The present article is a translation of the guideline recently published online (
https://www.awmf.org/uploads/tx_szleitlinien/179-015l_S1_Thromboembolieprophylaxe-bei-Querschnittlaehmung_2020-09.pdf). The annual incidence of deep leg vein thrombosis (DVT) varies between 90 and 130 per 100,000 persons, equivalent to an average of 0.1% in the general population [
13,
22]. The frequency of symptomatic and asymptomatic DVT in surgical and non-surgical medicine without prophylaxis (prevalence) arises as follows [
13]: Internal medicine diseases 10–20%, stroke 20–50%, polytrauma 40–80%, and spinal cord injury 60–80%. Venous thromboembolism (VTE) is a common complication in spinal cord injury with resulting paresis. Of all traumatic injuries, traumatic spine injuries affecting the spinal cord and/or the cauda equina bear the highest risk for VTE [
9]. Reasons for this are the failure of the muscle pump due to the paresis, a presumed transient hypercoagulative phase, and accompanying endothelial damage. Decoupling from supraspinal control is also discussed as a relevant prothrombotic factor [
21]. Pulmonary embolism, leg edema caused by postthrombotic syndrome and hemorrhage due to the required anticoagulation, represent complications of VTE. Also, patients can be burdened by frequently required laboratory controls undergoing therapy with vitamin K antagonists.
The frequency of VTE (particularly in the English literature the terms frequency, incidence, risk, and rate are used interchangeably) varies extremely depending on the study between 49 and 100% (older studies) or 1.6 to 45% (recent studies published between 2010 and 2019) in acute SCI (within 3 months after the date of injury), depending on the detection method, the observation period and the implementation of prophylactic measures [
22]. The risk (calculated in 3-month hazard intervals) for a VTE decreases with time since injury/disease onset [
11]. Thus, the risk of VTE is 34% within the first 3 months, 1.1% after 6 months, and 0.4% after 1 year. The neurological level of injury affects the likelihood of VTE. In paraplegic patients with a high thoracic injury level, higher incidences were found compared to quadriplegics: In quadriplegics with a level between C1 and C4, the incidence is 3.4%. Paraplegics with level T1-T6, on the other hand, have an almost twice as high incidence of 6.3%. Low thoracic (T7–12) or lumbar injury levels are associated with incidences comparable to cervical injuries (4.47 and 3.17%, respectively). The reason for the VTE cluster in high thoracic SCI has yet to be determined [
20]. The more pronounced the neurological deficits according to the American Spinal Injury Association Impairment Scale (AIS) are, the higher is the risk of suffering from VTE. The risk is particularly high in sensorimotor complete SCI. No evidence is available regarding the incidence of VTE in flaccid paralysis (lower motor neuron lesion due to conus medullaris and/or cauda equina lesion – typically caudal to the Th12 vertebral body) versus spastic paralysis (upper motor neuron lesion due to a spinal cord lesion – typically C1 and Th10–12 vertebral bodies). However, the absence of a spastic tone increase has been described as a risk factor for VTE [
6]. Concerning age, a study of more than 12,000 patients showed no correlation with VTE events [
11]. A previous VTE increases the risk of recurrent VTE by a factor of 6 [
10]. If thrombosis prophylaxis was started within the first 2 weeks after the onset of paraplegia, a significantly reduced risk of VTE was shown compared to a delayed start of prophylaxis [
25]. In respect to pre-existing thrombophilia, a possibly increased risk is described in the presence of a prothrombin or factor V Leiden gene mutation, antithrombin, protein C/protein S deficiency, hyperhomocysteinemia, or persistently increased factor VIII levels. However, so far neither the independent predictive value of a hereditary thrombophilia nor the clinical significance of the factors mentioned could be confirmed [
3]. The factors gender, obesity, alcohol/nicotine consumption, and insurance status do not show a clear correlation with the risk of VTE [
11], even if this is described in a retrospective analysis with a relatively low number of cases [
24]. In summary, paraplegia per se carries a high risk of VTE, regardless of the cause or concomitant disease.
The present guideline provides a concise overview of the risk of VTE and recommendations regarding diagnosis and prophylactic measures to prevent VTE in acute and chronic SCI. The pattern of paralysis is defined by the severity and level of SCI. The different types of paralysis require to properly adjust the method and duration of prophylaxis. Additional specific risk factors and their relevance for VTE prophylaxis in spinal cord injury need to be considered. The scope of the guideline extends to traumatic and non-traumatic SCI. The guideline covers the time from the subacute (patient transfer to dedicated spinal cord injury center typically within the first 1–4 weeks after injury) to the chronic phase (readmission for treatment of secondary complications of SCI). The acute phase immediately after injury will be addressed in a separate guideline.