Venous Insufficiency as a Late Complication After Tibial Fracture

Willén, Jan; Bergqvist, David; Hallböök, T

doi:10.3109/17453678208992193

Cited by 19 publications

(3 citation statements)

References 9 publications

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“…In spite of this, there are very few studies describing the true incidence or natural history of DVT in the trauma patient. Our review of the literature yielded only eight reports [3,4,[13][14][15][16][17][18] in which the diagnosis of DVT was firmly established in the trauma patient, by either autopsy examination or venogram ( Table 1). …”

Section: Incidencementioning

confidence: 99%

“…In addition, no blood tests are currently available that satisfactorily identify the patient at risk for DVT[32].Other Factors Increasing age appears to increase the risk of DVT and PE significantly. Willen and associates[17] observed that an age of more than 45 years increased the risk of DVT after tibial fracture. Sevitt and Gallagher[3] found an increase in the number and diameter of intramuscular calf veins (particularly in the soleal plexus) with advancing age.…”

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confidence: 98%

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Deep Venous Thrombosis and Pulmonary Embolism in Trauma Patients

Shackford

Moser

1988

J Intensive Care Med

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Trauma patients are at exceedingly high risk for the development of deep venous thrombosis and pulmonary embolism. The incidence, pathophysiology, diagnosis, prophylaxis, and therapy of deep venous thrombosis and pulmonary embolism in the trauma patient are reviewed. The type of injury, systemic pertubations, and enforced immobility are important factors in pathogenesis. Patients with lower extremity injuries and spine fractures with paraplegia appear to be at highest risk. Orthopedic devices used to treat these injuries often preclude the conventional noninvasive diagnostic modalities. Further, hemorrhagic risk often impacts the judgment regarding the use of prophylactic measures as well as the therapy once deep venous thrombosis is diagnosed. Better data regarding the incidence of venous thromboembolism and the applicability of existing diagnostic, prophylactic, and treatment approaches in this population are needed. Accidents are responsible for over 140,000 deaths and approximately 70 million nonfatal injuries annually in the United States [1]. Most of the fatalities occur within hours of injury as a result of exsanguination or a lethal head injury, but approximately 20% survive for days or weeks [2], usually in the intensive care unit. The primary causes of late death are sepsis and multiple-organ failure [2]. Increasing evidence, however, suggests that pulmonary embolism (PE) is now becoming a leading cause of late death, especially in some high-risk groups [3][4][5].The increase in the incidence of PE is due in part to improvements in trauma care, which have lowered the early mortality rate [6-8], leaving more patients at risk for late death. In addition, autopsy examinations, used more frequently to audit trauma care systems [6,9], have documented an increase in clinically unsuspected deep venous thrombosis (DVT) and PE.This review was prompted because of the apparent increase in DVT and PE in the trauma population, and because the trauma patient presents very difficult and unique problems compared with the nontrauma patient with regard to the diagnosis, prophylaxis, and treatment of these disorders. In this review, we address the incidence, pathophysiology, diagnosis, treatment, and prophylaxis of DVT and PE in the trauma patient. We do not consider the entities of fat embolism or pulmonary microemboli as a cause of late pulmonary failure.

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Section: Incidencementioning

confidence: 99%

mentioning

confidence: 98%

Deep Venous Thrombosis and Pulmonary Embolism in Trauma Patients

Shackford

Moser

1988

J Intensive Care Med

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“…They found oedema in 48 per cent, skin induration in 21 per cent and leg ulcer in 2 per cent; 79 per cent of the patients had no subjective complaints. Willen et al (1982) examined 38 patients with tibial fractures 13-17 years previously, using clinical examination and directional doppler measurement and in some cases phlebography; 15 patients had symptoms of DVI and in eight patients objective venous insufficiency was established; high energy trauma, long immobilisation and age over 45 years were significantly associated with venous insufficiency. Miehle (1982) found constant swelling of the leg in 13 per cent, eczema in 9 per cent, pigmentation in 29 per cent and leg ulcer in 3 per cent.…”

Section: Discussionmentioning

confidence: 99%

Venous function after fracture of the lower extremity: A 9-year follow-up of 150 cases

Lindhagen

Bergqvist

Hallböök

et al. 1985

Acta Orthopaedica Scandinavica

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One hundred and fifty patients were examined 8-10 years after a fracture of the lower limb to evaluate whether the frequency of deep venous insufficiency (DVI) was influenced by the type of fracture. The evaluation included clinical examination, subjective complaints, venous pressure, plethysmography and doppler sonography. Symptoms and signs of DVI were more common in the fractured than in the uninjured limbs, while objectively diagnosed DVI did not differ between the groups. Only minor differences were present in the development of DVI between limbs with various types of fracture (hip fractures were not included in the study). High age and incompetence of the popliteal valves were more important in the development of DVI than the earlier fracture. The frequency of objectively measured DVI in the fractured limbs was 35 per cent and in the uninjured limbs 30 per cent.

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Ankle fracture is associated with prolonged venous dysfunction

Tierney

Burke

Fitzgerald

et al. 1993

Journal of British Surgery

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Leg swelling is a significant problem following ankle fracture. Venous pump function and femoral and popliteal venous patency were assessed prospectively in 26 patients with ankle fractures requiring open reduction, internal fixation and immobilization in plaster. Functional venous volume, venous filling index (VFI), ejection volume fraction (EVF) and residual volume fraction (RVF) were measured using air plethysmography at 5 days and at 6, 12 and 18 weeks after fracture. The uninjured leg was used as a control. Popliteal and femoral venous patency was determined using duplex ultrasonography. No patient developed deep vein thrombosis during the study. At 5 days after fracture there was a significant reduction in mean(s.d.) EVF, 18.2(12.1) versus 55.9(19.5) per cent, and increase in RVF, 87.0(14.3) versus 42.5(22.2) per cent (both P < 0.001). Analogous values were similar at 6 weeks, EVF 28.5(21.2) versus 55.6(21.9) per cent, RVF 82.2(16.8) versus 48.5(23.8) per cent (both P < 0.001), and at 12 weeks, EVF 39.1(16.0) versus 60.3(14.9) per cent, RVF 64.7(18.8) versus 38.8(13.2) per cent (both P < 0.001). However, by 18 weeks there was no significant difference in venous function between fractured and control limbs. It is concluded that there is a significant and prolonged impairment in venous pump function following ankle fracture.

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Venous Insufficiency as a Late Complication After Tibial Fracture

Cited by 19 publications

References 9 publications

Deep Venous Thrombosis and Pulmonary Embolism in Trauma Patients

Deep Venous Thrombosis and Pulmonary Embolism in Trauma Patients

Venous function after fracture of the lower extremity: A 9-year follow-up of 150 cases

Ankle fracture is associated with prolonged venous dysfunction

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