Persistent hypercoagulation associated with heterotopic ossification in patients with spinal cord injury long after injury has occurred

Perkash, A; Sullivan, George H.; Toth, Louis A.; Bradleigh, L H; Linder, S.; Perkash, Inder

doi:10.1038/sc.1993.105

Cited by 17 publications

(12 citation statements)

References 12 publications

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“…Previous studies demonstrated a comorbidity of HO and DVT 18,19 which also presented in two of our patients. We agree with these authors that the expanding ectopic mass of HO associated with in¯ammation will compress vascular structures and irritate endothelial cells.…”

Section: Discussionsupporting

confidence: 76%

“…We agree with these authors that the expanding ectopic mass of HO associated with in¯ammation will compress vascular structures and irritate endothelial cells. As shown for the hip, this will result in hypercoagulability (elevated d-dimer levels) followed 19 or not 20 by DVT. In accordance with these ®ndings, acute HO involving the hip appears to increase the risk for development of secondary ipsilateral DVT through local presence of generally accepted risk factors as compression, in¯ammation and immobilisation.…”

Section: Discussionmentioning

confidence: 98%

“…18 ± 20 A related aetiology was proposed but never proved. 18,19 Perkash et al 19 demonstrated that an elevated level of d-dimer correlates with the activity of HO. Recent experimental studies suggest a central role of musclelocalised pluripotential mesenchymal cells and genes speci®c for enchondral ossi®cation in the formation of the new ectopic bone.…”

Section: Introductionmentioning

confidence: 99%

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Deep vein thrombosis and heterotopic ossification in spinal cord injury: a 3 year experience at the Swiss Paraplegic Centre Nottwil

et al. 2003

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Study design: Retrospective review of patient data. Objectives: (i) To determine the incidence and time of deep vein thrombosis (DVT) under low molecular weight heparin (LMWH) prophylaxis in spinal cord injury (SCI), (ii) to determine the incidence and time of heterotopic ossi®cation (HO) and (iii) to assess a possible aetiologic relationship in the pathogenesis of DVT and HO. Setting: Swiss Paraplegic Centre, Nottwil. Methods: We analyzed the incidence of DVT and HO in 1209 SCI patients (275 ®rst rehabilitations) at the Swiss Paraplegic Centre Nottwil from 1998 to 2000. Clinical ®les and laboratory data were scrutinised for particularities preceding DVT and HO. Results: The incidence of DVT was 6.55% for ®rst rehabilitation compared to only 1.59% in all patients hospitalised. DVT was complicated by pulmonary embolism (PE) in 1.45% and 0.47% respectively. Incidence of HO was 8% for ®rst rehabilitation and 1.82% for all patients hospitalised. In ®rst rehabilitation patients the peak for DVT occurred around day 30 contrary to HO with a peak around day 120. In single patients HO was identi®ed by MRI as a rapidly progressing process. Laboratory pro®les were in¯ammatory in both HO and DVT. Increased physical activity preceding HO was observed in four patients. In two patients acute HO was complicated by ipsilateral DVT. Conclusion: Prophylaxis with LMWH and elastic stockings signi®cantly reduces the frequency of DVT during ®rst rehabilitation in SCI. DVT and HO are both associated with laboratory parameters of non-infectious in¯ammation. The later onset of HO coinciding with ongoing mobilisation, argues for a di erent pathogenetic mechanism. Acute HO of the hip region appears to favour ipsilateral DVT by well known thrombogenic mechanisms.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Deep vein thrombosis and heterotopic ossification in spinal cord injury: a 3 year experience at the Swiss Paraplegic Centre Nottwil

et al. 2003

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“…High D. Dimer levels can also be due to extravascular thrombin formation in areas of ischemia related to pressure sores, which are common in spinal cord injury patients and favoured by the period of bedrest and oedema of lower limbs and sometimes heterotopic ossi®cation. 20 Dierent sets of factors associated with an increased risk of DVT are present in spinal cord injury patients. Venous stasis due to forced bedrest and absence of muscle contractions, in¯ammation, frequently present in spinal cord injury patients, are known to promote venous thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Endothelial fibrinolytic reactivity and the risk of deep venous thrombosis after spinal cord injury

et al. 1997

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Deep vein thrombosis (DVT) is a frequent event in patients with spinal cord injury, even with prophylactic anticoagulant therapy. Lower limb paralysis is a known major risk factor for venous thrombosis, supposedly due to the venostasis in relation with total immobility. The main goal of this study was to evaluate the endothelial response to anoxia to determine whether recovery of ®brinolytic potential occurs in patients subjected to forced bedrest because of a spinal cord injury and whether this recovery is related to the incidence and/or evolution of DVT. We evaluated vascular endothelium reactivity in the lower limbs no longer submitted to the hydrostatic pressure of the erected position in 15 patients with paraplegia or tetraplegia and in 10 normal volunteers after venous occlusion produced by the application of 10 cm Hg pressure to the lower limb for 15 min comparatively to the upper limb used as reference. Among the 15 patients, 10 whose spinal cord injury had occurred 1 to 6 months earlier were still receiving prophylactic anticoagulant therapy, whereas the ®ve other patients were not receiving prophylactic anticoagulants because the injury dated back 6 months or more. After venostasis, tissue plasminogen activator (tPA) increased signi®cantly in both patients and controls in the upper limb (tPA levels twofold and threefold respectively in controls and patients) but showed no signi®cant changes in the lower limb; prolonged immobility did not allow recovery in the lower limbs of a level of ®brinolytic responsiveness identical to that in the upper limbs. The plasminogen activator inhibitor (PAI 1 ) remained unchanged after anoxia, although wide interindividual variations were seen. Natural coagulation inhibitors and circulating blood stigmates of hypercoagulability were measured. None of the patients had abnormally low levels of coagulation inhibitors (ie, antithrombin III, protein C and protein S levels were normal). Seventy-®ve per cent of patients (prophylactically anticoagulated or not) had very high levels of ®brin degradation products (D. Dimer levels sevenfold to eightfold those of the controls), but all patients had normal levels of thrombinantithrombin complexes and prothrombin fragments 1+2. The permanence of the thrombotic process characterized by an increase in D. Dimer levels without recovery of ®brinolytic potential suggests a proposal for the patients an inde®nite antithrombotic treatment at curative doses.

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“…1 It is also known that patients with HO after SCI develop deep vein thrombosis 2,3 and are of a persistent hypercoaguable state. 4 Therefore increased D-Dimere levels are often noticed in patients with traumatic spinal cord disturbances, but it is not certain if all patients with increased D-Dimere levels develop an HO. HO is mostly diagnosed between 1-6 months after injury with a peak at 2 months.…”

Section: Introductionmentioning

confidence: 99%

Development of heterotopic ossifications, blood markers and outcome after radiation therapy in spinal cord injured patients

et al. 2014

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Study Design: Retrospective study. Objectives: This study was implemented to detect risk factors for the developing of heterotopic ossifications (HOs) in spinal cord injury (SCI) patients. Setting: This study was conducted in Murnau, Germany. Methods: All patients from 2008-2012 with acute SCI were routinely examined by ultrasound of the hips every 2 weeks. The sub group of SCI patients suffering of HO of the hips were extracted and the incidence of developing an HO was calculated. Parameters like age, level of injury, ASIA Impairment Scale (AIS), duration time of accident until diagnosis of HO, Brooker stage, localization of HO (magnetic resonance imaging (MRI)) and symptoms like thrombosis, emboli, decrease of range of motion (ROM), dermal symptoms, swelling, increase in D-Dimere level, were evaluated. Also accompanying injuries of the brain, lung and extremities were recorded. Results: From January 2008 until January 2012, 575 patients with an acute and traumatic SCI were treated in our Department. During this period 32 HOs were detected in the muscles surrounding the hip. In 10 cases a single side and in 22 cases both sides were affected. A total of 26 patients were detected showing up a Brooker 0, two patients Brooker 1, and five patients a Brooker stage 42. The adductor muscles showed an edema in 19 cases and the quadriceps muscles were affected in 15 cases. 26% of all SCI patients showed AIS A status, but in patients who developed HO, 64% have had an AIS A status. 19% of patients with a HO were AIS B and 9.5% showed an AIS C and D. Regarding the level of injury the distribution of patients suffering of HO was comparable to the distribution of SCI patients without HO. In mean HO were detected 9 weeks after SCI and no new HO were found after the 22nd (n = 1) week of injury. Clinical symptoms such as swelling, pain, redness or decrease in ROM or increase in D-Dimere levels were seen in 24 cases. Accompanying injuries like brain injury and lung contusions were found in 83% of patients developing HO. The incidence of thrombosis was comparable to SCI patients without HO. One patient with no accompanying injuries or clinical symptoms was detected by routinely performed ultrasound. Conclusions: The risk of developing HO in patients with traumatic SCI is 5.5% but increases when accompanying injuries of the brain and lung occur. Patients with a neurological status of AIS A must also be quoted as risk patients. When considering the described risk factors and clinical symptoms, 96% of all HO can be detected.

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Persistent hypercoagulation associated with heterotopic ossification in patients with spinal cord injury long after injury has occurred

Cited by 17 publications

References 12 publications

Deep vein thrombosis and heterotopic ossification in spinal cord injury: a 3 year experience at the Swiss Paraplegic Centre Nottwil

Deep vein thrombosis and heterotopic ossification in spinal cord injury: a 3 year experience at the Swiss Paraplegic Centre Nottwil

Endothelial fibrinolytic reactivity and the risk of deep venous thrombosis after spinal cord injury

Development of heterotopic ossifications, blood markers and outcome after radiation therapy in spinal cord injured patients

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