**8. References**


Pathophysiology and Clinical Aspects of 152 Venous Thromboembolism in Neonates, Renal Disease and Cancer Patients

an ironic association, since a key aspect of Virchow's work on venous thrombi was his threepart distinction between thrombus and clot and his demonstration that a DVT is formed when leukocytes as well as platelets swarm to the site of injury, the venous valve cusp. As a result, mainstream research in the DVT field since 1962 has taken on an increasingly haematological character, which has entailed a tacit dismissal of the important discoveries made prior to the mid-20th century, not least those of Virchow. The valve cusp hypoxia (VCH) thesis is founded on the recognition of these discoveries and on our knowledge of vascular physiology, particularly the dynamics of blood flow in venous valve pockets. It was advanced as a hypothesis in 1977 and was corroborated and validated by critical

In clinical terms, the VCH thesis adds nothing to accepted standards of treatment for actual, manifest thromboembolism other than to augment the rational basis for mechanical prophylaxis and to suggest reconsideration of prolonged muscle relaxant use during surgery, a potential 'silent killer'. Mechanical prophylaxis should be based not on altering the venous blood flow velocity, which is almost certainly irrelevant to thrombogenesis, but to ensuring that flow is always pulsatile. The pulses need not be frequent: once per hour will suffice to ensure that valve pocket hypoxaemia does not become seriously injurious to the endothelia, and should therefore preclude the formation of thrombi, though optimal timing can only be established on the basis of experience. The key point is to ensure that the valve pockets are emptied and refilled regularly with fresh venous blood. On the other hand, the VCH thesis indicates that anticoagulants do not prevent the initiation of deep venous thrombosis, though they restrict or retard the growth of thrombi that have already formed. The approaches to mechanical prophylaxis inferred from VCH are testable on experimental animals. Such tests should certainly be conducted before a randomised controlled clinical trial is initiated. We encourage colleagues throughout the world to undertake these experiments – and, subject to the results, clinical trials – since only by consistent findings from different laboratories and clinical establishments can a consensus be obtained that would make rational

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**7** 

*Denmark* 

**Venous Thromboembolism as a Preventable** 

**Insurance Association (1996 - 2010)** 

Jens Krogh Christoffersen1 and Lars Dahlgaard Hove2

*1Danish Patient Insurance Association,* 

*2Hvidovre Hospital, University of Copenhagen,* 

**Patient Injury: Experience of the Danish Patient** 

The mechanism of disease in venous thromboembolsm (VTE) is mentioned, with emphasis on the rarer types of the disease. Next the conditions for approval of claims under the Danish Patient Insurance law are drawn up, and the typical situations for approval of VTE are listed. In the database of the DPIA we found 688 claims with this disease, and of these 421 were approved. The different types of VTE are examined, and the possibilities for

Venous trombosis is usually located in the veins of the lower extremity. The thrombosis probably has its origin in the valve pockets of the veins of the lower leg. There are several pathogenetic factors, but a common denominator is reduction of flow velocity in the veins.

1. During aneasthesia it has been shown that the diameter of the veins increase, and thus the velocity of the flow decreases. At the same time the operative trauma increases the

2. In a number of different trauma situations to the leg, where immobilisation in casts or

These are classic examples of patients that may suffer a deep venous trombosis (DVT) or

The thrombosis may begin in the popliteal or femoral vein progressing centrally until it breaks off and sends its potentially fatal embolism to the lungs. It may also have its origin in the iliac veins, in which case the diameter of the ensuing embolism is sufficient large to close

splints is used, rendering the venous muscle pump dysfunctionate, 3. In acute stroke, the afflicted leg is left without its normal venous muscle pump

**1. Introduction** 

prevention are discussed.

**2. Of venous thromboembolism** 

This may occur in a varity of situations, e.g.:

readyness of the thrombotic system.

more severely a pumonary embolism (PE).

There are many clinical examples of variatons on the theme.

off the entire pulmonary artery, causing immediate death.

