My Clinical Notes

Varices are dilated veins and include varicose veins

 

Varicose veins

 

• Abnormally dilated veins produced by prolonged increased pressure within the vessel lumen and loss of vessel wall support
• Main sites are the superficial veins of the upper and lower leg
• 15-20% of the population develop varicose veins
• Venous pressure rises when the legs are dependant for long periods
• Risk factors;
  • Occupations that require long periods of standing, car and plane journeys
  • Age >50
  • Obesity
  • Female (due to increased venous pressure in the lower legs during pregnancy
  • Familial tendency – thought to be due to defective venous wall development

 

Morphology

• Macroscopically, the veins are dilated, tortuous, elongated and scarred. There is commonly thrombosis and valvular deformities
• Microscopically the changes consist of variations in the thickness of the vein caused by dilation in some areas and by compensatory hypertrophy of the smooth muscle and subintimal fibrosis in others
• Often there is phlebosclerosis with elastic tissue degeneration and calcifications within the media

 

Clinical course

• Dilation of veins renders the valves incompetent causing;
  • Venous stasis
  • Congestion
  • Oedema
  • Trophic skin changes leading to stasis dermatitis and ulceration
  • Pain
  • Thrombosis
• Embolism and serious consequences are rare in contrast to thrombosis of deep veins

 

Varicosities also occur in other sites;

• Oesophageal – in patients who have liver cirrhosis and portal hypertension. The can lead to massive GI haemorrhage
• Haemorrhoids – results from varicose dilation of the haemorrhoidal plexus at the anorectal junction. Seem to be caused by repeated straining at stool and pregnancy (prolonged pelvic congestion)

 

Thrombophlebitis

 

• Is inflammation of the veins with thrombus formation.
• Phlebothrombosis is thrombus formation in the absence of inflammation

 

• 90% occur in deep leg veins
• Causes;
  • Cardiac failure
  • Neoplasia
  • Pregnancy
  • Obesity
  • Post operative state
  • Prolonged bed rest/immobilisation
  • Genetic hypercoagulability syndromes

 

• In patients with cancer (particularly colonic adenocarcinoma), hypercoagulation seems to be part of a paraneoplastic syndrome. In these patients, the clot  tends to appear at one site, only to disappear and be followed by thrombosis in other veins – migratory thrombophlebitis (Trousseau sign)
• Thombophlebitis can also occur in the veins of the skull and venous sinuses when these vessels become inflamed by bacterial infections of the meninges, middle ear or mastoids
• Also infections in the abdominal cavity such as peritonitis, appendicitis, salpingitis ad pelvic abscesses may lead to inflammation and thrombosis of the portal vein

 

Symptoms and signs

• There may be few symptoms in the early stages
• Later there may be;
  • Oedema distal to the occluded vein
  • Dusky cyanosis
  • Dilation of the superficial veins
  • Heat
  • Tenderness
  • Redness
  • Swelling
  • Pain – may be absent in the bedridden patient
    • May be elicited by pressure over affected veins, squeezing the calf muscles or forced dorsiflexion of the foot (Homan sign)

 

• PE is a common and serious clinical sequel to DVT- where the contraction of the surrounding muscle milks the contents loose from their attachment to the leg veins

 

Pulmonary Embolism

 

• 95% of PE are caused by DVT in the legs
• Risk factors;
  • Cardiac disease
  • Cancer
  • Immobilisation
  • Hip fractures
  • Hypercoagualtion states
    • Primary
      • Factor V Leiden
      • Prothrombin 20210
      • Hyperhomocysteinaemia
      • Antiphospholipid syndrome
    • Secondary
      • Obesity
      • Recent surgery
      • Cancer
      • OCP
      • Pregnancy

 

• The pathophysiological response depends upon the extent of pulmonary artery obstruction, the number of emboli, the size of the occluded vessel, the overall status of the CVS
• There are 2 main pathophysiological consequences;
  • Respiratory compromise – due to the ventilated but non perfused segment
  • Haemodynamic compromise – due to increased resistance of pulmonary blood flow. This can cause pulmonary hypertension and cause acute right sided heart failure

 

Morphology

• Large emboli may impact in the main pulmonary artery or its major branches or it may lodge in the bifurcation as a saddle embolus. Sudden death may result due to the block of blood through the lungs
• Death may occur due to acute right sided heart failure
• Small emboli may travel into more peripheral vessels and cause infarction. Although only about 10% actually do so as the bronchial artery supply may be sufficient to sustain the lung parenchyma despite pulmonary obstruction
• Infarction generally only occurs in cases where the circulation is inadequate e.g. in heart and lung disease, therefore they tend to be uncommon in the young
• ¾ of all infarcts affect the lower lobes and in more than ½ multiple lesions occur
• Characteristically the are wedge shaped with the apex pointing toward the hilum of the lung
• The pulmonary infarct is generally haemorrhagic, goes from being red-blue in the early stages, to brownish to white due to fibrosis and scar formation
• Microscpically there is ischaemic necrosis of the lung substance within the walls of haemorrhage affecting the alveolar walls, bronchioles and vessels
• It the infarct is caused by an infected emboli there maybe neutrophils and an inflammatory reaction

 

Clinical course

• A large PE is one if the few causes of instantaneous death
• Patient may be in electromechanical dissociation – ECG has a rhythm but not there is no pulse
• If the patient survives the clinical syndrome may mimic MI;
  • Chest pain
  • Dyspnoea
  • Shock
  • Increased temperature
  • Increased serum lactate dehydrogenase
• Usually in individuals with normal CVS function, small emboli induce only transient chest pain and cough or possibly small haemorrhages without infarction
• A wedge shaped pulmonary infarct may appear on the CXR 12-36 hr after it has occurred
• Diagnosis is a via D-dimer detection and spiral CT
• After the initial insult small emboli generally resolve by fibrinolysis , unresolved multiple emboli over time may lead to;
  • Pulmonary hypertension
  • Pulmonary vascular sclerosis
  • Chronic cor pulmonale

 

Prevention of PE

• Early ambulation in postoperative and postpartum patients
• Graduated pressure stockings for bed ridden patients
• Preventative anti-coagulation
• IVC filter

 

Non thrombotic causes of PE

• Air – may be iatrogenic
• Bone marrow – after trauma of BM necrosis in sickle cell patients
• Fat – following trauma and surgery
• Amniotic fluid – during parturition
• Foreign bodies – I.V drug abusers

 

This entry was posted on Thursday, February 7th, 2008 at 6:37 am and is filed under Cardiovascular. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.