The human body has three systems of vascular channels. We all know and are principally aware of the arterial system which propels oxygenated blood to the periphery and the remotest tissues for the delivery of oxygen and proteinaceous nutrients. The lymphatic system is concerned mainly with the return of protein-rich fluid of an oily nature to the circulatory system. The veins and the venous system are extensive and diverse. Principally involved in returning deoxygenated blood to the lung ultimately, the distribution and mechanics defy imagination. Smaller veins unite to form larger veins and ultimately two large veins are formed draining the superior extremity and the head-neck, and the inferior extremity and the abdomen. The Superior Vena Cava is ultimately formed by the fusion and coalescence of the head-neck and upper extremity veins. Similarly, lower extremity veins fuse with the visceral veins of the abdomen and liver to form the Inferior Vena Cava to finally drain into the heart.
We know for a fact that the human circulatory system is in a series connection and the strong contraction of the heart is sufficient to propel blood along the pulsatile arterial system into the tissue capillaries via the precapillary arterioles. Venules are formed by the fusion of these capillaries which in their turn coalesce to form the larger veins. Venous return is also governed by this strong cardiac contraction and the presence of one-way valves in the various systems prevents significant regurgitation.
In general, even though the three basic lining layers, i.e., the adventitia, the media, and the endothelium are retained, the veins have a larger diameter than an artery of the same name. The lining layers are subjected to lower pressures than the corresponding arteries. They are thus thinner than the arteries and show the presence of less connective tissue in the adventitia with a lower number of muscle fibres in the media. The most intriguing additional structure in the veins is the valves. The veins nearer the heart and adjacent to visceral structures do not exhibit any interior valves. However, a distally located intramuscular vein always is provided with a one-way, perfectly formed semilunar tri-leaflet valve. The valves are re-duplicated internal endothelial linings with a few collagen and elastin thrown in to give the required strength and character. This not only ensures ideal hemodynamics but also synchronized unidirectional return with muscular contraction. This ensures stagnation does not happen and a continuous flow is maintained. This muscular activity augmented propulsion of the deoxygenated blood back, also called the peripheral heart, however, it lacks the automaticity and spontaneous rhythm generation capability of the normal native heart.
Another feature is a dilated region in the vein also known as the ' jugular bulb' and is a site where the intracranial lateral venous sinuses (the larger sigmoid sinus and the inferior petrosal sinus from the cavernous sinus) drain into the internal jugular vein in the neck. Essentially this is an extra-cranial structure and does not have any significance. A small percentage may have a high, intra-osseous (i.e., adjacent to the middle ear and inside the petrous temporal bone) jugular bulb which can lead to a degree of conductive deafness and/or pulsatile tinnitus. The jugular bulb is not present at birth and develops with time. The small dilatation at the origin of the internal jugular vein may be a release of the tortuosity and constraints of the bony canal. Thereafter it traverses along with the internal carotid artery in the confines of the carotid sheath. The neck like the lower limbs has a superficial and deep venous drainage system. Though the superficial system drains a lesser volume of blood, the systems are complementary.
Generally, the thickness and thinness of a venous radicle depend upon the flow and pressure within it. Usually, the low-pressure and low-flow veins have thin walls and should be handled accordingly. Awareness of the major portal system is also needed to understand the varicose appearance of selected systemic veins on endoscopic evaluation.
The venous drainage of the brain requires special mention. There are superficial and deep veins and there is a specific pattern that governs the return of deoxygenated venous blood and nutrient-extracted blood back to the enlarged venous sinuses which are a feature of the organ. The only vein named after its discoverer is the short great cerebral vein of Galen which is responsible for draining the cerebrum on each side via the Inferior cerebral veins of the respective sides. To reach the jugular veins, the brain has an intricate network of venous sinuses that drain not only the brain parenchyma, but the meninges, eyes, and cerebrospinal fluid as well. The drainage pathways can be differentiated as either superficial drainage to the dural sinuses, or deep drainage to the medullary veins and ultimately to the cerebral vein of Galen. These vessels are uniformly valve-less and as such, freely communicate with each other, which can facilitate the spread of infectious pathogens. The cerebral venous system is also quite delicate and, as the brain is suspended in fluid, mild trauma or even sudden changes in velocity can cause rupture of the cortical bridging vessels, leading to a subdural hematoma. The diploic veins are also valveless and thin-walled. They drain blood from the two tables of the skull bones (cancellous portion or diploe of skull bones) and internally communicate via subdural channels draining into the superior sagittal sinus, and meningeal veins. Externally these communicate with the external scalp veins and, although not efficiently, are involved in the dissipation of intracranial pressure and temperature in obstruction to a major venous channel draining the brain. The bridging veins (BV) require a mention in the same context. They are venous channels that are seen intercommunicating the brain veins with the larger dural venous sinuses and thus they are different. Rather the bridging veins traverse the pia and arachnoid maters to end up in the dural sinuses. The emissary veins, on the other hand, cross the tables of the skull bones as direct channels not receiving any tributaries on the way and communicating with external scalp veins. A complex system therefore exists, however, final drainage is into the systematic internal jugular veins (IJV) on each side. This constitutes brain venous drainage effectively.
The heart also has some unique venous drainage patterns. There are the major systemic veins but not on all occasions do they accompany corresponding systemic arteries. Rather they are organ-specific and involved in organ venous drainage. All manage to cover the common venous channel, the coronary sinus which ultimately drains into the right atrium. Other veins draining directly into the right atrium are the anterior cardiac veins. Tiny channels carrying venous blood, also called the Thebesian veins or the 'Venae cordis minimae', open directly into respective chambers. The pulmonary veins, two in number on each side, drain purely oxygenated blood into the left atrium. The heart happens to be the only organ where there is a role reversal, where the pulmonary arteries carry deoxygenated blood, and veins of the same name transport oxygenated blood from and to the heart.
The inferior vena cava (IVC) is the largest venous channel of the human body with the superior vena cava (SVC) a close second. The valved channels prevent a regurgitant and turbulent flow reversal into relatively compliant, low-pressure, and thin-walled venous channels and help in maintaining an optimal preload to the heart. Usually, channels close to the heart are devoid of valves.
The superior vena cava or the SVC carries all the venous blood from the brain, head-neck, and upper extremities to the heart. The inferior vena cava or the IVC is involved in a similar way in transporting de-oxygenated blood from the lower extremities and abdominal viscera, the only difference being the interposition of the portal system. Drainage of the thoracic organs other than the heart follows a mathematical division where blood from the upper half is drained by the SVC while the lower half goes to the IVC. However, the SVC is the more accessible vein, but the oesophagal and diaphragmatic venous return is into the IVC.
The diseases affecting veins very much are the same as in diseases of other organs and the general rule of traumatic, congenital, acquired, and iatrogenic can be applied. Hitherto traumatic disruption of veins accidental or otherwise was never given much attention unless the vein was very big and there was a question about the venous return. The repair principles are the same as in other vascular procedures, but unnecessary time-wasting should be avoided as usually there are alternative pathways for venous return. Whenever there is a superficial and a deep venous system, the more accessible superficial system can be sacrificed. However, the hint of disease in the deep system makes the clinician think otherwise and the question of sacrificing the superficial system does not arise.
In general, one should have some idea about the various venous sinuses in the body. These are a congregation of valve-less, multiple small intercommunicating venous radicles that form an intricate, lattice-like network composed of slowly flowing blood. That they are veins that can be made out on both sagittal and axial MR images as areas of increased signal intensity. There are numerous venous sinuses in the body, and in addition to the eleven dural sinuses these are:
Basilar plexus
Batson plexus
Internal vertebral venous plexus
Pterygoid plexus
Submucosal venous plexus of the nose
Uterine plexus
Vaginal plexus
Venous plexus of the hypoglossal canal
Vesical plexus,
Soleal plexus, etc. in cephalo-pedal order.
There is an intricate network of sinuses in the arachnoid, pia, and dura mater of the brain with interconnecting veins as well. The dural sinuses are large and the sinuses help return blood to the heart the same way as the veins do. Characteristically the sinuses are devoid of or minimally have a muscular coat and instead a connective tissue layer and the periosteum of the adjacent bone is incorporated into the layer. The sinuses are so thin-walled and fragile that inadvertent surgical trauma may even lead to uncontrollable massive haemorrhage. Even though interruption of a smaller sinus is without any Ill effects, usually the sinuses are spacious, valve-less, thin-walled channels that carry venous blood back into a nearby large conventionally valved vein. Cerebral Venous Sinus Thrombosis is a rare and recognized form of stroke that may affect the larger dural sinuses in any age group. The eventual function of the sinuses consists in the return of venous blood, however, in the brain the dural sinuses also carry the cerebrospinal fluid (CSF).
The veins are return pathways where the blood flow is slow. Consequently, the chances and indications of thrombotic and occlusive disorders are higher than the corresponding arterial pathway. When affecting a small segment with alternative pathways, no symptoms other than discomfort, oedema, tiredness or heaviness of the affected part, and pain are features. Thrombotic piles or haemorrhoids are an example of visceral affliction in such a condition. When longer segments are affected, it is called venous thrombosis. Deep vein thrombosis typically happens in the deeply situated intramuscular veins of the lower limbs. A large majority go unnoticed and the condition becomes symptomatic with pain and swelling of the affected limb when a major vein is affected. The classic signs of DVT are leg swelling, pain to deep pressure over the calf, and pain in the calf when the foot is dorsiflexed (i.e., Homan's sign). Unfortunately, fewer than 50% of patients with a documented DVT have the classic findings on clinical examination. Tenderness, tight limbs, and reddish discolouration occur in severe cases.
Intravascular thrombosis does not occur normally, as the balancing act of the heparin-antithrombin III system helps in preventing this substantially. Other factors potentiate the tendency and these are usually inherited conditions, though more stress is there to prevent the acquired and preventable ones. The primary causes are seldom heard, and are as follows:
Factor V Leiden (the most common).
Prothrombin gene mutation.
Deficiencies of natural proteins that prevent clotting (such as antithrombin, protein C, and protein S).
Elevated levels of homocysteine.
Elevated levels of fibrinogen or dysfunctional fibrinogen (dysfibrinogenemia).
Elevated levels of factor VIII (still being investigated as an inherited condition) and other factors including factor IX and XI.
Abnormal fibrinolytic system, including hypoplasminogenemia, dysplasminogenemia, and elevation in levels of plasminogen activator inhibitor (PAI-1).
Cancer and some medications used to treat cancer, such as tamoxifen, bevacizumab, thalidomide, and lenalidomide.
Recent trauma or surgery.
Central venous catheter placement.
Obesity.
Pregnancy.
Supplemental estrogen use, including oral contraceptive pills (birth control pills).
Hormone replacement therapy.
Prolonged bed rest or immobility.
Heart attack, congestive heart failure, stroke, and other illnesses lead to decreased activity.
Heparin-induced thrombocytopenia (decreased platelets in the blood due to heparin or low molecular weight heparin preparations).
Lengthy aeroplane travel is also known as "economy class syndrome".
Antiphospholipid antibody syndrome.
Previous history of deep vein thrombosis or pulmonary embolism.
Myeloproliferative disorders such as polycythemia vera or essential thrombocytosis.
Paroxysmal nocturnal hemoglobinuria.
Inflammatory bowel syndrome.
HIV/AIDS.
Nephrotic syndrome (too much protein in the urine).
The list is long and exhaustive, and it is prudent to take measures against preventable causes before the precipitation of such a situation. The next priority is the alleviation of symptoms when the condition has set in, and the diagnosis has been made. Most often proper counseling to allay the fears of impending amputation is needed and at the same time, the patient should be made to understand that a long time is required for treatment.
Usually, patients present with features that are consistent with symptoms and signs of deep vein thrombosis. Treatment is conventionally conservative with an agent which prevents intravascular coagulation and contains the disease. The main goal is to prevent a buildup of clots on the already formed one. Symptomatic management is important as the symptoms and signs often appear to be aggressive. To the patient, and near kin of the patient, the appearance may be so bad that imminent action may be warranted. In most cases, an assurance that this condition will not lead to a loss of limb works wonders. A detailed clinical history and a thorough physical examination are required next. Often this helps in establishing the relatively rarer causes of DVT. Sophisticated and target-oriented investigations may be needed in some extremely rare situations. However, investigations for the anti-phospholipid antibody syndrome increasingly need to be done to rule out the increase in the number of DVTs without a discernible cause in the Southeast Asian population.
There should be a clear understanding of the role of anticoagulants and or antiplatelet agents. The latter by their inhibitory effect on platelets prevents new clot formation in the vascular system. The initial anticoagulation should be with a low molecular weight un-fractionated heparin in adequate repeat doses so that an acceptable INR is achieved. This prevents new clot formation. Thereafter low molecular weight heparins (LMWH), any one of the many, may be continued. The anti-platelets or the direct-acting oral anticoagulants all have similar effects and are to be continued orally to prevent repeat intravascular thrombosis. There have been numerous trials to find out the best-suited agent. The Einstein trial and the Recovery trial are a couple of examples. The former is a multi-centre, open-assessed, randomized, company-sponsored trial, and the latter is an observational study. All these trials and studies are mainly directed at finding out a view of whether direct oral anticoagulants have a non-inferior role in atrial fibrillation than traditionally used agents. Next comes their role in pulmonary embolism and its prevention.
There are no clear-cut guidelines for DVT treatment. Five types of agents are used and these are unfractionated heparin, Vitamin K antagonists, low molecular weight heparins, antiplatelet agents, and direct-acting oral anticoagulants. The low molecular weight heparins (LMWHs) are usually single or double-dosed and have the anti-thrombin III effect almost similar to unfractionated heparin and may be used in place of unfractionated heparin and a domiciliary patient as it requires a single or, at the most, a double subcutaneous injection for administration. Fondaparinux, though clubbed as an LMWH, has a slightly different action. It binds to the an-thrombin III and this complex then neutralizes the action of factor Xa in a 300 times manner to decrease the conversion of prothrombin to thrombin and subsequently fibrinogen to fibrin. Direct oral anticoagulants (DOAC) have mainly an action on the factor substrate and oral rivaroxaban is gaining popularity after FDA approval. Oral use, less interaction with foods, and a predictable effect have made it popular. Vitamin K antagonists are the first and true anticoagulants. Coumarin derivatives are commonly used and are preferred in prosthetic valve replacement situations. The Coumarins were accidentally discovered, and they have been found to effectively block the action of 2,3 epoxy reductase reaction necessary for hepatic production of Vitamin K and consequently the essential coagulation factors, e.g., prothrombin.
These agents take some time to act and this is why unfractionated heparin is used in the intervening period to achieve an INR of > 2. One must use and fall back on heparin in acute situations. The other antiplatelet agents and the novel-acting direct oral agents are used for preventing any new intravascular or intracardiac clots. Though no INR quantitation or other laboratory tests are required, and these can be used with little ill effects, they do not ensure the prevention of thromboembolic events in prosthetic valve-replaced patients. These patients are maintained on Coumarins like Warfarin or Acenocoumarol (also known as Nicoumalone). Periodic INR is done for both monitoring and dose adjustment.
When a Doppler suggests stabilization of a venous clot, a compression stocking may be worn. First, it prevents dislodgment and migration of the stabilized clot and there is an attempt at preventing post-phlebitic incompetence of the perforators which will lead to superficial system varicosity with attendant symptoms and signs. The post-phlebitic syndrome is an example and chronic leg pain, swelling, and ulceration. Early prevention of this situation is required. This condition often makes the patient think about the cure of the disease and as symptoms may be similar, one is not sure of the effectiveness of the treatment given. Experience tells one to be frank and counsel the patient about the possibility of the development of a post-phlebitic varicosity of the superficial venous system. As no operative solution is available, patients are condemned to a chronic condition for the rest of life.
Venous thrombectomy is a rarely performed operation in recurrent deep vein thrombosis involving large veins. The intervention may be needed for the severe state of phlegmasia caerulea dolens. Even in a post-delivery state of phlegmasia alba dolens, an expectant attitude with anticoagulants is usual. However, with an established cause of hypercoagulability and recurrent deep vein thrombosis affecting the larger veins, this operation may be done. An IVC filter is placed at the same time.
Trans-catheter venous clot extraction is becoming popular nowadays. This can be a manual extraction against a mechanically operated continuous thrombolysis and aspiration. Some companies have come up with devices after the access of a large axial vein and placement of an 8 or 9 F catheter at the appropriate site is attached to the appliance. The device, though operator-driven, can do the thrombolysis and aspiration at the same time. As a precaution, a retrievable umbrella is always positioned upstream to prevent pulmonary embolism. Any catheter-driven procedure or otherwise on the venous systems is carried out only when the chances of pulmonary embolism are very high. One has to remember that a large embolus can cause right heart failure and death. Smaller emboli burden leads to repeated attacks of chest pain and shortness of breath, and ultimately lung destruction may reach a point of no return. These trans-catheter procedures are minimally invasive and are successful in 60% of situations. Prior placement of a retrievable umbrella in a large central vein is always a necessity for both reductions of the embolic load and sudden massive pulmonary embolism. An early intervention theoretically reduces the chances of development of post-phlebitic varicosity and may be done in those who can afford it. Stents to maintain venous patency where needed are indicated. Recanalization of the returning venous pathway, relief from debilitating symptoms, minimization of development of chronicity, and prevention of development of pulmonary embolism of any form are the goals of management.
Varicosity means a serpiginous elongation and tortuosity of the draining veins. It is visible and symptomatic when it affects the superficial lower limb veins. Visceral veins of the oesophagus and other organs may be affected in certain conditions where there is an increase in pressure or obstruction in the drainage pathway. When submucosal, the varicose dilatations of the venous radicles may rupture leading to torrential hemorrhage. Usually, obesity, work or lifestyle where there is a long sedentary period, pregnancy, portal hypertension, and pelvic tumours compressing the main draining veins are the common causes of this condition. Varicosity affecting the lower limb superficial venous system is quite common and usually, no cause is found. A genetic predisposition and gradual weakening of the venous valves may be responsible. The Klippel-Trenaunay syndrome is a rare genetic disorder where there is a triad of vascular malformations and or varicose veins with both soft tissue and bone architectural anomalies. The patients are often brought to a Vascular surgeon with the hope of an operative cure but other than laser ablation of vascular stains and minor varicosities, not much can be done. The gender of female heritage is associated with a higher preponderance for this condition. One explanation is a pregnancy where the enlarging uterus compresses the main draining veins. Whether other causes like an inherent weakness of the venous wall or the valves a factor cannot be ruled out. Old age and weakness of venous valves contribute to the development of varicose dilatations, however, serpiginous elongation can only be explained if there is a simultaneous increase in the drainage pressure. The existing venous channels elongate to compensate for accommodating the increased amount of blood first then the dilatations occur. Obesity and a sedentary lifestyle deprive an individual of the inherent tone of a structure and are thus a factor. A thorough clinical and physical examination is necessary to find out the state of the disease. The objective structured clinical examination guideline (OSCE) should be followed when indicated and it has the added advantage of unfurling an arterial disease in a case. The examination should be started with a detailed inspection of the affected limb. Proper exposure of the whole body is ideal, but due to convenience and lack of time, often an examination that involves minimal exposure and the examiner's choice, a provisional diagnosis is made. This may be error-prone and is dependent on the examiner's experience. Chances of missing or omission in an odd case cannot be ruled out. The structured examination system is stepwise and designed to unearth hidden problems. The examination should always be preceded by a detailed history and the role of diabetes and smoking in peripheral arterial disease has to be emphasized. Inspection is mandatory and comparing bilaterally symmetrical limbs often helps in establishing distinct color changes. Visually obvious swelling and the presence of blisters alert the physician of a possible vascular compromise. The prominence of serpiginous and subcutaneous channels tells the physician of varicosity, but even then the changed direction of blood flow often is an indication of the site and nature of obstruction to venous drainage. Palpatory confirmation of the presence of peripheral pulses is necessary and there is no harm in not appreciating a Popliteal pulse due to difficulties. The brisk nailbed return, satisfactory tissue turgor, and good colour often are indicative of adequate circulation. Brodie-Trendelenburg percussion test, named, both after Benjamin Collins Brodie and Friedrich Trendelenburg, helps in determining the level of perforator incompetence in superficial varicosity affecting the great saphenous system. The classical Brodie-Trendelenberg test. The Brodie-Trendelenburg test was primarily designed to find competence at the saphenofemoral junction. The variations of the test are later additions.
Anatomical dissection of the lower limb shows around 55-75 communicating perforators. For clinical ease, these have been grouped as ankle, calf, and below-knee perforators. Of these again there are 3 ankle (5, 10, and 15 cm from the ankle joint), 2 calf, and 1 below-knee perforator having clinical significance. The thigh perforators of significance are the upper thigh and lower thigh ones. A similar test with multiple tourniquets circumferentially tied to occlude the superficial system only may be done to locate the level of perforator incompetence. In that situation also the test is performed with the subject lying down and standing. The tourniquets are successively removed. The release is somewhat below the level of a presumed group of perforators. Refilling of the superficial system of veins happens from the deeper system in a rostral direction the moment incompetence at the perforator is encountered. If the valves in the superficial system are leaking as well, then the filling of the superficial system happens in both directions up to the incompetent segment of veins.
There is another test called the Perthes test which tells about the competence of the deep venous system. Here the superficial veins of the affected limb are rendered inoperative by an elastic bandage and then the individual is asked to walk for at least 5 minutes. The subject complains of deep-seated pain in the calf if the deep venous system is not capable of draining the blood. In the simple modern variation, the long saphenous vein is occluded at the top where it joins the femoral vein. The same results occur and these tests are a must before any interruptive procedure.
So in varicose veins, the Brodie-Trendelenburg test and the Perthes test both have immense clinical value for diagnosis and treatment and one can proceed once a corroborative Doppler study is done.
Venous ulcers are typical, shallow, and with irregular margins. Venous stasis and poor circulation due to the damaged venous valves in the proximity are considered the usual causes. Ache and characteristic tiredness of the affected limb are the usual symptoms. Elevation, compression, and wound care are the mainstay of treatment. Graduated compression with stockings with a protective dressing gives the best results and though time takes most of these ulcers to heal completely.
Localized cellulitis followed by lipodermatosclerosis is often seen. The best treatment is a conservative change in the lifestyle, leg elevation, graduated compression stockings, and exercises to increase muscle tone.
Venous gangrene is rare nowadays and most often there is a deep-seated malignancy. Often the vascular surgeon is c requested to close a venous offshoot drainage in a side-to-side distal A-V fistula for dialysis access. Micro-embolism and poor circulation are implicated here.
Management aims to correct obesity, sedentary lifestyle, and coagulation issues initially. Sophisticated interventional methods need employment in advanced situations only. The first step should be assurance and counselling. The individual must understand the value of changing their lifestyle. An increase in the muscular tone enhances venous return. Also, bodily shape is important in psychological well-being. The foot raised while resting, or even during a sedentary job, lowers the pressure in the affected veins. Application of a graduated pressure stocking or at the least a crepe bandage alleviates the aching associated with increased venous pressure. By compressing the incompetent perforators, pressure application reduces the load on the superficial system and induces the deep system to work more with the help of an improved muscular tone. The damaged valves are prone to clot formation and hence even in varicosity, with no apparent evidence of increased coagulability, a low-dose anticoagulant is prescribed.
An operation is indicated only when the conservative measures fail. It must be understood that psychologically the patient is against any major operative intervention. Also, the physician needs to know that when multiple operations are there for a pathology, none is satisfactory, and each method has an insurmountable flaw. Surgical stripping and ligation is a time-honoured and still practised surgical method of managing varicosity. However, one should remember that the management is highly specific, and it is important to realize a patient’s individualistic needs. One must additionally understand that for a successful surgery, there must be unsightly superficial lower limb varicosity, Doppler evidence of pooling of blood, and incompetence of perforators. It is mandatory to be aware of the course of both the long and short saphenous systems and knowledge of the saphenofemoral and/or the saphenopopliteal junctions. The number of venous radicles draining into these regions and the necessity of ligating these not only tells on a long-term result but also is responsible for preventing recurrence. The actual operation consists of a junctional flush ligation with exposure of the dilated proximal or distal saphenous vein. The introduction of the specially designed stripper not only shears off the offending and pathological vein but also takes care of the perforating communication with the deep venous system. It hardly matters whether the direction of introduction of the stripper is from above or below but being introduced from below upwards definitely avoids injury to the long saphenous nerve. The Rindfleisch-Friedel procedure of the early 1900s was extremely invasive and only has a historic value now. There is a documented Linton's operation (introduced in the 1930s) for varicose veins. However, because of the long length of the incision along the whole pathologic length of the vein, it is seldom practised. The practice of varicose vein surgery mainly was centred around the unsightly long and short saphenous systems and the evolution from a major invasive approach to a minimally interventional procedure is a testament to the understanding of the underlying pathology and the realization that the same things can be achieved by these methods. Classically short 2 to 3 cm long incisions are needed, in the groin in GSV flush ligation and the Popliteal fossa when a sapheno-popliteal ligation is required. Still, shorter incisions at the knee region and ankle region are required for dilated varicose vein localization. It is necessary to understand the nature and evolution of the various venous strippers. The Mayo stripper was extraluminal while the Babcock stripper was intraluminal. A recent attitude is the use of a self-fabricated slightly stiff intraluminal stripper for the extirpation of the pathological vein after its localization. The perforation-invagination (PIN) technique and the use of an intraluminal Keller stripping device are still in vogue. In the districts and small health units of mofussil towns a modified automobile (commonly a scooter or a motorcycle) accelerator or clutch-wire has been observed to be used as vein strippers.
Doppler evaluation of the varicosity of a limb and localization of a dilated pathological vein is important. The surgeon should best know how to localize dilated veins and how they should look collapsed when a minimal laser or thermal treatment of varicosity is being done. Doppler examination is necessary also to find out the degree of vascular reflux, at the groin or popliteal regions. Identification of veins in an ultrasound examination should stress the following points:
Large veins and the deep arteries usually lie side by side and the color away from the transducer is blue while toward the transducer is red.
Veins are larger and circular.
Veins are easily collapsible and often the weight of the transducer pencil is enough to lead to a luminal obliteration.
The Vascular flow is usually streamlined and unidirectional. Regurgitant flow reversal usually indicates right heart failure.
There are numerous unidirectional valves along a vein course.
The recent attitude is to set up a vein clinic in a hospital and then categorize the varicose vein patients in a manner according to the method of management required. Most of the time a less invasive conservative method will be required. Less invasive procedures involve laser, thermal or radio-frequency obliteration of dilated and pathological veins. Injection sclerotherapy with foam is also there. Each method has its advantages and disadvantages and the results are operator-dependent. Vein hook phlebectomy may be practised under local anaesthesia in the clinic. An ambulatory phlebectomy, common in dermatological practice, rids the patient of superficial varicose unsightly lesions. Surgery should be reserved for those situations where getting rid of the troublesome superficial limb varicosity becomes mandatory. But one should remember at the same time that the slightest doubt about the integrity of the deep system negates the need for any operation on the superficial system.
Endoscopic sclerotherapy is reserved for oesophagal varices mainly and rarely in troublesome anorectal varicose lesions. This form of therapy provides some relief and can prevent troublesome bleeding. Such therapy inaccessible to hollow visceral varicosity at least provides the physician some time to tackle the primary pathology.
These two are the major areas of venous diseases that require knowledge and intervention by the physician/physicians. It should be remembered that DVT requires judicial use of proper anti-coagulants at the right times and knowledge about venous Doppler. Seldom, if ever, an operation is needed. Superficial thrombophlebitis is often a harbinger of other conditions, especially when there are recurrent attacks. This condition can be easily controlled.
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