DVT is the result of a number of factors that include stasis of blood, endothelial injury and hypercoagulability of blood. PE is a major complication of DVT and occurs when a thrombus or blood clot detaches itself and is carried by the blood stream to the lungs. [J32]
Proximal DVT carries a higher risk of PE than distal DVT. [J30, Havig]
We focused on proximal DVT because it is much more reliably detected by ultrasonography and is considered to be clinically more important. [J53: 11,12, ç„¡è½K list,真係用先改]
DVT can occur in any veins. (near neck, etc.) However, it is not including in this literature review because…
Upper limb DVT is being reported, particularly associated with central venous catheters. (K66, from J20:54)
After a stroke, blood clots can form in the veins of the legs (deep vein thrombosis, or DVT). These clots can break off and be carried in the blood stream to the heart and lungs (causing pulmonary embolism). This can be life threatening. [J30]
Deep venous thrombosis may lead to pulmonary emboli, a frequent cause of avoidable deaths. [K52, from J53:1]
Virchow’s triad
The pathophysiological mechanisms underlying DVT include venous stasis and hypercoagulability linked to an increase in thrombin formation and platelet hyperactivity (Virchow 1858). [J30]
The occurrence of one or more factors of Virchow’s triad (stasis of blood, endothelial injury and hypercoagulability of blood) in the venous system often leads to deep vein thrombosis (DVT) (Virchow 1858). [J18]
DVT =
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Lower extremity DVT can be anatomically be divided into proximal DVT involving the popliteal vein and proximal veins or distal DVT involving the calf vein and distal veins. [J59]
DVT in the paralyzed legs of patients with stroke was reported as early as 1810 by Ferriar and again by Lobstein in 1833. [J45]
Pathophysiology of DVT formation
According to the Medsurg, Venous return is aided by the calf muscle pump. When the legs are inactive or the pump is ineffective, blood pools by gravity in the veins. Thrombus development is a local process. It begins by platelet adherence to the endothelium. Several factors promote platelet aggregation, including thrombin, fibrin, activated factor X, and catecholamines. In addition, where the platelets adhere to collagen, adenosine diphosphate (ADP) is released. ADP is also released from the damaged tissues and disrupted platelets. ADP produces platelet aggregation that results in a platelet plug.
Deep vein thrombi vary from 1mm in diameter to long tubular masses filing main veins. Small thrombi are found commonly in the pocket of deep vein valves. As thrombi become larger in diameter and length, they obstruct the veins, the resulting inflammatory process can destroy the valves of the veins; thus; venous insufficiency and postphlebitic syndrome are initiated.
Newly formed thrombi may become pulmonary emboli. Probably 24 to 48 hours after formation, thrombi undergo lysis or become organized and adhere to the vessel wall. Lysis diminishes the risk of embolization.
Pulmonary emboli, most of which start as thrombi in the large deep veins of the leg, are an acute and potentially lethal complication of DVT.
Venous thrombosis is the process of clot (thrombus) formation within veins. Although this can occur in any venous system, the predominant clinical events occur in the vessels of the leg, giving rise to deep vein thrombosis, or in the lungs, resulting in a pulmonary embolus (PE). [J56]
In fact, about 90% of DVT are of the ascending type. The potential for embolism depends on the speed and the extent of the dynamic, ascending clot growing process. Almost all clinical PE originate from distal DVT. Only the remaining 10% are derived from clots without connection to the lower leg veins (e.g. isolated iliac vein thrombosis, transfascial great or small saphenous vein thrombosis, subclavian vein thrombosis, or catheter-related thrombosis). [J58]
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Damage to the epithelial cell lining of the blood vessel is one of the extrinsic factors triggering the clotting cascade. The damaged endothelium attempts to maintain vascular integrity by adhesion and aggregation of platelets. As the clotting cascade continues, the final step is the formation of thrombin, which leads to the conversion of fibrinogen to fibrin and the formation of a fibrin clot. (Arcangelo & Peterson, 2006) (from K84, J40: Arcangelo)
Abnormal blood clots that adhere to the vessel wall are known as thrombi. These are composed of blood cells, platelets, and fibrin. Arterial thrombi are composed mainly of platelet aggregates and fibrin. Venous thrombi are composed of mainly red blood cells. The difference in composition is caused by the conditions in which the thrombus forms. In the artery, the blood flow is high in comparison with the low flow conditions in the vein. The thrombus may become large enough to interfere with blood flow within the vein or artery. (Mansen & McCance, 2002) (from K85, J40: Mansen)
If the thrombus detaches from the vessel wall, it becomes an embolus. This mobile clot travels thought the circulation until it lodges in a blood vessel that is smaller than the clot. Distal to this point, blood flow is blocked and tissues or organs are deprived of oxygen and nutrition. (Mansen & McCance, 2002). The signs and symptoms associated with an embolus depend on the vein or artery where th clot becomes lodged. (from K85, J40: Mansen)
In 1856, Virchow described the factors that predispose to venous thrombosis, including stasis, vascular damage, and hypercoagulability. These three factors are referred to as Virchow’s triad. Stasis of blood may occur because of immobility, age, obesity, or disease processes. Trauma (including surgery), intravenous (IV) cannulation, medications, and toxins are some of the many sources that may precipitate vascular damage. Hypercoagulability of the blood may be caused by various disease processes and medications. (Mansen & McCance, 2002) (from K85, J40: Mansen)
Why focus on DVT rather than PE and VTE?
A high proportion of patients with DVT also have subclinical PE. [K15, from J45:14]
Most of the PE results from DVT (please find literature to support)
Since lower limb DVT is the major origin of PE, and the characteristic of prolong bed rest of stroke, this literature review will mainly focus on the DVT at lower limbs.
Approximately two thirds of these are below-knee DVTs, in contrast to unselected (nonstroke) patients presenting with symptomatic DVT, in whom the majority are proximal. [J43]
Most studies show that PE seems to be much more common in patients with proximal and symptomatic DVT. [K41, from J46:1]
Clinical symptoms of DVT were developed by six patients (oedema or pain of the lower extremity, no cases of PE). (out of 28, =21.4%) (J48’s result)
Why stroke patient easy to have DVT
The general stroke population is at risk for DVT because of the following factors. First, there is an alteration in blood flow due to weakness in the lower limb and a resulting hypercoagulable state related to changes in the blood. Second, vessel wall intimal injury occurs related to changes in blood and blood flow. Stroke patients may also have similar symptoms associated with DVT, such as swelling and Homan’s sign, that may be misinterpreted as being related to the stroke. [J50]
Stroke patients are often bed-ridden, especially during the acute phase, because of paresis. [J50]
Most of the stroke patients are elderly. (age > ), while aging is a significant factors of the occurrence of DVT.
Patients with stroke are at particular risk for developing deep venous thrombosis (DVT) and pulmonary embolism (PE) because of limb paralysis, prolonged bed rest, and increased prothrombotic activity. [J45 (also code at J51)]
Sioson et al. [46] reported 19 DVT events in the paretic limb, nine bilateral events and four contralateral in 32 patients prospectively followed. (K49 from J46:46)
Why important to prevent
WHO estimates that 15 million people have a stroke every year, and this number is rising. (K91, from J39:2)
Venous thromboembolism is a common but preventable complication of acute ischaemic stroke, and is associated with increased mortality and long-term morbidity and substantial health-care costs for its management. (K92, from J39:6)
Without venous thromboembolism prophylaxis, up to 75% of patients with hemiplegia after stroke develop deep vein thrombosis and 20% develop pulmonary embolism, (K93, from J39:8) which is fatal in 1-2% of patients with acute ischaemic stroke and causes up to 25% of early deaths after strokes. (K94, from J39:9)
low molecular weight heparin and unfractionated heparin are therefore recommended in guidelines from expert consensus groups.10-14 (K95, from J39:10-14)
The best treatment for VTE is prevention. [J34]
Cause preventable death [J06]
Deep venous thromboembolism (DVT) is an important health issue in the hospitalized patients that leads to increased length of stay, morbidity, and mortality. [J50]
Early detection of DVT is important because of the risk of pulmonary embolism and its potentially fatal consequences. However, it is well known that clinical features of DVT and PE are notoriously nonspecific. [J09]
Despite improvements in prevention (SPARCL 2006), little progress has been made in treating stroke with specific interventions once it has occurred. (K72, from J44)
the occurrence of venous thromboembolism was about two-fold higher in patients with an NIHSS score of 14 or more than in those with a score less than 14 (in line with previous studies25) (K99, from J39:25 + J39self)
Patients with intracerebral hemorrhage (ICH) or ischemic stroke are at high risk for development of venous thromboembolism (VTE). (K103, from J29:1)
In comparison to patients with ischemic stroke, the risk for VTE is higher in the hemorrhagic stroke population. (K104, from J29:2)
Without preventative measures, 53% and 16% of immobilized patients develop deep venous thrombosis (DVT) or pulmonary embolism (PE), respectively, in this population. (K105, from J29:3)
One study detected DVT in 40% of patients with ICH within 2 weeks and 1.9% of those patients had a PE.4 (K106, from J29:4)
Development of VTE in the patient with ICH adds further detrimental complications to an already lethal disease with a 1-month case-fatality rate of 35% to 52%.5 (K107, from J29:5)
DVT also prolongs the length of hospital stays, delays rehabilitation programs, and introduces a potential risk for PE. (K108, from J29:6)
DVT prolongs hospitalization and increases healthcare costs. [J01]
DVT is the pathophysiological precursor of pulmonary embolism (PE). However, half of the DVT cases were asymptomatic. [J01, K1 from J37:18, J37,J27]. Approximately one third of patients with symptomatic venous thromboembolism (VTE) manifest pulmonary embolism (PE), whereas two thirds manifest deep vein thrombosis (DVT) alone. Moreover, death occurs in 6% of DVT cases and 12% of PE cases within 1 month of diagnosis. [J46, J27]
Clinically apparent DVT was reported in 1.7% to 5.0% of patients with stroke. Subclinical DVT occurred in 28% to 73% of patients with stroke, usually in the paralyzed limb. [J45]
The frequency of asymptomatic PE in patients with DVT to be 40%. [J50]
Prevention of VTE is highly effective in lowering the morbidity and mortality rate of stroke patients since PE accounts for up to 25% of post-stroke early deaths. [J43]
Bounds JV, Wiebers DO, Whisnant JP, Okazaki H: Mechanisms and timing of deaths from cerebral infarction. Stroke 1981, 12:474-477.The rate of PE is likely to be underestimated because they are not routinely screened for, and autopsies are rarely performed. Fifty percent of patients who die following an acute stroke showed evidence of PE on autopsy. [K68, from J13:7]
The annual incidence of DVT in the general population is estimated to be about 1 per 1000 (8), however, it should be noted that much of the published data are derived from patients who present with symptoms at medical institutions. Diagnosis of DVT has traditionally been based on clinical presentation, however, evidence from postmortem studies indicates that a substantial proportion of VTE cases are asymptomatic. [K10 from J55]
Clinically apparent DVT confirmed on investigation is less common but DVTs may not be recognised and may still cause important complications. Pulmonary embolism (PE) is an important cause of preventable death after stroke [K67, from J13:4]
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