Enoxaparin for VTE thromboprophylaxis during inpatient rehabilitation care: assessment of the standard fixed dosing regimen.

BACKGROUND: We aimed to examine the efficiency of fixed daily dose enoxaparin (40 mg) thromboprophylaxis strategy for patients undergoing inpatient rehabilitation. METHODS: This was an observational, prospective, cohort study that included 63 hospitalized patients undergoing rehabilitative treatment following sub-acute ischemic stroke (SAIS) or spinal cord injury (SCI), with an indication for thromboprophylaxis. Anti-Xa level measured three hours post-drug administration (following three consecutive days of enoxaparin treatment or more) was utilised to assess in vivo enoxaparin activity. An anti-Xa level between 0.2-0.5 U/ml was considered evidence of effective antithrombotic activity. RESULTS: We found sub-prophylactic levels of anti-Xa (<0.2 U/ml) in 19% (12/63). Results were within the recommended prophylactic range (0.2-0.5 U/ml) in 73% (46/63) and were supra-prophylactic (>0.5 U/ml) in 7.9% (5/63) of patients. Anti-Xa levels were found to inversely correlate with patients' weight and renal function as defined by creatinine clearance (CrCl) (p<0.05). CONCLUSIONS: Our study confirmed that a one-size-fits-all approach for venous thromboembolism (VTE) prophylaxis may be inadequate for rehabilitation patient populations. The efficacy of fixed-dose enoxaparin prophylaxis is limited and may be influenced by renal function and weight. This study suggests that anti-Xa studies and prophylactic enoxaparin dose adjustments should be considered in certain patients, such as those who are underweight, overweight and or have suboptimal renal function. TRIAL REGISTRATION: No. NCT103593291, registered August 2018.

Cognitive Dysfunction: Part and Parcel of the Diabetic Foot.

OBJECTIVE: The presence of a foot ulcer increases the self-treatment burden imposed on the individual with diabetes. Additionally, this condition increases the cognitive demands needed for adherence to medical recommendations. A potential gap could exist between medical recommendations and the individual's ability to implement them. Hence, the goal of this study was to examine whether the cognitive profile of people with diabetic foot ulcers differs from that of people with diabetes without this complication. RESEARCH DESIGN AND METHODS: This was a case-control study. Ninety-nine individuals with diabetic foot ulcers (case patients) and 95 individuals with type 2 diabetes (control subjects) (age range 45-75 years), who were matched for diabetes duration and sex, underwent extensive neuropsychological evaluation using a NeuroTrax computerized battery, digit symbol, and verbal fluency tests. A global cognitive score after standardization for age and education was computed as well as scores in the following six cognitive domains: memory, executive function, reaction time, attention, psychomotor abilities, and estimated premorbid cognition. RESULTS: Individuals with diabetic foot ulcers had significantly (P < 0.001) lower cognitive scores than individuals with diabetes without this complication, in all tested cognitive domains, excluding estimated premorbid cognition. Individuals with diabetic foot ulcers demonstrated a significant difference between precognitive and current cognitive abilities, as opposed to the nonsignificant difference among control subjects. The differences persisted in multivariable analysis after adjusting for depression and smoking. CONCLUSIONS: Individuals with diabetic foot ulcers were found to possess fewer cognitive resources than individuals with diabetes without this complication. Thus, they appear to face more self-treatment challenges, while possessing significantly fewer cognitive resources.

The nature and course of sensory changes following spinal cord injury: predictive properties and implications on the mechanism of central pain.

Central pain below the injury level after spinal cord injury is excruciating, chronic and resistive to treatment. Animal studies suggest that pretreatment may prevent central pain, but to date there are no measures to predict its development. Our aim was to monitor changes in the sensory profile below the lesion prior to the development of below-level central pain in order to search for a parameter that could predict its risk and to further explore its pathophysiology. Thirty patients with spinal cord injury and 27 healthy controls underwent measurement of warm, cold, heat-pain and touch thresholds as well as graphaesthesia, allodynia, hyperpathia and wind-up pain in intact region and in the shin and feet (below level). Patients were tested at 2-4 weeks, 1-2.5 months and 2.5-6 months after the injury or until central pain had developed. At the end of the follow-up, 46% of patients developed below-level central pain. During the testing periods, individuals who eventually developed central pain had higher thermal thresholds than those who did not and displayed high rates of abnormal sensations (allodynia and hyperpathia), which gradually increased with time until central pain developed. Logistic regressions revealed that the best predictor for the risk of below-level central pain was allodynia in the foot in the second testing session with a 77% probability (90.9% confidence). The results suggest that neuronal hyperexcitability, which may develop consequent to damage to spinothalamic tracts, precedes central pain. Furthermore, it appears that below-level central pain develops after a substantial build-up of hyperexcitability. To the best of our knowledge, this is the first systematic report establishing that neuronal hyperexcitability precedes central pain. Predicting the risk for central pain can be utilized to initiate early treatment in order to prevent its development.

Risk factors for failure of heparin thromboprophylaxis in patients with acute traumatic spinal cord injury.

UNLABELLED: Venous thromboembolism (VTE) is a well-recognized complication of Acute Traumatic Spinal Cord Injury (ATSCI). Despite prophylaxis by heparins, VTE occurs in a substantial number of ATSCI patients without an obvious explanation. In this matched case-control study we examined whether thrombophilia and other risk factors are associated with failure of thromboprophylaxis. Cases and controls receiving heparin thromboprophylaxis were selected from consecutively admitted ATSCI patients. Patients who developed a new, objectively confirmed, symptomatic VTE despite prophylaxis at hospital were matched by gender, age, level and mechanism of ATSCI with 2-3 controls without VTE. Patients were interviewed about VTE risk factors and tested for factor V Leiden (FVL), prothrombin G20210A (PT), methylenetetrahydrofolate reductase C677T homozygosity (MTHFR), lupus anticoagulant, homocysteine (Hcy) and plasma factor VIII (FVIII) levels. Twenty-two patients with new VTE episodes and 64 controls were ascertained. The total number of gene alterations for MTHFR, FVL and PT or elevated levels of Hcy or FVIII was significantly more common in patients compared to controls (82% vs. 48%, p=0.006). Multiple logistic regression proved the PT mutation, a positive family history of thrombosis and elevated levels of either FVIII or Hcy to be predictors of thrombosis. CONCLUSION: A positive family history of VTE, carriership of the prothrombin mutation and elevated FVIII or Hcy levels were significantly associated with failure to prevent VTE by heparin therapy following ATSCI. Testing for thrombophilia in patients with ATSCI and possibly a more intense thromboprophylactic regimen seem desirable but need to be verified by a prospective study.