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Deep vein thrombosis and heterotopic ossification following spinal cord injury--a clinical perspective for physiotherapists.


Deep vein thrombosis (DVT) and heterotopic ossification (HO) are known complications following spinal cord injury (SCI). This report documents contemporary preventive measures, diagnosis and management for these complications in order to highlight the role of the physiotherapist within the multidisciplinary team. Mechanisms behind the development of DVT and HO remain somewhat unclear. The detection and diagnostic pathway also contains uncertainties. This study reviews and postulates the relationships between DVT and HO to provide information and understanding of the relationship between managements used in the prevention and treatment of DVT and HO. Persons with spinal cord injury need to share this understanding to assist with self management. Beilby J, Mulligan H (2008): Deep vein thrombosis and heterotopic ossification following spinal cord injury--a clinical perspective for physiotherapists. New Zealand Journal of Physiotherapy 36(1): 7-14.

Key Words: Spinal cord injury, deep vein thrombosis, heterotopic ossification, physiotherapy


Persons with spinal cord injury (SCI) are at great risk of developing an array of debilitating and potentially life-threatening complications (Jones 1992). Two important complications are deep vein thrombosis (DVT) and heterotopic ossification (HO). These conditions are significant because they can be life threatening due to risk of pulmonary embolism (PE), can complicate rehabilitation, can delay discharge, or can hinder function in the already discharged individual. Figure One illustrates the development and potential consequences of these complications.

As part of the multi-disciplinary team, it is important that physiotherapists have an understanding of as well as the ability to assist in the recognition, diagnosis and treatment of complications following SCI (Campagnolo and Merli 2002). Physiotherapists also play a major role in patient education regarding self management to ensure the person with a SCI attains the knowledge and skills necessary to stay healthy throughout the years following their initial rehabilitation phase (Jones 1992). Therefore, physiotherapists assume a key role as educators concerning DVT and HO

This paper will discuss the incidence, etiology, risk factors, detection, diagnosis and management of DVT and HO by the multidisciplinary team with specific reference to the role of the physiotherapist. The association between these two conditions that has been suggested by some authors (Colachis and Clinchot 1993, Perkash et al 1993) will also be reviewed.


Deep vein thrombosis is one of "the most significant indirect cardiovascular complications" following a SCI (Campagnolo and Merli 2002 p. 127) particularly in the initial acute phase (Svensson et al 1995). Detection has been documented as early as seventy-two hours following injury, with a peak in incidence between days five and twelve post injury (Merli et al 1993).

It has been reported that venous thromboembolism (DVT and pulmonary embolism) develops in 8% to 25% of patients with SCI (Chen et al 1999, Deep et al 2001, Weingarden 1992). Clinical studies diagnosing venous thromboembolism (VTE) by contrast venography have reported the incidence of asymptomatic VTE to be as high as 48% to 100% (Deep et al 2001, Green 2003). The introduction of thromboprophylaxis from the late 1970's to the early 1990's led to a sharp reduction in the incidence of VTE in the SCI population (Jones et al 2005). A recent large retrospective cohort study by Jones et al (2005) showed no further change in incidence between 1991 and 2001, and updates the reported incidence to the following: a VTE incidence of 4.8% during the hospital stay, 5.4% within 91 days of acute SCI, and 6 percent within one year after hospitalization.

The reason the person with a SCI is at risk of developing a DVT is multifactorial. Vessel injury from the spinal cord injury, surgery after injury, immobilization and paralysis can all lead to venous stasis, hypercoagulability and vessel injury - three factors collectively referred to as Virchow's Triad (Campagnolo and Merli 2002, Kumar et al 2003, Lee et al 2002, Merli et al 1993, Svensson et al 1995). Of these, venous stasis and hypercoagulability are thought to be the major contributing factors to development of thrombus formation and possible DVT (Merli et al 1993).


Venous stasis may result from a combination of (i) peripheral vasodilatation, (ii) a reduction in the velocity of blood flow with loss of the gastrocnemius muscle pump and (iii) gravitational pressure exerted on the leg of a bedridden patient (Campagnolo and Merli 2002, Lee et al 2002, Merli et al 1993). Vasodilatation can result from the release of vasoactive amines after blunt trauma, the effects of anaesthesia if surgery is required, and secondary to injury to the spinal cord itself (Merli et al 1993).

Hypercoagulability is thought to be the result of a series of events leading to thrombus formation in the veins of persons with lower extremity paralysis (Myllenen et al 1987, Rossi et al 1980). A marked elevation in von Willebrand factor antigen (factor VIII:Ag), an elevation in ristocetin cofactor (VIII:RcoF) (Rossi et al 1980) and a slight elevation in factor VIII:C, has been observed to occur prior to the development of DVT (Myllenen et al 1987, Rossi et al 1980). The factor antigens (produced by epithelial cells and the liver respectively) result in platelet adhesion and formation of a thrombus (Campagnolo and Merli 2002, Rossi et al 1980).

Of importance is that an increased ratio of F VIII:Ag/F VIII:C was predictive of DVT in patients with SCI (Campagnolo and Merli 2002, Myllenen et al 1987, Rossi et al 1980). Measurement of this ratio may be valuable in identifying patients who require anti-coagulation therapy, particularly in the initial post-injury phase when the occurrence of DVT most often commences in the absence of clinical symptoms (Myllenen et al 1987). However, the ratio of FVIII:Ag to FVIII:C is a complicated mechanism that is not well understood. Further investigation is required to determine the clinical importance of this elevated ratio and its use as a potential marker of DVT (Campagnolo and Merli 2002).

Risk factors for DVT

Jones and colleagues (2005) identified specific risk factors for venous thromboembolism (DVT and PE) in a large recent retrospective cohort analysis of all SCI cases (16,240) presenting to Public Hospitals in California from 1991 to 2001. Strong risk factors included being male, having complete paraplegia (relative to complete tetraplegia), and being an African American. A modest increase in the risk of developing DVT (named as VTE in this report) was noted in patients with an increasing number of chronic comorbid conditions including cancer, chronic neurological disease, history of psychiatric disease, and anxiety/depression. A significantly lower risk of developing DVT was noted in younger patients below the age of adolescence.

Prevention of DVT

Preventative measures are essential in this population in order to avoid resultant complications. Pulmonary embolism (PE) is the most serious complication following DVT with an incidence of 8%--14 % and a mortality rate of 2.5%--4.7 % in persons with acute SCI (Merli et al 1988, Merli et al 1993, Rossi et al 1980). Another complication may be the post-thrombotic syndrome, which includes persistent oedema, purpura (bleeding into the skin), increased skin pigmentation, pain, eczema-like dermatitis, pruritis (itchiness), cellulitis, ulceration, and possibly spasticity or autonomic dysreflexia (Powell et al 1999, Warrell et al 2003).

To reduce hypercoagulability and venous stasis and therefore prevent the likelihood of DVT immediately after injury, a number of interventions are commonly employed: low dose anticoagulants, physiotherapy (passive movements and mobilization), pressure stockings, neuromuscular electrical stimulation, alternating pressure devices (inflatable boots or sleeves) and optimal hydration (Campagnolo and Merli 2002, Green et al 2003, Riklin et al 2003).

Campagnolo and Merli (2002) highlight the guideline developed under the auspices of the Paralysed Veterans of America in 1997, which recommends that persons with SCI receive both pharmacological prophylaxis (anticoagulation) and a form of mechanical prophylaxis. The present review will examine these different forms of prophylaxis here under.

In a retrospective review on data from 1209 patients with acute SCI, Riklin et al (2003) found a reduced incidence of DVT (from around 70% before the advent of anti-thrombotic prophylaxis) to 6.55% with anti-thrombotic prophylaxis and elastic stockings. Aito et al (2002) in a prospective clinical trial on 275 patients found that application of mechanical and pharmacological prophylaxis within 72 hours of injury produced a reduction to 2%.

The main pharmacological agents used for DVT prevention are low-molecular weight forms of heparin or adjusted-dose un-fractionated heparin. Common pharmacologicals used in DVT prophylaxis include Innohep, Orgaran and Clexane (New Ethicals Compendium 2004). Anticoagulation prophylaxis continues for eight to twelve weeks following injury, or longer if a patient continues to be at risk of DVT development (Campagnolo and Merli 2002).

Mechanical prophylaxis includes antiembolic stockings, graduated compression stockings (GCS) and external pneumatic compressive (EPC) hoses or devices, and can be applied to the legs of all patients for the first two weeks following injury (Campagnolo and Merli 2002). These devices are intended to enhance venous return from the lower extremities and prevent venous stasis. A Cochrane review by Amaragiri and Lees (2005) concluded that the use of GCS lowers the risk of DVT in post surgical patients. These authors suggest therefore that GCS should be considered in all patients who are at risk of developing a DVT unless contraindicated.

Antiembolic stockings provide moderate constant compression to the legs from the toes to either the thighs or knees. The application of GCS provides different degrees of compression along the leg. Pressure is greatest at the ankle, recorded as 100%, then decreases to 70% at the mid-calf region, and further decreases to 40% at the mid-thigh region (Maxwell-Thompson and Reid 2003). External pneumatic compression devices are soft plastic sleeves that are applied to the legs. An air pump regulating the flow of air into the sleeve is attached, providing intermittent compression by inflating and deflating the sleeves at regular intervals to encourage venous return. GCS and EPC devices are contraindicated in patients with severe oedema, arterial disease, phlebitis, skin breakdown, or leg fractures (Maxwell-Thompson and Reid 2003).

Another mechanical technique applied by physiotherapists, is known as "passive movements". Passive movements are a traditional component of the rehabilitation programme in the acute phase while the person with SCI is still on bed-rest. While performed to maintain a functional range of motion of the joints for the individual, passive movements have traditionally been thought to reduce venous stasis and consequently reduce the risk of thrombosis (Svensson et al 1995). There is however, no conclusive evidence to support this belief. Svensson et al (1995) investigated the effect of passive leg movements on lower extremity blood flow in a cohort of six patients with acute SCI. The purpose of their study was to determine if flexion-extension movements increased blood flow in the lower limbs and whether there was a difference in flow when comparing five and 30 movement repetitions. In this well executed and clearly documented study that used validated methods of measuring arterial blood flow (such as venous occlusion plethysmography to measure changes in volume of the calves, and laser-doppler to measure change in skin blood flow) they found that the increase in blood flow was not, or only slightly increased after both treatments. They concluded therefore that five or 30 flexion-extension passive repetitions in the lower limbs would not have any useful effect on prevention of thrombosis in the acute phase. These authors conservatively acknowledge that passive movements are still necessary to maintain joint range of motion, although more recent work by Harvey's group (Harvey et al 2000, Harvey and Herbert, 2002, Harvey et al 2003, Ben et al 2005) questions the effectiveness of short or long term passive movement treatment for maintaining joint range of motion in persons with SCI.

A different form of mechanical prophylaxis used in the prevention of DVT is neuromuscular electrical stimulation of lower limb muscles. In a study of 48 patients with acute SCI randomized to receive low dose heparin, a placebo heparin injection or low dose heparin with neuromuscular electrical stimulation, Merli and Colleagues (1988) found that prophylactic electrical stimulation in combination with low-dose heparin significantly lowers the incidence of DVT more than low dose heparin alone.

Detection, treatment and management of DVT

Signs and symptoms of DVT include unilateral swelling, (bilateral swelling if DVT is in the vena cava), local pain or tenderness, skin discolouration, tension over the site, and local or systemic temperature elevation (Jones 1992, Maxwell-Thompson and Reid 2003, Svensson et al 1995). Detection of some of these symptoms may however be difficult due to a loss of sensation in this population (Svensson et al 1995). It is therefore essential that patients are regularly monitored for signs. If the thrombus is restricted to the popliteal and calf veins, swelling will be constrained below the knee. Swelling of the thigh is anticipated if the thrombus develops in the femoral and pelvic veins. A one centimeter difference in the circumference of the calves measured 10cm below the tibial tuberosity is abnormal (Sands 2003). Sands (2003) also suggests that calf and thigh circumference are monitored at least once a day, and skin is assessed for discolouration or warmth each time compression devices are removed for skin care. It is a good idea to mark the measurement position on the patient's skin so that measurements can be made from a fixed point (Warrell et al 2003).

However, swollen limbs have a number of differential diagnoses including heterotopic ossification, DVT, fracture, cellulitis, joint sepsis, haematoma formation, and neoplasm (Bradleigh et al 1992). It is therefore important to confirm or refute the diagnosis of DVT with appropriate investigations such as ultrasonography, contrast venography and measurement of D-dimer.

Duplex doppler ultrasonography is the preferred first line diagnostic procedure because it is inexpensive and has the ability to non-invasively examine the major veins in a limb for detection of a thrombus. This technique is an imaging method used to monitor moving substances (Tierney et al 2002). Ultrasonic waves directed at an artery or vein reflect off red blood cells, producing a waveform or audible sound (Huffstutler 2003). An acute clot is not usually able to be visualised directly, but the presence is inferred from a lack of normal change in blood flow rate with respiration. It has been shown to have both good sensitivity in symptomatic patients, and also high specificity (Warrell et al 2003). This type of ultrasound may miss smaller thrombi in the calf veins when there are collateral channels present. It may however be helpful in detecting an extension of a small thrombus in the calf vein into the popliteal and femoral veins on a follow up test (Tierney et al 2002).

Contrast venography, involving the injection of a radiopaque contrast medium into the veins to provide a graphic representation of the venous pulse (Tierney et al 2002), is the 'gold standard' for detection of DVT in the leg veins. It can define the location, extent, and degree of thrombus attachment. However, due to the expense, discomfort to the person, and time required, it is not used as a screening tool and is unsuitable for repeated monitoring (Warrell et al 2003). It is useful predominantly when the clinical picture suggests DVT, but ultrasound is equivocal. Of note is that on rare occasions it can worsen, or generate a thrombotic process (Tierney et al 2002).

A D-dimer is a fragment produced during the degradation of a clot and its presence provides a reliable indication that clotting has begun (Warrell et al 2003). The test does however have a large number of false positive tests (Warrell et al 2003).

Guidelines for Treatment of DVT

Once the presence of DVT has been established, the person will be treated with Warfarin (Campagnolo and Merli 2002). Common pharmacological forms of Warfarin are Coumadin and Marevan Tablets (New Ethicals Compendium 2004). It is important to note that anticoagulants have no effect on an established thrombus, nor do they reverse ischaemic damage. Once a thrombus has occurred however, anticoagulant treatment aims to prevent further extension of the formed clot and prevents secondary thromboembolic complications which may result in serious and fatal events (New Ethicals Compendium 2004).

For the person in whom anticoagulant prophylaxis has failed, or for those in whom anticoagulation is contraindicated, placement of an inferior vena cava filter is indicated. Filter insertion is also often considered in patients with SCI who are at greater risk of developing DVT because they have (i) complete motor paralysis due to a high cervical cord injury, (ii) poor cardiopulmonary reserve, or (iii) developed a thrombus in the inferior vena cava despite receiving anticoagulant prophylaxis (Lee et al 2002).

Once a person has been diagnosed with a DVT, it is recommended that they have a period of immobility to prevent the thrombus breaking away from the vein's lining, causing a pulmonary embolism (PE) (Kiser and Stefans 1997). The exact duration of immobilization required to prevent complications following detection of a DVT is still unclear (Kiser and Stefans 1997). Despite this recommendations have been made.

Kiser and Stefans (1997) compared the occurrence of PE among patients who were mobilized early versus those who were mobilized later following DVT diagnosis. This retrospective case-controlled study analyzed the clinical records of 127 patients (14 of these patients were persons with SCI) admitted to an urban rehabilitation hospital. Outcome measures included time to return to physical therapy following DVT detection, and presence or absence of PE. The authors noted that an increased risk of PE occurred in persons who returned to physical therapy less than 48--72 hours following diagnosis of a DVT. The authors concluded that the affected limb should be immobilized for 48--72 hours at minimum whilst the person is receiving anticoagulation therapy.

More recently, Ciccone (2002) performed a literature search to establish the immobilization period required following an episode of DVT. Several studies were reviewed including the study above by Kiser and Stefans (1997). In Ciccone's (2002) review, a study by Aschwanden and colleagues (2001) found no difference in the incidence of PE in those who were mobilized immediately following DVT detection, and those who were immobilized for four days. Ciccone (2002) however, was reluctant to accept the suggestion that early mobilization is therefore safe due to the high incidence of PE in both groups of Aschwanden & colleagues (2001) study population. Despite unequal patient subgroups and retrospective design of the study by Kiser and Stefan (1997), Ciccone (2002) felt that this particular study 'provided a preliminary benchmark for when ambulation should be resumed' (p. 88) and recommended that ambulation activities should be withheld for at least 48 hours following a DVT episode, then progressively increased. More research is required in the specific population with SCI to determine an appropriate immobilization period following DVT in this group of people.


Heterotopic ossification (HO), a process where true bone forms outside the bone within muscle tissue (Banovac and Banovac 2002, Lal et al 1989) is a common complication following SCI, occurring below the level of the lesion in the paralyzed limbs (Banovac and Gonzalez 1997) . I t has an incidence of approximately 50% (Banovac and Banovac 2002). The severity of the condition varies from incidental findings on plain radiographs, to significant joint restriction (20% of persons with SCI) (Banovac and Banovac, 2002), or ankylosis (5% of individuals with SCI) (Banovac and Banovac 2002, Banovac and Gonzalez 1997, Colachis and Clinchot 1993, Garland 1988). It most commonly occurs in the first four months following the SCI, but can occur up to one year after injury (Bradleigh et al 1992, Lal et al 1989). The most common site for HO formation is within soft tissue surrounding the hip joint (Banovac and Banovac 2002, Lal et al 1989) which subsequently adversely affects mobility, functional independence and self care (Lal et al 1989).

The etiology of HO following SCI is uncertain (Banovac and Gonzalez 1997) and too complex to be included in the current review. Hypotheses on the cause of the condition include bone metabolic changes, traumatic lesions, and vaso-motor disturbances (Bravo-Payno et al 1992, Chantarine et al 1995, Garland 1991, Lotta et al 2001, Uebelhart et al 1995).

Risk Factors for HO

Lal et al (1989) reviewed 843 patients with SCI and identified the risk factors related to the formation of HO as some or all of being older than 30 years of age, having a complete lesion, having increased spasticity, and having pressure sores. Support for the last three risk factors was also found in a cross sectional study of 654 patients by Bravo-Payno et al (1992). The relationship between these factors and HO is, however, unclear. Muscle spasticity and skin pressure sores occur most commonly prior to HO formation, and less commonly following HO development. Existing spasticity however, can be exacerbated with the onset of HO (Lal et al 1989).

Detection, diagnosis, prophylaxis and management of HO

One of the first symptoms of HO formation is fever, especially at night. Joint swelling that limits range of motion occurs several days later and those persons with preserved sensory function may experience pain in the affected area. The knee and thigh may show oedema if the hip is involved. Symptoms experienced in the later stage of HO depend on the site and size of the lesion in relation to surrounding joint structures (Banovac and Banovac 2002) so that, for example, a large formation of bone growth close to the hip joint may inhibit seating or transfer ability due to pain or a significant loss of hip range of motion.

It is important to remember that a number of other medical complications could be responsible for a person presenting with the signs and symptoms above. These complications include DVT, impending pressure ulcer, cellulitis, septic arthritis, or fracture of the lower extremity. Therefore, investigations are required in order to differentially diagnose HO (Banovac and Banovac 2002). The most commonly used tests in the diagnosis of HO are bone scintigraphy and radiography (Banovac and Gonzalez 1997) although laboratory studies may also be used (Banovac and Banovac 2002). Measurement of serum alkaline phosphatase (ALP) is the most commonly used laboratory study. ALP is released into the serum from the membrane of osteoblasts, is often elevated in the early stage of HO, and may increase further as the bone growth progresses (Banovac and Banovac 2002).

No definitive protocol for prophylaxis against the development of HO exists, therefore the goal is to detect and treat HO in the early stage of development prior to the formation of mineralized tissue. The pharmacological agent Etidronate inhibits mineralization and also has an antiinflammatory effect by decreasing the production of cytokines (Banovac and Gonzalez 1997).

Surgical resection is another intervention that can be performed. The indications for surgical resection include a reduction in joint range of motion leading to loss of function (for example, seating problems), pressure sores, and an increase in spasticity and pain (Banovac and Gonzalez 1997, Meiners et al 1997). Complications following surgical resection of HO are common. These complications include recurrence of HO, infection, gradual loss of motion, and excessive bleeding. Patients should be monitored closely following the procedure and should continue physiotherapy for six months or until their range of motion has stabilized as, as noted above, a gradual loss of range of motion has been demonstrated during this period (Garland and Orwin 1989).


It appears that a relationship exists between DVT and HO (Colachis and Clinchot 1993, Perkash et al 1993). Colachis & Clinchot (1993) reviewed the records of 209 patients with SCI and found that more than 36% of the patients with DVT had HO, and approximately 31% of those patients with HO developed a DVT at some time during their acute or rehabilitation hospitalization. In all cases, HO was present on the same side of the body affected by the lower limb DVT. Perkash et al (1993) studied three patients presenting with traumatic SCI complicated by acute HO and concurrent DVT. HO preceded DVT in all patients. Therefore, management and monitoring of persons with HO is required to prevent or detect DVT.

Speculations have been proposed regarding the relationship between HO and DVT. One hypothesis is that the expanding HO bone and its inflammatory reaction may compress vascular structures leading to venous stasis, endothelial cell irritation and vessel injury (Colachis and Clinchot 1993). This would result in hypercoagulability, which could increase the likelihood of DVT (Perkash et al 1993). In this hypothesis, the events resulting in DVT following HO onset are clearly due to changes associated with acute HO (Riklin et al 2003).

Riklin et al (2003) proposed a different view. They identified clinical characteristics that suggest there is an independent mechanism for the development of HO and the development of DVT; (i) the time point of DVT and HO onset are dissimilar, (ii) DVT is an acute complication developing soon after the initial event or during immobilization following surgery, (iii) HO occurs later when the person is participating in rehabilitation with intensive physiotherapy, and (iv) the benefit of low molecular weight heparin (LMWH) in DVT prevention was not noted in the prevention of HO. Riklin et al (2003) therefore hypothesised that ongoing (possible forceful) mobilization (for example in the performance of passive range of motion exercises by physiotherapists or the person themselves) may trigger development of HO. With this in mind, longitudinal studies are needed to further clarify the relationship between HO and DVT (Colachis and Clinchot 1993).

The role of passive movements in management of both DVT and HO is unclear. Recent evidence suggests that passive movements performed gradually over a long period of time do not worsen the HO already present (Scalzitti 2003). Traditionally, mobilization of the affected joint/s was believed to be beneficial in maintaining or improving joint mobility (Stover et al 1975). However, Banovac and Banovac (2002) suggest that passive motion should not begin until the acute inflammatory signs of HO have subsided. Evidence for the use of passive movements by physiotherapists to maintain joint range of motion (see work by Harvey et al 2000-2005) needs to be extended to examine efficacy of passive movements in prevention of DVT.


This article has investigated the causes and mechanisms of DVT and HO, the possible relationship between these two conditions after spinal cord injury, and the evidence for management. While much is now known about risk factors, mechanisms of pathology, and effects of medication, there remains inconclusive evidence around certain aspects of prevention and management of these conditions, including the role of passive movements and optimal timeframes for immobilization. Physiotherapists need to be familiar with current methods of prevention, detection, diagnosis and management, and to review their role accordingly. Education of patients about these conditions, including risk factors, might lead to important preventative measures being followed by the person and their carers.

Key Points:

* DVT and HO are common complications following SCI and physiotherapists play a key role in educating the person with SCI about such complications

* The relationship between DVT and HO remains somewhat unclear and the detection and diagnostic pathways of HO and DVT are fraught with uncertainties

* A combination of pharmacological and mechanical prophylaxis produces the greatest reduction in DVT incidence

* Conflicting evidence exists around the use of passive movements for the prevention of DVT as well as a cause of HO development

* Passive movements may not prevent DVT formation and recent research questions their worth in addressing range of motion


Thanks is extended to Dr Rick Acland and staff at the Burwood Spinal Unit for the opportunity to gain experience and knowledge in this area, and to Karen Peebles and Heather Patterson for assistance with editing of an early draft of this paper. In particular we wish to gratefully acknowledge the expertise and efforts of the unknown reviewers in assisting us with this review.


Amaragiri SV and Lees TA (2005): Elastic compression stockings for prevention of deep vein thrombosis. [Software, Research, Systematic Review] The Cochrane Library (Oxford.) (1); (ID #cd001484).

Aito S, Pieri A, D'Andrea M, Marcelli F and Cominelli E (2002): Primary prevention of deep venous thrombosis and pulmonary embolism in acute spinal cord injured patients. Spinal Cord 40 (6): 300-303.

Banovac K and Banovac F (2002): Heterotopic ossification. In Krishblum A,

Campagnolo DI and DeLisa JA (Eds): Spinal Cord Medicine. USA: Lippincott, Williams & Wilkins, pp. 253--359.

Banovac K and Gonzalez F (1997): Evaluation and management of heterotopic ossification in patients with spinal cord injury. Spinal Cord 35: 158-162.

Ben M, Harvey L, Glinsky J, Goehl, G, Chee S and Herbert RD (2005): Does 12 weeks of regular standing prevent loss of ankle mobility and bone mineral density in people with recent spinal cord injuries? Australian Journal of Physiotherapy. 51(4):251-256.

Bradleigh LH, Perkash A, Linder S, Sullivan GH, Bhatt HK and Perkash I (1992): Deep venous thrombosis associated with heterotopic ossification. Archives of Physical Medicine and Rehabilitation 73: 293-294.

Bravo-Payno P, Esclarin A, Arzoz T, Arroyo O and Labarta C (1992): Incidence and risk factors in the appearance of heterotopic ossification in spinal cord injury. Paraplegia 30: 740-745.

Campagnolo DA and Merli GJ (2002): Autonomic and cardiovascular complications of spinal cord injury. In Krishblum A, Campagnolo DI and DeLisa JA (Eds). Spinal Cord Medicine. USA: Lippincott, Williams & Wilkins. pp. 123-134.

Chantarine A, Nusgens B and Lapiere CM (1995): Biochemical analysis of Heterotopic ossifications in spinal cord injury patients. Paraplegia 33: 398-401.

Chen D, Apple D, Hudson L, Bode R (1999): Medical complications during acute rehabilitation following spinal cord injury--current experience of the model systems. Archives of Physical Medicine and Rehabilitation 80: 1397-1401.

Ciccone CD (2002): Does ambulation immediately following an episode of deep vein thrombosis increase the risk of pulmonary embolism? Physical Therapy 82(1): 84-88.

Colachis SC and Clinchot DM (1993): The association between deep vein thrombosis and heterotopic ossification in patients with acute traumatic spinal cord injury. Paraplegia 31: 507-512.

Deep K, Jigajinni MV McLean AN, Fraser MH (2001): Prophylaxis of thromboembolism in spinal injuries--results of enoxaparin used in 276 patients. Spinal Cord 39: 88-91.

Garland DE (1991): Surgical approaches for resection of heterotopic ossification in traumatic brain injured patients. Clinical Orthopaedics and Related Research 263: 59-70.

Garland DE (1988): Clinical observations on fractures and heterotopic ossification in the spinal cord and traumatic brain injured population. Clinical Orthopaedics and Related Research 233: 86-108.

Garland DE and Orwin JF (1989): Resection of heterotopic ossification in patients with spinal cord injuries. Clinical Orthopaedics and Related Research 242: 169-176.

Green D (2003): Diagnosis, prevalence, and management of thromboembolism in patients with spinal cord injury. Journal of Spinal Cord Medicine 26: 329-334.

Green D, Hartwig D, Chen D, Soltysik RC and Yarnold P (2003): Spinal cord injury risk assessment for thromboembolism (SPIRATE Study). American Journal of Physical Medicine and Rehabilitation 82(12): 950-956.

Harvey LA, Byak AJ, Ostrovskaya M, Glinsky J, Katte L and Herbert RD (2003). Randomized trial of the effects of four weeks of daily stretch on extensibility of hamstring muscles in people with spinal cord injuries. Australian Journal of Physiotherapy. 49(3):176-181.

Harvey LA and Herbert HR (2002). Muscle stretching for treatment and prevention of contracture in people with spinal cord injury. Spinal Cord. 40:1-9.

Harvey LA, Batty J, Crosbie J, Poulter S and Herbert RD (2000): A randomized trial assessing the effects of 4 weeks of daily stretching on ankle mobility in patients with spinal cord injuries. Archives of Physical Medicine and Rehabilitation. 81(10):1340-1347.

Huffstutler SY (2003): Assessment of the cardiovascular system. In Phipps WJ, Monahan FD, Sands JK, Marek JF and Neighbors M (Eds.): Medical-Surgical Nursing: Health & Illness Perspectives (7th ed.). USA: Mosby. pp. 611-644.

Jones MF (1992): Spinal Cord Injury: Functional Rehabilitation. Connecticut: Appleton and Lange.

Jones T, Ugalde V, Franks P, Zhou H and White RH (2005): Venous thromboembolism after spinal cord injury: incidence, time course, and associated risk factors in 16,240 adults and children. Archives of Physical Medicine and Rehabilitation 86: 2240-2247.

Kiser TS and Stefans VA (1997): Pulmonary embolism in rehabilitation patients: relation to time before return to physical therapy after diagnosis of deep vein thrombosis. Archives of Physical Medicine and Rehabilitation 78: 942-944.

Kumar F, Cotran R and Robbins SL (2003): Robbins Basic Pathology (7th ed.). Pennsylvania: Saunders.

Lal S, Hamilton BB, Heinemann A and Betts HB (1989): Risk factors for heterotopic ossification in spinal cord injury. Archives of Physical Medicine and Rehabilitation 70: 387-390.

Lee BY, Dasilva MC and Ostrander LE (2002): Deep venous thrombosis in spinal cord injured patients. In Lee BY and Ostrander LE (Eds.): The Spinal Cord Injured Patient (2nd ed.). New York: Demos Medical Publishing Inc. pp. 140-147.

Lotta S, Scelsi L and Scelsi R (2001): Microvascular changes in the lower extremities of paraplegics with heterotopic ossification. Spinal Cord 39: 595-598.

Maxwell-Thompson CL and Reid KB (2003). Vascular problems. In Phipps WJ Monahan FD Sands JK Marek JF & Neighbors M (Eds.). Medical-Surgical Nursing: Health & Illness Perspectives (7th ed.). USA: Mosby. pp. 760-800.

Meiners T, Abel R and Gerner HJ (1997): Resection of heterotopic ossification of the hip in spinal cord injured patients. Spinal Cord 35: 443-445.

Merli GJ, Crabbe S, Paluzzi RG and Fritz D (1993): Etiology, incidence and prevention of deep vein thrombosis in acute spinal cord injury. Archives of Physical Medicine and Rehabilitation 74: 1199-1205.

Merli GJ, Herbison GJ, Ditunno JF, Weitz HH, Henzes JH, Park CH and Jaweed MM (1988): Deep vein thrombosis: prophylaxis in acute spinal cord injured patients. Archives of Physical Medicine and Rehabilitation 68: 661-664.

Myllynen P, Kammonen M, Rokkanen P, Bostman O, Lalla M, Laasonen E and Vahtera E (1987): The blood F VIII:Ag/F VIII:C ratio as an early indicator of deep venous thrombosis during post-traumatic immobilization. Journal of Trauma 27 (3): 287-290.

New Ethicals Compendium (2004). 8th Edition. Adis International Ltd.

Perkash A, Sullivan G, Toth L, Bradleigh LH, Linder SH and Perkash I (1993): Persistent hypercoagulation associated with heterotopic ossification in patients with spinal cord injury long after injury has occurred. Paraplegia 31: 653-659.

Powell M, Kirshblum S, and O'Connor KC (1999): Duplex ultrasound screening for deep vein thrombosis in spinal cord injured patients at rehabilitation admission. Archives of Physical Medicine and Rehabilitation 80: 1044-1046.

Riklin C, Baumberger M, Wick L, Michel D, Sauter B and Knecht H (2003): Deep vein thrombosis and heterotopic ossification in spinal cord injury: a three year experience at the Swiss Paraplegic Centre Nottwil. Spinal Cord 41: 192-198.

Rossi EC, Green D, Rosen JS, Spies SM and Jao ST (1980): Sequential changes in factor viii and platelets preceding deep vein thrombosis in patients with spinal cord injury. British Journal of Haematology 45: 143-151.

Sands JK (2003). Spinal cord & peripheral nerve problems. In Phipps WJ Monahan FD

Sands JK Marek JF & Neighbors M (Eds.): Medical-Surgical Nursing: Health & Illness Perspectives (7th ed.). USA: Mosby. pp. 1404-1436.

Scalzitti DA (2003): Because of the risk of developing heterotopic ossification, are passive range of motion exercises contraindicated following traumatic injuries? Physical Therapy 83(7): 659-667.

Stover SL, Hataway CJ and Zeiger HE (1975): Heterotopic ossification in spinal cord injured patients. Archives of Physical Medicine and Rehabilitation 56: 199-204.

Svensson M, Siosteen A, Wetterqvist H and Sullivan L (1995): Influence of leg blood flow in patients with complete spinal cord injury lesions. Physiotherapy Theory and Practice 11: 97-107.

Tierney LM, McPhee SJ and Papadakis MA (2002): Current Medical Diagnosis & Treatment (41st ed.). New York: Lange Medical Books/McGraw-Hill.

Ubelhart D, Demiaux-Domenech B, Roth M and Chantraine A (1995): Bone metabolism in spinal cord injured individuals and others who have prolonged immobilization. A review. Paraplegia 33: 669-673.

Warrell DA, Cox TM, Firth JD, and Benz Jr EJ (Eds.) (2003). Oxford Textbook of Medicine (4th ed.). Volume Two. Oxford: University Press.

Weingarden SI (1992): Deep vein thrombosis in spinal cord injury; overview of the Problem. Chest 102: 636S-639S.


Jacqui Beilby, Christchurch Centre, School of Physiotherapy, University of Otago, P O Box 4345, Christchurch, New Zealand. Fax: (03) 364 0692

Jacqui Beilby, BPhty, BPhEd, Physiotherapist, Ward 2A, The Princess Margaret Hospital, Christchurch

Hilda Mulligan, BSc (Physiotherapy), MHSc Professional Practice Fellow, Christchurch Centre, School of Physiotherapy, University of Otago
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Title Annotation:Clinical Perspective
Author:Beilby, Jacqui; Mulligan, Hilda
Publication:New Zealand Journal of Physiotherapy
Geographic Code:8NEWZ
Date:Mar 1, 2008
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