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Mark A Crowther

Publications and source records attributed to Mark A Crowther.

At least 19 recordsLinked to original sources
PubMed2007

Systematic review: efficacy and safety of rituximab for adults with idiopathic thrombocytopenic purpura.

BACKGROUND: Rituximab, a monoclonal anti-CD20 antibody, is increasingly used to treat idiopathic thrombocytopenic purpura (ITP). PURPOSE: To systematically review the literature on the efficacy and safety of rituximab for the treatment of adults with ITP. DATA SOURCES: MEDLINE, EMBASE, the Cochrane Library, abstracts from the American Societies of Hematology and Clinical Oncology annual meetings, and bibliographies of relevant articles and reviews were searched in duplicate until April 2006. STUDY SELECTION: Descriptive and comparative studies in any language that met predefined inclusion criteria were eligible. Efficacy analysis was restricted to studies enrolling 5 or more patients. DATA EXTRACTION: Platelet count response, toxicities, dose, previous treatments, baseline platelet count, duration of ITP, study design, and sources of funding were extracted in duplicate. DATA SYNTHESIS: We identified 19 eligible reports on efficacy (313 patients) and 29 on safety (306 patients). Weighted means for complete response (platelet count > 150 x 10(9) cells/L) and overall response (platelet count > 50 x 10(9) cells/L) with rituximab were 43.6% (95% CI, 29.5% to 57.7%) and 62.5% (CI, 52.6% to 72.5%), respectively. Responses lasted from 2 to 48 months. Nearly all patients had received corticosteroids, and 53.8% had undergone splenectomy. Nine patients (2.9%) died. LIMITATIONS: There were no controlled studies, and no studies met all criteria for study quality. Reported deaths could not necessarily be attributed to rituximab. Overall, the number of rituximab-treated patients with ITP reported in the literature is small. CONCLUSIONS: Rituximab resulted in an overall platelet count response in 62.5% of adults with ITP. However, this finding derives from uncontrolled studies that also reported significant toxicities, including death in 2.9% of cases. These data suggest that providers should avoid indiscriminate use of rituximab and that randomized, controlled trials of rituximab for ITP are urgently needed.

Antibodies, Monoclonal↗
PubMed2007

Paper-based dosing algorithms for maintenance of warfarin anticoagulation.

We examined the quality of anticoagulation produced by two paper-based warfarin dosing algorithms in a randomized clinical trial of warfarin therapy. Fifty-eight patients were randomized to receive warfarin at a target international normalized ratio (INR) range of 2.1-3.0 and were followed for an average of 2.7 years. As a proportion of total patient-time, the percentage of time spent above, within, and below the therapeutic range was 11%, 71%, and 19% respectively. Fifty-six patients were randomized to receive warfarin at a higher target INR range (3.1-4.0) and had INRs within the therapeutic range for 40% of total patient time. We conclude that the performance, minimal cost, and ease-of-use of these algorithms make them well-suited for patient management within primary-care and research settings.

Adult↗
PubMed2007

Prevalence of thalassemia in patients with microcytosis referred for hemoglobinopathy investigation in Ontario: a prospective cohort study.

In Ontario, Canada, beta-thalassemia is easily detected through measurement of hemoglobin A2, but most laboratories do not do exhaustive DNA investigations for alpha-thalassemia. Therefore, the prevalence of thalassemia in microcytic samples for hemoglobinopathy investigation in Ontario is unknown. To address this, we performed a prospective cohort study in which samples referred for hemoglobinopathy investigation were also evaluated for alpha-thalassemia by DNA testing. Of 800 samples submitted, 664 were evaluable. Of the 664 patients represented, 163 (24.5%) were beta-thalassemia major carriers, 68 (10.2%) were hemoglobin Bart's hydrops fetalis carriers and, in total, 361 (54.4%) had some form of thalassemia. We conclude that microcytosis due to thalassemia is common in Ontario and that major forms of thalassemia, including forms predisposing to hemoglobin Bart's hydrops fetalis and beta-thalassemia major, are frequent. This illustrates the importance of adequate prenatal and laboratory investigation for these abnormalities in Ontario and other similar multiethnic jurisdictions worldwide.

Adolescent↗
PubMed2006

An evaluation of D-dimer in the diagnosis of pulmonary embolism: a randomized trial.

BACKGROUND: It may be safe to omit additional diagnostic testing in selected patients with suspected pulmonary embolism (PE) who have a negative D-dimer test, but this approach has never been evaluated in a randomized, controlled trial. OBJECTIVE: To determine if additional diagnostic testing can be safely withheld in patients with suspected PE who have negative erythrocyte agglutination D-dimer test results. DESIGN: Randomized comparisons in 2 subgroups of a prospective multicenter study. SETTING: 7 university hospitals. PATIENTS: 1126 outpatients or inpatients with suspected PE; of these, 456 patients with negative erythrocyte agglutination D-dimer test results were randomly assigned to the intervention groups. Patients were classified into 2 clinical probability groups: those with a low clinical probability of PE (low-probability group) and those with a moderate or high clinical probability of PE, a nondiagnostic ventilation-perfusion lung scan, and no evidence of proximal deep venous thrombosis on bilateral ultrasonography (moderate- or high-probability group). INTERVENTIONS: The experimental intervention for both probability groups was no further diagnostic testing for PE. The control intervention for the low-probability group was a ventilation-perfusion lung scan followed by ultrasonography of the proximal deep veins of the legs on the same day. If the lung scan was nondiagnostic, ultrasonography of the legs was repeated 7 and 14 days later. The control intervention for the moderate- or high-probability group was ultrasonography of the proximal deep veins of the legs after 7 and 14 days. In the control and experimental groups, anticoagulation was withheld or withdrawn if PE was not diagnosed. MEASUREMENTS: Symptomatic venous thromboembolism (VTE) during 6 months of follow-up. RESULTS: Prevalence of VTE was 15.2% in the 1126 enrolled patients. In the low-probability group, VTE occurred during follow-up in 0 of 182 patients who had no additional diagnostic testing and in 1 of 185 patients who had additional testing (difference, -0.5 percentage point [95% CI, -3.0 to 1.6 percentage points]). In the moderate- or high-probability group, VTE occurred during follow-up in 1 of 41 patients who had no additional diagnostic testing and in 0 of 41 patients who had additional testing (difference, 2.4 percentage points [CI, -6.4 to 12.6 percentage points]). LIMITATIONS: The authors could not enroll 2000 patients as originally planned; 3 randomly assigned patients did not receive the allocated intervention, and 7 received inadequate follow-up. Personnel who performed follow-up evaluations were not blinded to the results of diagnostic testing at enrollment or to allocation group assignments. CONCLUSION: In patients with a low probability of PE who have negative D-dimer results, additional diagnostic testing can be withheld without increasing the frequency of VTE during follow-up. Low clinical probability and negative D-dimer results occur in 50% of outpatients and in 20% of inpatients with suspected PE.

Fibrin Fibrinogen Degradation Products↗
PubMed2006

Safety of dalteparin for the prophylaxis of venous thromboembolism in elderly medical patients with renal insufficiency: a pilot study.

The aim of this prospective cohort study was to determine the incidence of dalteparin bioaccumulation (measured using anti-Xa levels), and bleeding during thromboprophylaxis in elderly patients with renal failure who were admitted to hospital with an acute medical illness. Patients who met the criteria for being at high thromboembolic risk received dalteparin 5,000 IU subcutaneously once daily while the other patients (low risk) received 2,500 IU daily. Thromboprophylaxis was administered for at least 6 days. Anti-Xa activity was determined before the first dalteparin dose and again on day 6, 4 hours after the administration of the dalteparin dose. Bleeding was assessed daily. Compression ultrasonography was performed to identify any deep vein thromboses. There was no evidence of bioaccumulation on day 6 of therapy, irrespective of renal function. No episodes of major bleeding or venous thromboembolism occurred. Larger, randomized studies are warranted to confirm the safety of dalteparin in this patient population.

Aged↗
PubMed2006

Meta-analysis: low-molecular-weight heparin and bleeding in patients with severe renal insufficiency.

BACKGROUND: Dose adjustment or laboratory monitoring of low-molecular-weight heparin (LMWH) is commonly recommended for patients with severe renal insufficiency (creatinine clearance < or =30 mL/min), but the basis for this recommendation is unclear. PURPOSE: To compare levels of anti-Xa heparin and risk for major bleeding in LMWH-treated patients with a creatinine clearance of 30 mL/min or less versus those with a creatinine clearance greater than 30 mL/min by using standard weight-adjusted therapeutic doses, empirically adjusted doses, or prophylactic doses of LMWH. DATA SOURCES: Electronic databases (MEDLINE, EMBASE, and the Cochrane Library) searched to December 2005 with no language restrictions. The authors also searched reference lists and contacted experts. STUDY SELECTION: Observational or subgroups of randomized studies that included non-dialysis-dependent patients with varying degrees of renal function who were treated with LMWH and reported creatinine clearance and anti-Xa levels or major bleeding. DATA EXTRACTION: Two reviewers independently selected studies and extracted data on patient characteristics, renal function, LMWH treatment, anti-Xa levels, and major bleeding. The pooled odds ratio of major bleeding in patients with a creatinine clearance of 30 mL/min or less was calculated by using the Peto method. DATA SYNTHESIS: Eighteen studies using 3 preparations of LMWH (15 studies using enoxaparin, 2 using tinzaparin, and 1 using dalteparin) were included. Peak anti-Xa levels measured 4 hours after a subcutaneous injection were statistically significantly higher in patients with a creatinine clearance of 30 mL/min or less compared with those with a creatinine clearance greater than 30 mL/min in studies that used a standard therapeutic dose of enoxaparin (4 studies) but not in studies of empirically dose-adjusted enoxaparin (3 studies). Data were insufficient to assess the relationship between anti-Xa and renal function for prophylactic doses of enoxaparin and therapeutic doses of tinzaparin or dalteparin. In 12 studies involving 4971 patients, LMWH was associated with a statistically significant increase in the risk for major bleeding in patients with a creatinine clearance of 30 mL/min or less compared with those with a creatinine clearance greater than 30 mL/min (5.0% vs. 2.4%; odds ratio, 2.25 [95% CI, 1.19 to 4.27]; P = 0.013). When analyzed according to LMWH preparation, major bleeding was increased when a standard therapeutic dose of enoxaparin was used (8.3% vs. 2.4%; odds ratio, 3.88 [CI, 1.78 to 8.45]) but may not be increased when an empirically adjusted dose of enoxaparin is used (0.9% vs. 1.9%; odds ratio, 0.58 [CI, 0.09 to 3.78]; P = 0.23 for heterogeneity). There were insufficient studies to assess the risk for major bleeding with tinzaparin, dalteparin, and prophylactic doses of enoxaparin. LIMITATIONS: The data for tinzaparin and dalteparin were limited. Data are observational, and the potential for confounding cannot be excluded. CONCLUSIONS: Non-dialysis-dependent patients with a creatinine clearance of 30 mL/min or less who are treated with standard therapeutic doses of enoxaparin have elevated levels of anti-Xa and an increased risk for major bleeding. Empirical dose adjustment of enoxaparin may reduce the risk for bleeding and merits additional evaluation. No conclusions can be made regarding other LMWHs.

Anticoagulants↗
PubMed2006

Natural history of cerebral vein thrombosis: a systematic review.

UNLABELLED: Cerebral vein thrombosis (CVT) has been considered, until a few years ago, an uncommon disease with significant long-term morbidity and high mortality rate. New noninvasive diagnostic techniques have increased the frequency with which this disease is diagnosed; despite this, there continues to be little data on its natural history. The objectives of this study were to evaluate the mortality rate, the rate of disability at long-term follow-up, and the incidence of recurrence after a first episode of CVT; to determine clinical and radiologic predictors of death and dependence; and to identify possible risk factors for recurrence. ( DATA SOURCE: MEDLINE and EMBASE databases, reference lists of selected articles and authors' libraries.) Nineteen studies were identified. Mortality rate during peri-hospitalization period is 5.6% (range, 0%-15.2%) and 9.4% (range, 0%-39%) at the end of follow-up period. Eighty-eight percent of surviving patients recover completely or have only a mild functional or cognitive deficit. Two thirds of patients with CVT recanalized within the first few months after presentation, and 2.8% (range, 0%-11.7%) had objectively confirmed recurrence. We conclude that patients with CVT have a low risk of death and that most patients have a good long-term prognosis.

Diagnosis, Differential↗
PubMed2006

Management of antiphospholipid antibody syndrome: a systematic review.

CONTEXT: Antiphospholipid antibodies are autoantibodies directed against proteins that bind to phospholipid. Antiphospholipid antibody syndrome (APS) refers to the association between antiphospholipid antibodies and thrombosis risk or pregnancy morbidity. Patients with APS may be at increased risk of recurrent arterial or venous thrombosis or pregnancy loss. OBJECTIVE: To systematically review the evidence for treatment of thrombosis risk in patients with antiphospholipid antibodies or APS. EVIDENCE ACQUISITION: Search of MEDLINE (1966 to November 2005) and Cochrane Library electronic databases (2005) and reference lists for randomized trials, meta-analyses of randomized trials, and prospective cohort studies of the treatment of thrombosis risk in patients with antiphospholipid antibodies or APS. Studies were selected on the basis of clinical relevance. EVIDENCE SYNTHESIS: Among patients with antiphospholipid antibodies, the absolute risk of developing new thrombosis is low (<1% per year) in otherwise healthy patients without prior thrombotic events, may be moderately increased (up to 10% per year) in women with recurrent fetal loss without prior thrombosis, and is highest (>10% in the first year) in patients with a history of venous thrombosis who have discontinued anticoagulant drugs within 6 months. Compared with placebo or untreated control, anticoagulation with moderate-intensity warfarin (adjusted to a target international normalized ratio [INR] of 2.0-3.0) reduces the risk of recurrent venous thrombosis by 80% to 90% irrespective of the presence of antiphospholipid antibodies and may be effective for preventing recurrent arterial thrombosis. No evidence exists that high-intensity warfarin (target INR, >3.0) is more effective than moderate-intensity warfarin. For patients with a single positive antiphospholipid antibody test result and prior stroke, aspirin and moderate-intensity warfarin appear equally effective for preventing recurrent stroke. Treatment issues that have not been addressed in clinical trials, or for which the evidence is conflicting, include the role of antithrombotic prophylaxis in patients with antiphospholipid antibodies without prior thrombosis, the optimal treatment of noncerebrovascular arterial thrombosis, recurrent thrombosis despite warfarin therapy, and treatment of women with antiphospholipid antibodies and recurrent fetal loss. CONCLUSIONS: In patients with APS, moderate-intensity warfarin is effective for preventing recurrent venous thrombosis and perhaps also arterial thrombosis. Aspirin appears to be as effective as moderate-intensity warfarin for preventing recurrent stroke in patients with prior stroke and a single positive test result for antiphospholipid antibody. The optimal treatment of other thrombotic aspects of APS needs to be addressed in well-designed prospective studies.

Antibodies, Antiphospholipid↗
PubMed2006

Azathioprine and inhibition of the anticoagulant effect of warfarin: evidence from a case report and a literature review.

BACKGROUND: Warfarin and azathioprine may be prescribed concurrently in patients requiring both anticoagulation and immunosuppression. However, a potential interaction between the 2 drugs, resulting in an increased warfarin requirement, may be overlooked in clinical practice. CASE SUMMARY: A 67-year-old woman was treated with warfarin (initial mean dose, 24 mg/wk [3.5 mg/d]) for >3 years for recurrent deep vein thrombosis associated with systemic lupus erythematosus. Soon after commencing warfarin, azathioprine 150 mg/d was introduced for its steroid-sparing effect. Warfarin was titrated to a mean dose of 60 to 75 mg/wk (8.5-10.5 mg/d) over the next 18 months. Her dose of azathioprine was then increased to 200 mg/d. Subtherapeutic international normalized ratio (INR) levels required an increase in the warfarin dose to a mean of 130 mg/wk (18.5 mg/d). Subsequent discontinuation of azathioprine resulted in a dramatic increase in her INR levels (from 1.8 to 14.0 four weeks after discontinuation). DISCUSSION: A temporal relationship, demonstrating the interaction between warfarin and azathioprine, was evident at various times during therapy for our patient. This case, together with 7 additional published cases, is comprehensively reviewed here using previously described criteria for establishing a definite interaction between warfarin and other drugs. CONCLUSIONS: The evidence supports a clinically important inhibitory action of azathioprine on warfarin and calls for closer monitoring of INR levels when azathioprine doses are altered during concurrent administration with warfarin.

Aged↗
PubMed2006

New anti-thrombotic agents: emphasis on hemorrhagic complications and their management.

Our advanced knowledge of coagulation has led to the synthesis of novel procoagulant substances, such as recombinant activated factor VII (rFVIIa; NovoSeven, Novo Nordisk, Bagsvaerd, Denmark). Similarly, in-depth understanding of the interaction between anticoagulant proteins and their natural inhibitors has led to the synthesis of various novel anticoagulants. Novel anticoagulants are characterized by highly specific coagulation-inhibiting activities and, frequently, a complete lack of effective antidotes. This lack of antidotes is particularly important in the case of novel inhibitors with extended half-lives; for example, idraparinux may produce effective anticoagulation for as long as one week after subcutaneous administration. As novel anticoagulants complete licensing evaluations and are used in clinical practice, the likelihood of anticoagulant-associated hemorrhage will increase. This will require physicians to have an understanding of the mechanism of action of these anticoagulants, and to have an advanced degree of knowledge of the potential specific and nonspecific inhibitors of these anticoagulant agents. This paper will briefly review the biochemistry of coagulation, focusing on the complexes inhibited by currently available and novel anticoagulants. Specific and nonspecific prohemostatic agents will be reviewed and discussed. The ability of nonspecific procoagulant agents (particularly rFVIIa) to reverse the effects of novel anticoagulants will also be reviewed.

Blood Coagulation↗
PubMed2006

Reliability of electrocardiogram interpretation in critically ill patients.

OBJECTIVE: To assess the intrarater and interrater reliability of electrocardiogram (ECG) interpretation in critically ill patients and to assess the effect of knowledge of cardiac troponin values on these reliability estimates. DESIGN: Prospective cohort study. SETTING: Fifteen-bed medical-surgical intensive care unit. PATIENTS: Consecutive adults admitted over a 2-month period. MEASUREMENTS AND RESULTS: All consecutive 12-lead ECGs were interpreted independently by two raters for the presence of myocardial ischemia or infarction and secondarily for specific ischemic ECG abnormalities. The ECGs were first interpreted blinded to the patient's troponin levels and reinterpreted on two separate occasions, blinded and unblinded to the troponin values. Results are reported using chance-independent agreement (phi) with associated 95% confidence intervals. For the presence of ischemia or infarction, the intrarater reliability ranged from fair to moderate (phi = 0.35 [95% confidence interval = 0.16, 0.52] and 0.59 [0.33, 0.77] for the two raters, respectively); interrater reliability was slight when blinded to troponin levels (phi = 0.18 [0.03, 0.32]) and increased to moderate when the raters were unblinded to troponin values (phi = 0.52 [0.33, 0.66], p value for the difference = .004). For specific ECG changes, the intrarater and interrater reliability were low for T-wave flattening, whereas detection of a left bundle branch block showed high reliability. CONCLUSIONS: ECG interpretation in critically ill patients for the presence of myocardial ischemia or infarction showed moderate reliability at best; however, there was high reliability for specific ECG changes. Knowledge of the patient's troponin values increased the reliability for all studied ECG changes and resulted in a statistically significant increase in the interrater reliability for diagnosing myocardial ischemia or infarction. Additional studies assessing the appropriate methods of diagnosing myocardial ischemia and infarction and assessing the reliability of these diagnostic tests in critically ill patients are required.

Critical Illness↗
PubMed2006

Utilization of platelet transfusions in the intensive care unit: indications, transfusion triggers, and platelet count responses.

BACKGROUND: A description of current platelet (PLT) transfusion practice in the intensive care unit (ICU) is needed. STUDY DESIGN AND METHODS: All thrombocytopenic patients (PLT count, <150 x 10(9)/L) who received PLT transfusions were identified from a previous prospective study of consecutive medical-surgical ICU patients; trauma, orthopedic, and cardiac surgery were exclusions. Risk factors for ineffective transfusions were examined. RESULTS: Of 261 ICU patients, 118 (45.2%) had thrombocytopenia and a PLT count nadir of less than 50 x 10(9) per L (n = 22), 50 to 99 x 10(9) per L (n = 37), and 100 to 149 x 10(9) per L (n = 59). Twenty-seven (22.9%) patients received PLT transfusions (n = 76 transfusions) and 37 (31.4%) had major bleeding. PLT dose was approximately 3 to 4 x 10(11) per L transfusion. Therapeutic (n = 24) and prophylactic (n = 52) PLT transfusion triggers were 51 x 10(9) per L (interquartile range [IQR], 26 to 68) and 41 x 10(9) per L (IQR, 20 to 57), respectively, as measured at a median of 4.5 hours (IQR, <1.6 to 6.9) before transfusion. A single PLT transfusion resulted in a median PLT increase of 14 x 10(9) per L (IQR, -2 to 30) measured at 5.2 hours (IQR, 1.8 to 8.8) after the transfusion; however, no PLT count increase was observed after 17 transfusions given to 13 (48.1%) patients. No risk factors for ineffective transfusions were identified. CONCLUSIONS: Among critically ill patients, most PLT transfusions were administered to prevent, rather than to treat, bleeding, with a transfusion trigger of 40 to 50 x 10(9) per L. Nearly half of ICU patients who received transfusions failed to mount a PLT count increase after a single transfusion. Prospective studies are needed to determine the effects of PLT transfusions on bleeding and predictors of ineffective transfusions in the ICU.

Aged↗
PubMed2006

Elevated cardiac troponin levels in critically ill patients: prevalence, incidence, and outcomes.

BACKGROUND: Levels of cardiac troponin, a sensitive and specific marker of myocardial injury, are often elevated in critically ill patients. OBJECTIVES: To document elevated levels of cardiac troponin I in patients in a medical-surgical intensive care unit and the relationship between elevated levels and electrocardiographic findings and mortality. METHODS: A total of 198 patients expected to remain in the intensive care unit for at least 72 hours were classified as having myocardial infarction (cardiac troponin I level >or=1.2 microg/L and ischemic electrocardiographic changes), elevated troponin level only (>or=1.2 microg/L and no ischemic electrocardiographic changes), or normal troponin levels. Events were classified as prevalent if they occurred within 48 hours after admission and as incident if they occurred 48 hours or later after admission. Factors associated with mortality were examined by using regression analysis. RESULTS: A total of 171 patients had at least one troponin level measured in the first 48 hours. The prevalence of elevated troponin level was 42.1% (72 patients); 38 patients (22.2%) had myocardial infarction, and 34 (19.9%) had elevated troponin level only. After the first 48 hours, 136 patients had at least 1 troponin measurement. The incidence of elevated troponin level was 11.8% (16 patients); 7 patients (5.1%) met criteria for myocardial infarction, and 2 (1.5%) had elevated troponin level only. Elevated levels of troponin I at any time during admission were associated with mortality in the univariate but not the multivariate analysis. CONCLUSIONS: Elevated levels of cardiac troponin I in critically ill patients do not always indicate myocardial infarction or an adverse prognosis.

Adult↗
PubMed2005

Elevated troponin and myocardial infarction in the intensive care unit: a prospective study.

INTRODUCTION: Elevated troponin levels indicate myocardial injury but may occur in critically ill patients without evidence of myocardial ischemia. An elevated troponin alone cannot establish a diagnosis of myocardial infarction (MI), yet the optimal methods for diagnosing MI in the intensive care unit (ICU) are not established. The study objective was to estimate the frequency of MI using troponin T measurements, 12-lead electrocardiograms (ECGs) and echocardiography, and to examine the association of elevated troponin and MI with ICU and hospital mortality and length of stay. METHOD: In this 2-month single centre prospective cohort study, all consecutive patients admitted to our medical-surgical ICU were classified in duplicate by two investigators as having MI or no MI based on troponin, ECGs and echocardiograms obtained during the ICU stay. The diagnosis of MI was based on an adaptation of the joint European Society of Cardiology/American College of Cardiology definition: a typical rise or fall of an elevated troponin measurement, in addition to ischemic symptoms, ischemic ECG changes, a coronary artery intervention, or a new cardiac wall motion abnormality. RESULTS: We screened 117 ICU admissions and enrolled 115 predominantly medical patients. Of these, 93 (80.9%) had at least one ECG and one troponin; 44 of these 93 (47.3%) had at least one elevated troponin and 24 (25.8%) had an MI. Patients with MI had significantly higher mortality in the ICU (37.5% versus 17.6%; P = 0.050) and hospital (50.0% versus 22.0%; P = 0.010) than those without MI. After adjusting for Acute Physiology and Chronic Health Evaluation II score and need for inotropes or vasopressors, MI was an independent predictor of hospital mortality (odds ratio 3.22, 95% confidence interval 1.04-9.96). The presence of an elevated troponin (among those patients in whom troponin was measured) was not independently predictive of ICU or hospital mortality. CONCLUSION: In this study, 47% of critically ill patients had an elevated troponin but only 26% of these met criteria for MI. An elevated troponin without ischemic ECG changes was not associated with adverse outcomes; however, MI in the ICU setting was an independent predictor of hospital mortality.

Cohort Studies↗
PubMed2005

Uremic bleeding: pathophysiology and clinical risk factors.

Renal insufficiency appears clinically to be associated with a bleeding tendency. This has been documented in clinical settings including as a complication of medical interventions such as surgery and also in spontaneous bleeding events at gastrointestinal and intracranial sites. The pathophysiology that underlies this tendency appears to involve platelet dysfunction and an imbalance of mediators of normal endothelial function. It is also may be complicated by the co-morbidities in this population, such as vascular disease, hypertension and anemia, and the medical interventions required to treat such co-morbidities. This article reviews the evidence, the pathophysiology and the risk factors for increased bleeding in patients with chronic renal insufficiency.

Hemorrhage↗