Interview Dr. Toni Feodor - Primary doctor General Surgery / Vascular Surgery Specialist doctor
Content
Chronic venous disease (BVC) includes a wide range of signs and symptoms ranging from the absence of visible or palpable signs or just cosmetic complaints related to the presence of dilated veins to severe irreversible microcirculation damage leading to varicose ulcer formation.
The severity of the disease occurs in the advanced stages of venous disease such as leg ulcers and lipodermatosclerosis, but also in the appearance of complications such as thrombosis and variceal hemorrhage. These complications can occur in the early stages and can lead to death from pulmonary thromboembolism or death from hemorrhagic shock, especially in elderly patients.
Therefore, BVC is a serious effect when complications occur, especially thrombotic and in the advanced stages of the disease.
On the other hand, the high prevalence of BVC has a significant negative impact on both the quality of life of many patients and the high social and economic costs.
The trigger mechanism of this pathology is not known, so in the appearance of BVC we are talking about risk factors.
These risk factors are hereditary, constitutional (obesity, female gender, static foot disorders) and occupational (orthostatism and sedentary lifestyle).
The pathogenic mechanisms of venous hypertension are reflux and / or obstruction. Furthermore, the pathophysiological chain includes the appearance of stasis with the entry of leukocytes in this process by adhesion, migration and activation in the interstitial space. The last stage is the appearance of inflammation, venous pain, destruction of the valves and remodeling of the venous wall that will maintain the vicious pathophysiological circle.
Moreover, the 2 theories of varicogenesis by destroying venous valves (1. the valvular theory or the descending theory in which venous reflux determines the occurrence of venous hypertension and 2. the parietal or ascending theory in which the remodeling of the venous wall is the first process that appears in the pathophysiological chain of BVC) are found in practice in the same way, but more important is the fact that the lesions once initiated progress with the destruction of new valves with the involvement of several venous segments.
BVC is a multifactorial disease, but heredity is considered the most important risk factor for this disease, as evidenced by family, epidemiological and genetic studies.
All these studies show that BVC is an autosomal dominant genetic disease with variable penetration in offspring:
These data are of practical importance in active prophylaxis since childhood, by practicing certain sports and avoiding those that would aggravate the disease.
These measures reduce the rate of progression of BVC and prevent the occurrence of irreversible lesions in the microcirculation.
Structurally, the quality of collagen tissue is inherited, the ratio of soluble collagen to insoluble collagen, the number of valves, both in macro and in microcirculation, a feature in the distribution of deep veins such as nontrombotic lesions of the iliac veins.
Metabolically we can inherit an increased activity of metalloproteinases or a decrease in the activity of inhibitors of these processes.
Genetically, we can inherit a mutation in the FOX C2 gene, which is involved in vascular differentiation, but also in the development of venous and lymphatic valves.
Unfortunately, there is no specific BVC genetic test because BVC is a multifactorial disease.
Given the fact that the disease is hereditary, we can see in practice children and adolescents with incipient lesions that progress slowly insidiously with the appearance of lesions in young adults.
This group of patients is at high risk of developing severe BVC lesions and gambit ulcers.
That is why our efforts to communicate with the patient, to actively follow up and to adopt personalized long-term strategies must be directed primarily to this group of patients in order to prevent those extremely serious injuries and to improve the quality of life in the long run. long. Therefore, with an early diagnosis, prophylactic measures can delay or prevent the onset of severe forms of BVC.
I do not know of a study of the prevalence of BVC in aviation personnel, but long air travel is an important risk factor for deep vein thrombosis that can be clinically expressed or insidious, leading to valve damage and reflux and venous hypertension.
Also, long trips by plane can be aggravated in BVC by the sedentary nature and lack of leg muscle activity.
BVC is a slow-progressing disease in which we have enough time to organize ourselves in advance to perform a specialized consultation in which we will receive information and personalized therapeutic strategies.
There are two clinical situations of concern when it is necessary to take prompt therapeutic action:
It is better, easier and cheaper to prevent than to treat, so the right time would be at the first symptoms or signs.
The onset symptoms of BVC are nocturnal muscle cramps, heavy, tired legs, swollen feet, and pain that worsens after prolonged orthostatism. The early signs of BVC are skin deformation caused by varicose veins that return to the cynostatic position, reticulated veins, and telangiectasias. These signs are convincing elements to present to the doctor.
It is good to present to the family doctor from the first symptoms, who, depending on the extent of the symptoms and / or lesions, will request either an ultrasound examination and then the consultation of a specialist in venous pathology, or a direct phlebological consultation. It is also important that the follow-up of the patient with BVC be done in the same team: family doctor and specialist.
In addition to obtaining classic historical data, a phlebological consultation involves analyzing symptoms and examining the patient (as in any medical consultation); in addition, the phlebology consultation must answer the following questions:
BVC has two important pathophysiological elements: inflammation and venous hemodynamic changes.
Our treatment strategy combats these two elements:
An important practical element is the benefit of combining the two therapeutic components (inflammation control and hemodynamic correction.
BVC is found in both women and men, both the thin and the overweight, both vegetarian and full-diet patients, both athletes and sedentary people.
There are currently no data showing a specific method or lifestyle that can prevent BVC.
However, we hope that the near future will show us that it is possible to prevent the occurrence of these pathologies.
Yes, but not for all patients.
We see from practice that a good part of the operated patients no longer develop BVC and do not show recurrence of the disease, both clinically and ultrasound.
On the other hand, the speed of disease progression differs from one patient to another and depends on the presence and persistence of risk factors, venous rehabilitation measures, adherence to venoactive and compressive treatment.
Even if in some situations the evolution of the disease cannot be stopped, by taking the listed measures, we will be able to reduce with certainty the rate of progression of the disease, significantly improving the quality of life.