: newer, better treatments available.

Varicose veins are not only a cosmetic annoyance: they can lead to complications that result in lost time from work and lost wages. Treatment has improved with the use of minimally invasive techniques that reduce recovery time and complications and offer better long-term results--encouraging news, considering that the problem affects 10% to 20% of adult men and 25% to 33% of adult women.

Humans↗
PubMed2005

Heparin-induced thrombocytopenia: principles for early recognition and management.

Heparin-induced thrombocytopenia (HIT) is a potentially devastating complication of therapy with either unfractionated or low-molecular-weight heparin. Thrombocytopenia is no longer essential for the diagnosis of HIT, since a 50% drop in the platelet count may be a more specific indicator. Once HIT is clinically suspected, heparin should be stopped immediately and direct thrombin inhibitor therapy started; waiting for laboratory confirmation may be catastrophic.

Anticoagulants↗
PubMed2004

Smokeless tobacco and cardiovascular risk.

This article discusses the evolution of smokeless tobacco in the United States and interprets the available data on cardiovascular risk factors and cardiovascular mortality associated with its use. There has been a resurgence of smokeless tobacco use since 1970. Smokeless tobacco consistently produces levels of nicotine higher than those seen with smoking and causes similar sympathetic neural stimulation and acute cardiovascular effects. However, there is conflicting evidence from prospective and case-control studies about cardiovascular mortality or myocardial infarction caused by smokeless tobacco use. Smokeless tobacco use is also associated with oral cancers and high-risk behavior in adolescents. Although the evidence is not conclusive, the adverse cardiovascular effects of smokeless tobacco use are less than those caused by smoking but are more than those found in nonusers. It is advisable to counsel all current users of smokeless tobacco to quit. Behavioral counseling, sustained-release bupropion hydrochloride therapy, and nicotine replacement therapy may be safe therapeutic modalities for treatment of smokeless tobacco use.

Blood Pressure↗
PubMed2004

Warfarin-induced skin necrosis and venous limb gangrene in the setting of heparin-induced thrombocytopenia.

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a common, often catastrophic, syndrome that produces the most hypercoagulable of states. Emerging therapeutic strategies use alternative anticoagulants; warfarin's place is being reexamined. Early in the course of warfarin therapy, there may be net procoagulant effects because of the inhibition of protein C. With HIT, it has been suggested that unopposed warfarin can precipitate venous limb gangrene. There are also reports of warfarin-induced skin necrosis. We seek to confirm and increase awareness of the risks of warfarin with HIT. METHODS: We describe 6 patients with HIT seen at 3 medical centers in whom frank or impending venous limb gangrene, central skin necrosis, or both were temporally related to warfarin initiation. RESULTS: At warfarin initiation, 5 patients had recognized HIT and 1 had it recognized later. Complications emerged after 2 to 7 days, and consisted of warfarin-induced skin necrosis (n = 5) and venous limb gangrene (n = 2); 1 patient had both. This emerged with unopposed warfarin in 4 patients and as a direct thrombin inhibitor was being withdrawn in 2. All had supratherapeutic international normalized ratios. One patient required leg and breast amputations, and another one died. CONCLUSIONS: Because of the early effects on protein C, warfarin can precipitate venous limb gangrene and/or skin necrosis in the extreme hypercoagulable milieu of HIT. With HIT, unopposed warfarin should be avoided and caution is needed during transition from a direct thrombin inhibitor. Warfarin should be initiated at modest doses in patients with HIT after platelet recovery. Implications extend to warfarin initiation with other thrombotic diatheses.

Adult↗
PubMed2003

Patients with acute pulmonary embolism should have an echocardiogram to guide treatment decisions.

A 62-year-old man with a past medical history notable for hypertension, osteoarthritis, and calf deep vein thrombosis at age 55 following a total hip arthroplasty presents to the emergency department with acute-onset dyspnea and right-sided pleuritic chest pains. His medications consist of a calcium channel blocker and a COX-2 inhibitor. Pretest clinical suspicion for pulmonary embolism (PE) is high. Ventilation and perfusion lung scintigraphy are interpreted as being high-probability for PE. The nurse asks if a stat transthoracic echocardiogram should be ordered.

Acute Disease↗
PubMed2002

Lepirudin anticoagulation for heparin-induced thrombocytopenia.

Lepirudin is indicated for anticoagulation in patients with heparin-induced thrombocytopenia (HIT). We describe 2 cases of HIT and thrombosis in children with heart disease, including one that required extracorporeal membrane oxygenation. Lepirudin, dosed in the recommended adult weight--based fashion, was an effective antithrombotic agent in pediatric patients with HIT.

Anticoagulants↗