Chronic venous insufficiency

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Chronic venous insufficiency
Classification and external resources
ICD-10 I87.2
ICD-9 459.81
DiseasesDB 13734
MedlinePlus 000203
eMedicine article/461449
MeSH D014689

Chronic venous insufficiency or CVI is a medical condition where the veins cannot pump enough oxygen-poor blood back to the heart.[1] It is sometimes referred to as an "impaired musculovenous pump", this is due to damaged or "incompetent" valves as may occur after deep vein thrombosis (when the disease is called postthrombotic syndrome) or phlebitis. Ordinarily, women make up the largest demographic for this problem. Paratroopers, utility pole linemen, and men with leg injuries can suffer from damaged leg vein valves and develop this condition.

Venous insufficiency in the legs[edit]

Venous valves

As functional venous valves are required to provide for efficient blood return from the lower extremities, CVI often occurs in the veins of the legs. The condition has been known since ancient times and Hippocrates used bandaging to treat it. It is sometimes described as chronic peripheral venous insufficiency. Whilst usually caused by incompetent valves, it may occur when an artery strangulates a vein, or be caused by an arteriovenous fistula (an abnormal connection or passageway between an artery and a vein).

Symptoms[edit]

Symptoms of CVI in the leg include the following:

  • Itching (pruritus)
  • Hyperpigmentation
  • Phlebetic lymphedema
  • Chronic swelling of the legs and ankles

Effects[edit]

CVI in the leg may cause the following:

  • Venous stasis
  • Ulcers.[2]
  • Stasis dermatitis,[2] also known as varicose eczema
  • Contact dermatitis.[2] Patients with venous insufficiency have a disrupted epidermal barrier, making them more susceptible than the general population to contact sensitization and subsequent dermatitis.
  • Atrophie blanche.[2] This is an end point of a variety of conditions, appears as atrophic plaques of ivory white skin with telangiectasias.
  • Lipodermatosclerosis.[2] This is an indurated plaque in the medial malleolus.
  • Malignancy.[2] Malignant degeneration is a rare but important complication of venous disease since tumors which develop in the setting of an ulcer tend to be more aggressive.
  • Pain.[2] Pain is a feature of venous disease often overlooked and commonly undertreated.
  • Anxiety.[2]
  • Depression.[2]
  • Inflammation
  • Discoloration
  • Skin thickening
  • Cellulitis

Causes[edit]

CVI in the leg may be caused by the following:

Palliative treatment[edit]

Palliative treatment of CVI in the leg involves managing the symptoms (and preventing the symptoms getting worse) instead of effecting a cure. It is sometimes called conservative treatment. Conservative treatments include:

  • Manual compression lymphatic massage therapy
  • Skin lubrication
  • Sequential compression pump
  • Ankle pump
  • Compression stockings
  • Blood pressure medicine,
  • Frequent periods of rest elevating the legs above the heart level
  • Tilting the bed so that the feet are above the heart. This may be achieved by using a 20 cm (7-inch) bed wedge or sleeping in a 6 degree Trendelenburg position.[citation needed] Obese or pregnant patients might be advised by their physicians to forgo the tilted bed.

Surgical treatments[edit]

Surgical treatment of CVI attempts a cure by physically changing the veins with incompetent valves. Surgical treatments include:

Venous insufficiency in the central nervous system[edit]

CVI has been reported in the CNS of several persons.[3] When it appears into the CNS is called Chronic cerebrospinal venous insufficiency (CCSVI). It can be seen using Transcranial doppler sonography or MRV (magnetic resonance venography)

This disease was only recently described (2006) and the first international symposium took place on September 8, 2009 in Bologna, Italy. The causes of venous insufficiencies were discussed, and it was mostly shown that it is due to venous stenosis which is subsequently due to genetics or embryonic problems.[4]

The known consequences of the disease are hypoxia, delayed perfusion and iron deposits in the blood vessels, with unknown final effects for the health of the patients. A connection with MS has been proposed (all cases of CCSVI in one particular study were found in MS patients[3]) but the possible relationship is still under study.

It can be treated currently in two ways: Balloons to open the veins, in the hope they will remain open, and venous stents, to keep them open permanently.

Other research groups have found jugular veins reflux in other neurological diseases. In particular in Transient Global Amnesia,[5][6] Leukoaraiosis,[7] and general myelopathies.[8] All of them have been linked to venous reflux with different names like Cerebral Venous Outflow Impairment. At this moment is unknown if these conditions can be considered related to CCSVI.

Venous insufficiency in the liver[edit]

Budd–Chiari syndrome is the condition caused by occlusion of the hepatic veins. It presents with the classical triad of abdominal pain, ascites and hepatomegaly. Examples of occlusion include thrombosis of hepatic veins. The syndrome can be fulminant, acute, chronic, or asymptomatic. It occurs in 1 out of a million individuals[9] and is more common in females. Some 10–20% also have obstruction of the portal vein.

Any obstruction of the venous vasculature of the liver is referred to as Budd-Chiari syndrome, from the venules to the right atrium. This leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates. The increased portal pressure causes: 1) increased filtration of vascular fluid with the formation of protein-rich ascites in the abdomen; and 2) collateral venous flow through alternative veins leading to gastric varices and hemorrhoids. Obstruction also causes centrilobular necrosis and peripheral lobule fatty change due to ischemia. If this condition persists chronically what is known as Nutmeg liver will develop. Renal failure may occur, perhaps due to the body sensing an "underfill" state and subsequent activation of the renin-angiotensin pathways and excess sodium retention.

See also[edit]

References[edit]

  1. ^ "Chronic Venous Insufficiency". Society for Vascular Surgery. December 1, 2009. 
  2. ^ a b c d e f g h i [1] Ann Vasc Surg. 2007 Sep;21(5):652-62. Dermatologic complications of chronic venous disease: medical management and beyond. Barron GS1, Jacob SE, Kirsner RS. PMID: 17823046
  3. ^ a b Zamboni, P; Galeotti, R; Menegatti, E; Malagoni, A M; Tacconi, G; Dall'ara, S; Bartolomei, I; Salvi, F (2008). "Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis". Journal of Neurology, Neurosurgery & Psychiatry 80 (4): 392–9. doi:10.1136/jnnp.2008.157164. PMC 2647682. PMID 19060024. 
  4. ^ Bologna conference notes [2][unreliable medical source?]
  5. ^ Chung, C; Hsu, H; Chao, A; Sheng, W; Soong, B; Hu, H (2007). "Transient Global Amnesia: Cerebral Venous Outflow Impairment—Insight from the Abnormal Flow Patterns of the Internal Jugular Vein". Ultrasound in Medicine & Biology 33 (11): 1727–35. doi:10.1016/j.ultrasmedbio.2007.05.018. 
  6. ^ Chung, C; Hsu, H; Chao, A; Wong, W; Sheng, W; Hu, H (2007). "Flow Volume in the Jugular Vein and Related Hemodynamics in the Branches of the Jugular Vein". Ultrasound in Medicine & Biology 33 (4): 500–5. doi:10.1016/j.ultrasmedbio.2006.10.009. 
  7. ^ Chung, Chih-Ping; Hu, Han-Hwa (2010). "Pathogenesis of leukoaraiosis: Role of jugular venous reflux". Medical Hypotheses 75 (1): 85–90. doi:10.1016/j.mehy.2010.01.042. PMID 20172657. 
  8. ^ Leriche, H; Aubin, ML; Aboulker, J (1976). "Cavo-spinal phlebography in myelopathies. Stenoses of internal jugular and azygos veins, venous compressions and thromboses". Acta radiologica. Supplementum 347: 415–7. PMID 207127. 
  9. ^ Rajani, Rupesh; Melin, Tor; Björnsson, Einar; Broomé, Ulrika; Sangfelt, Per; Danielsson, Åke; Gustavsson, Anders; Grip, Olof et al. (2009). "Budd-Chiari syndrome in Sweden: epidemiology, clinical characteristics and survival – an 18-year experience". Liver International 29 (2): 253–9. doi:10.1111/j.1478-3231.2008.01838.x. PMID 18694401. 

^ Bologna conference notes [1][unreliable medical source?]

Link correction ^ Bologna conference notes [1][3]

Further reading[edit]