4: Thromboembolic disorders

Chapter 4 Thromboembolic disorders



CHAPTER CONTENTS


Introduction 43

Relevant anatomy and physiology 44
Haemostasis (cessation of bleeding) 45

Pathophysiology of thromboembolism 46
Aetiology 46

Thromboembolic related conditions 47

Thromboembolic disorders in pregnancy 51
Introduction 51

Physiological changes in pregnancy 51

Incidence 52

Prevention 52

Prenatally 52

Labour 53

Puerperium 53

Pulmonary embolism 54

Neonatal considerations 54

Future pregnancies 54

References 54


INTRODUCTION


Thromboembolic disorders are the leading cause of direct maternal death in the UK (Lewis & Drife 2004).


From 2000–2002, 30 women died from thrombosis and/or embolism in the UK. Some 25 deaths were as a result of a pulmonary embolism and five from cerebral vein thrombosis. Ofthe deaths from pulmonary embolism, four deaths occurred in pregnancy, one in labour and 17 postnatally. Some 16 of these women had riskfactors for thromboembolic disorders. In 57% of all cases, there was evidence of substandardcare. Prophylactic anticoagulants are strongly recommended in all areas of healthcare where mobility is limited and this must be a consideration in the care of women undergoing childbirth dependent on risk (RCOG 2004). The majority of thromboembolic events during the childbearing process are not fatal, but may be responsible for considerable long-term morbidity (Gates 2000).


The midwife is the leading care giver in the majority of pregnancies and as such must be fully aware of all risk factors that may lead to a negative outcome. It is essential therefore, that she has a thorough understanding of thromboembolic disorders and their treatment in order to recognize those at risk and ensure prompt referral and treatment.



RELEVANT ANATOMY AND PHYSIOLOGY


The control and role of blood pressure in the movement of blood through the circulatory system has already been explained (seeCh. 2). The continued brisk movement of blood through blood vessels is one of the factors that prevents coagulation and thrombosis. Control of the coagulation cascade is another.


The circulating fluid in the cardiovascular system, blood, is composed of two main elements. Plasma is a fluid and blood cells are suspended within this.


Plasma is a straw coloured substance similar in composition to interstitial fluid. It makes up approximately 55% of the blood volume and is essential for the maintenance of homeostasis. Plasma is composed of 90% water plus dissolved or suspended substances. These include nutrients, wastes, proteins and the products of cell metabolism. Chemicals and proteins involved in the coagulation of blood are transported in this way.


The remaining 45% of blood is composed of blood cells:


• Erythrocytes – red blood cells – are responsible for transporting oxygen from the lungs to all parts of the body; 99% of blood cells are erythrocytes

• Leucocytes – white blood cells – make up approximately 1% of blood cells and are involved in infection control and the inflammatory response

• Thrombocytes – platelets – are very small fragments of cellular material. These contain the substances essential to blood clotting (Fig. 4.1a,b).

image

Figure 4.1 Diagrammatic representation of a platelet.(a) Inactive platelet. (b) Activated platelet.


Movement of blood through the circulation is controlled primarily by contraction of the heart. Blood pressure exerted by this process and by the constraining influence of the walls of the blood vessels moves blood rapidly through the arterial network. Blood pressure gradually drops as blood vessels become narrower, and once blood has passed through the capillary network, pressure is comparatively low. Additionally gravity plays a role (seeCh. 2). Venous return of blood to the heart is therefore more easily disrupted and it is in the venous system that there is increased risk of the formation of a thrombus particularly in lower limbs.


The venous system of the lower limbs consists of three distinct types of vein; deep veins which lie within the skeletal muscles (femoral, tibial and popliteal); superficial veins which lie outside this sheath (long and short saphenous veins); and joining the two systems, perforating or communicating veins (Fig. 4.2).


image

Figure 4.2 Veins of the lower limb.


Venous circulation in lower limbs returns blood to the heart in an upward direction against the force of gravity. This upward flow is maintained by valves which prevent backflow.


Valves are folds of the tunica intima which lines the veins (Fig. 4.3). The tunica intima is a very thin layer consisting of the basement membrane and endothelium. Valves can thus be easily damaged by injury to the blood vessels. In some individuals, valves are inherently incompetent and the upward flow is more difficult to maintain.


image

Figure 4.3 Comparison of the anatomy of an artery and a vein.


Venous return depends therefore on several factors:


• Difference in blood pressure between venules, approximately 16 mmHg, and the right atrium, 0 mmHg. Although this is a comparatively small pressure differential, resistance in veins is very low. Additionally, as the right atrium empties with each contraction of the heart, blood is sucked into the vacuum that is left

• Skeletal muscle contractions: Deep veins running through skeletal muscle are squeezed by muscle contraction and raise blood pressure. Blood is forced along the veins in the direction of the heart and backflow is prevented by the presence of the valves. When the muscles relax, the valves close and prevent backflow (Fig. 4.4). Normal daily activities require regular skeletal muscular contraction during walking, working etc. and thus contribute to this process

• Respiration: During inspiration, the diaphragm moves downward. This results in a decrease in pressure in the thorax and an increase in the abdominal cavity. As a result, blood moves from compressed abdominal veins into decompressed thoracic veins. During expiration, the presence of valves in veins again prevents backflow.

image

Figure 4.4 Movement of blood by skeletal muscle contraction. (a) Relaxed skeletal muscle. (b) Contracting skeletal muscle.



Haemostasis (cessation of bleeding)


Blood is essential to life. It is imperative that any loss of this substance due to trauma of a bloodvessel is corrected as quickly as possible. The body has a range of measures it can bring into play to seal the blood vessel and minimize blood loss (Fig. 4.5).


image

Figure 4.5 Haemostasis.


Initially, on detecting a damaged blood vessel, thrombocytes release serotonin which, along with other chemicals released by the damaged cells, causes local vasoconstriction of the blood vessel to minimize blood loss. Around the site of the trauma, thrombocytes clump together and release substances such as ADP, which attract many more platelets to the area, adding to the size of the temporary plug formed (Walthall 2006). Coagulation of blood occurs around the plug forming a permanent clot.


Coagulation is a complex process involving two pathways and a series of steps in each (Fig. 4.6). In summary, strands of fibrin are synthesized by a plasma protein, fibrinogen, which combines with water and solutes to form a gel in which blood cells become trapped. This is the thrombus – blood clot. As further chemicals become involved, the thrombus hardens and seals the blood vessel, and also acts as scaffolding for the repair of the damaged blood vessel. Finally, on completion of the repair, the fibrin thrombus is dissolved by the process of fibrinolysis to re-open the blood vessel fully for effective blood flow.


image

Figure 4.6 The coagulation cascade.


In undamaged blood vessels, various anti-clotting mechanisms restrict and prevent clot formation. Normal blood flow depends on a delicate balance between circulating and endothelial anticoagulant and procoagulating factors. It is when this fine balance is disrupted that an inappropriate thrombus forms. The hormonal changes of pregnancy disrupt this balance to some extent in all women; in women with an additional risk factor, this may result in the production of a thrombus.



PATHOPHYSIOLOGY OF THROMBOEMBOLISM


Any situation in which blood flow is slow or disrupted places the individual at risk of a thromboembolic event. Recent press has highlighted this risk in publicizing the dangers of immobility aggravated by dehydration on ‘long haul’ flights (Box 4.1). This risk has been well recognized for many years in healthcare and has led to rapid mobilization and physiotherapy in all patients post-surgery. Despite this, thromboembolic disorders continue to result in high mortality and morbidity rates, with commensurate healthcare costs.



Box 4.1 DVT and long haul flying


Pathophysiological changes associated with flying give rise to several significant predisposing factors for developing a DVT (Shepherd & Edwards 2004). Hypoxia and vasoconstriction develop over time and at high altitudes due to an increase in blood pressure and heart rate. Cabin pressure is set for 6000 feet andlong haul flights take place at much higher levels. These changes are aggravated by immobility anddehydration. After 1 h at these high altitudes, thereis a decrease in blood flow to the lower limbs and pooling of plasma proteins (Willcox 2004), thus increasing the risk of thrombosis. Additionally, pressure from the seat on the back of the leg and the cramped conditions in economy seats increasethe risk factors. Antiembolic stockings can be considered to reduce this risk but these are not suitable for some people with pre-existing disease (Scurr et al 2001). Walking around the aisles of the aircraft and preventing dehydration by drinking water (not alcohol) will help reduce the risks of DVT.



Aetiology


A thrombosis is the formation of a clot – thrombus –inside a blood vessel, thus obstructing the flow of blood through the circulatory system. The term ‘thromboembolism’ is a term applied to the formation of a thrombus complicated by the risk of embolization. An embolus is a moving clot.


Classically, the development of an inappropriate thrombosis is caused by a disruption in one or more of the following (Virchow’ striad 1856):


• Alteration of blood flow (haemostasis)

• Injury of the vascular endothelium

• Alterations to the constitution of the blood (hypercoagulability).

Commonly, the formation of the thrombus is caused by an injury to the blood vessel wall, either by trauma or infection, or by slowing or stagnation of blood flow past this injury. Abnormalities in the coagulation process may aggravate or initiate this process.


Alternatively and frequently the issue in caring for those in hospital, the formation of a thrombus is initiated in the first instance by venous stasis.


Venous stasis describes any condition in which venous blood flow slows or stagnates and occurs as a result of an overabundance of, or decreased removal of fluid. Common causes of venous stasis are (Gutierrez & Peterson 2002):


• A sedentary lifestyle

• Compression of blood vessels as in obesity or an abdominal tumour

• Congestive heart failure

• Chronic venous disease.

There are two main types of thrombus – venous and arterial. Venous thrombosis can occur in any of the veins of the body, for example a deep venous thrombosis. Common arterial thromboses are found in the coronary arteries, resulting in a myocardial infarction, or in cerebral arteries, causing a cerebrovascular accident (‘stroke’). Both of these disorders can also be caused by an embolism, but a myocardial infarction is often the result of damage to the blood vessel walls by atherosclerotic plaque to which platelets are attracted. A cerebrovascular accident (CVA) can have many causes including thrombosis due atherosclerosis (seeCh. 8).



Thromboembolic related conditions



Varicose veins


Blood flow in legs can slow and pool during inactivity of skeletal muscle. This is particularly true for those whose occupations require them to stand for long periods (Bentley 2003). When the plantar veins are compressed, as in walking, blood flow is increased into deep veins. Pressure in the veins is highest on standing but decreases on walking. In the supine position, blood pressure in the veins is negligible.


Varicose veins, or varicosities, are veins in which blood flow has become sluggish on its return to the heart, usually as a result of increased resistance. The valves in the veins are weak and incompetent and allow backflow, and as a result, the vessel walls become dilated and tortuous. Superficial and perforating veins, unsupported by skeletal muscle, are particularly susceptible. This aggravates venous stasis and predisposes to the formation of a thrombus. Although increased resistance leads to the development of varicose veins, there is a strong familial tendency to have inherently weak vessel walls.


Common sites for varicosities are:


• In the legs where the body’s upright stance and the effect of gravity slow blood flow

• In the anal canal, haemorrhoids

• In vulvar veins in pregnant women due to pressure from the enlarging uterus.

The presence of varicose veins is commonly indicated by localized swelling, which on examination can be felt, and subsequently seen, as being the result of swollen and knotty superficial veins. The patient complains of heavy, aching legs. Discolouration is seen due to the accumulation of waste products and dry itchy skin develops over the varicose vein. The veins readily become inflamed – phlebitis – and occasionally the vessel wall ruptures causing haemorrhage. Feet and ankles may become swollen and symptoms increase during the course of the day, particularly if the woman has been standing for a long time.


Diagnosis is determined by the Trendelenburg test. In this procedure, the leg is elevated from a horizontal position to empty the veins, and on standing, the veins are observed as they refill. Normally filling is comparatively slow: in the presence of varicosities, filling is much more rapid as the incompetent valves allow filling from above as well as below. Doppler studies will confirm the structure and functioning of the veins.


Medical management involves the use of support stockings and advice to avoid prolonged standing. Elevation of the limb will assist drainage and can be achieved by raising the foot of the bed at night. However, surgical treatment is often required. Affected veins are ligated and stripped, encouraging blood to return to the heart via the deep veins of the leg.


Haemorrhoids are varicosities of the anus and rectum. These can occur both at the anal margin and in the rectum. Haemorrhoids are a common complaint and occur as a result of inherently weak vessel walls combined with other factors, such as constipation and pregnancy.

< div class='tao-gold-member'>

Related posts:

  1. 1: The midwife’s role
  2. 7: Renal disorders
  3. 8: Epilepsy and other neurological conditions
  4. 6: Asthma

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 11, 2016 | Posted by in MIDWIFERY | Comments Off on 4: Thromboembolic disorders

Full access? Get Clinical Tree
Get Clinical Tree app for offline access