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Commonest cause of A-V fistulae is – (AI 88)

a) Congenital b) Traumatic

c) Surgical creation d) Tumour erosion


Congenital A-V fistulas in the thigh will be associated with all except – (PGI 89)

a)Increased cardiac output

b)Increased skin tempreture

c)Gigantism of limb

d)Superficial venous engorgement


Continuous murmur is not found in- (AIIMS 89)


b)Systemic A-V fistula

c)Rupture of sinus of valsalva

d)Double outlet right ventricle


AV fistula leads to all except – (AIIMS 98)

a)Sinus tachycardia

b)Increased preload

c)Cardiac arrythm ias

d)Increased cardiac output


AV fistula causes – (PGI 98)

a) dec Diastolic b) inc Venous return

c) dec Venous congestion d) inc Systolic fillin


Nicoladoni branham sign is – (PG198)

a)Compression cause bradycardia

b)Compression cause tachycardia


d)Systolic filling


True regarding AV fistula is – (PGI 02)

a)Leads to cardiac failure

b)Causes local gigantism

c)Can cause ulcers

d)Cause excess bleeding on injury

e)Closes spontaneously


Complications arising out of A – V fistula done for renal failure include the following EXCEPT –

a)Infection (Jipmer 03)


c)High output cardiac failure

d)Necrosis of the distal part


Ans. is ‘d’ i.e., Necrosis of the distal part [Ref Sabiston 161"/e p.1456; Love & Bailey 246/e p.950 ; 23"//e p.23]


Pulsating varicose vein in a young adult is due to-

a)Arteriovenous fistula (AIIMS 92)

b)Sapheno femoral incompetence

c)Deep vein thrombosis

d)Abdominal tumour


In Osler Weber Rendu syndrome A.V. fistulas occur.


The clinical features depend on the location and size of the fistula. Frequently, a pulsatile mass is palpable, and a thrill and bruit lasting throughout systole and diastole are present over the fistula. With longstanding fistulas, clinical manifestations of chronic venous insufficiency, including peripheral edema; large, tortuous varicose veins; and stasis pigmentation become apparent because of the high venous pressure. Evidence of ischemia may occur in the distal portion of the extremity. Skin temperature is higher over the arteriovenous fistula. Large arteriovenous fistulas may result in an increased cardiac output with consequent cardiomegaly and high-output heart failure.


The diagnosis is often evident from the physical examination. Compression of a large arteriovenous fistula may cause reflex slowing of the heart rate ( Nicoladoni -Branham sign).


Physiological effect

The combination of an uncontrolled leak from the high-pressure arterial system and an enhanced venous return and venous pressure results in an increase in pulse rate and cardiac output. The pulse pressure is high if there is a large and persistent shunt. Left ventricular enlargement and, later, cardiac failure occur. A congenital fistula in the young may cause overgrowth of a limb. In the leg, indolent ulcers may result from relative ischaemia below the short circuit.

Clinical signs

Clinically, a pulsatile swelling may be present if the lesion is relatively superficial. On palpation, a thrill is detected and auscultation reveals a buzzing continuous bruit. Dilated veins may be seen, in which there is a rapid blood flow. Pressure on the artery proximal to the fistula causes the swelling to diminish in size, the thrill and bruit to cease, the pulse rate to fall [known variously as Nicoladoni’s (1875) or Branham’s (1890) sign] and the pulse pressure to return to normal.




AV (arteriovenous) fistulas are recognized as the preferred access method. To create a fistula, a vascular surgeon joins an artery and a vein together through anastomosis. Since this bypasses the capillaries, blood flows rapidly through the fistula. One can feel this by placing one’s finger over a mature fistula. This is called feeling for "thrill" and produces a distinct ‘buzzing’ feeling over the fistula. One can also listen through a stethoscope for the sound of the blood "whooshing" through the fistula, a sound called bruit.


Fistulas are usually created in the nondominant arm and may be situated on the hand (the ‘snuffbox‘ fistula’), the forearm (usually a radiocephalic fistula, or so-called Brescia-Cimino fistula, in which the radial artery is anastomosed to the cephalic vein), or the elbow (usually a brachiocephalic fistula, where the brachial artery is anastomosed to the cephalic vein). A fistula will take a number of weeks to mature, on average perhaps 4–6 weeks. During treatment, two needles are inserted into the fistula, one to draw blood and one to return it.


The advantages of the AV fistula use are lower infection rates, because no foreign material is involved in their formation, higher blood flow rates (which translates to more effective dialysis), and a lower incidence of thrombosis. The complications are few, but if a fistula has a very high blood flow and the vasculature that supplies the rest of the limb is poor, a steal syndrome can occur, where blood entering the limb is drawn into the fistula and returned to the general circulation without entering the limb’s capillaries.


Maximum tourniquet time for the upper limb is –

a) 1/2 hour b) 1 hr (JIPMER 87)

c) 1-1/2 hrs. d) 2 hrs

e) 2-1/2 hrs


Sabiston:- Tourniquet Application:- The tourniquet is used to provide a bloodless field so that clear visualization of all structures in the operative field is obtained. Penrose drains, rolled rubber glove fingers, or commercially available tourniquets can be used on digits. Great care must be taken in using any constrictive device on digits because narrow bands cause direct injury to underlying nerves and digital vessels. With the use of an arm tourniquet, the skin beneath the cuff must be protected with several wraps of cast padding. During skin preparation, this area must be kept dry to prevent blistering of the skin under an inflated cuff over moist padding. The cuff selected needs to be as wide as the diameter of the arm. Standard pressures used are 100 to 150 mm Hg greater than systolic blood pressure. The cuff is deflated every 2 hours for 15 to 20 minutes (5 minutes of reperfusion for every 30 minutes of tourniquet time) to revascularize distal tissues and to relieve pressure on nerves locally before reinflating the cuff for more extensive procedures. Exsanguination of the extremities is performed by wrapping the extremity with a Martin’s bandage in all cases, except those involving infection or tumors. In these latter cases, because of the possibility of embolization by mechanical pressure, exsanguination by bandage wrapping needs to be avoided. Simple elevation of the extremity for a few minutes before tourniquet inflation suffices.


Bailey:- Tourniquet:- A bloodless field is essential for accurate surgery. A well-padded tourniquet above the elbow, inflated to 75 mmHg pressure over the systolic blood pressure, is usually satisfac­tory. The time should not exceed 2 hours. An Esmarch bandage or a rubber-tube exsanguinator are effective, but should be avoided for tumour or infection cases lest the pathology is spread systemically. In the finger, a tourniquet can be made by placing a sterile glove on the patient, snipping off the tip and then rolling the glove down to the base of the finger.



Thromboembolism after pelvic surgery is usually from the veins – (A189)

a) iliac b) Calf

c) Femoral d) Pelvic


An obese patient develops acute oedematous lower limb following a Pelvic surgery. Deep vein thrombosis is suspected . The most useful investigation in this case would be – (UPSC 2002)

a) Doppler imaging b) Fibrinogen uptake

c) Venography d) Plethysmography


Which of these is not a risk factor for thromboembolism – (TN 2001)

a)Myocardial infarction


c)Estrogen therapy

d)Superficial thrmbophlebitis


Most common cause of death in patients with

Burger’s disease is – (AIIMS 87)

a) Gangrena b) Pulmonary embolism

c) Myocardial infarction d) Carcinoma lung


Which of the following best responds to sympathectomy – (JIPMER 86)

a) Burger’s disease b) Hyperhydrosis

c) Raynaud’s disease d) Acrocyanosis


Intermittent claudication at the level of the hip indicates – (PGI 87)

a)Popliteal artery occlusion

b)Bilateral iliac artery occlusion

c)Common femoral occlusion

d)superficial femoral artery occlusion


The artery commonly involved in cirsoid aneurysm is – (PGI 88)

a) Occipital b) Superficial temporal

c) Internal carotid d) External carotid


Plusating tumours include all except – (PGI 88)

a)Bone sarcoma


c)Secondaries from hyper nephromas

d)Secondary from prostate


Preferred material for femoro popliteal bypass –

a) Dacron b) PTFE (PGI 89)

c) Saphenous vein d) Gortex


Prosthetic materials For bypass of the aortoiliac segment the favoured material is Dacron (Fig. 15.21a). Prostheses come in two types: woven and knitted. Woven grafts tend to leak less when first exposed to blood flow during surgery, but newer knitted prostheses may be sealed with gelatin or collagen by the manufacturer and may leak even less than their woven counterparts. In the final analysis, there is probably little to choose between any of the styles of Dacron graft; all achieve satisfactory results. For bypass in the femoropopliteal region, if autogenous long saphenous vein (or other veins such as the short saphenous or arm vein) is not available, PTFE (Fig. 15.21b) or glutaraldehyde-tanned, Dacron-supported, human umbilical vein (Fig. 15.21c) may be employed. In general, any vein used requires a diameter of at least 3.5mm. For profundaplasty, a small piece of vein may be used or, alternatively, PTFE or Dacron. Suture materials for vascular surgery are usually monofilament in nature; polypropylene has been particularly popular. In the aorta it is usual to use 2/0 or 3/0 polypropylene. In the femoral artery at the groin it is usual to use 4/0 or 5/0 polypropylene. Finer sutures, up to 7/0, may be needed further down the limb. PTFE may (alternatively) be stitched using a suture of the same material. PTFE sutures tend to cause less bleeding through stitch holes in the graft substance.




Most common cause of aneurysm of abdominal aorta is – (A196)

a) Trauma b) Atherosclerosis

c) Syphilis d) Cystic medial necrosis


The most common complication of an aortic aneurysm size 8 cm is – (Delhi, PG 96)

a) Rupture b) Intramural thrombosis

c) Embolism d) Calcification


Management of a cause of iliac artery embolism requires – (JIPMER 81, UPSC 86)


b)Injection of vasodilators

c)Hypotensive therapy



Intermittent claudicatin is caused by – (TN 89)

a)Venous occlusion

b)Arteria insufficiency

c)Nerual compression

d)Muscular dystrophy


Burger’s disease is seen in – (PGI 88)

a) Only male b) Age less than 40

c) Age more than 40 d) Smoker


In the abdomen, aneurysms of the …. commonly occur next only to the aorta …. – (PGI 88)

a)Internal iliac artery

b)External iliac artery

c)Splenic artery

d)Inferior mesentric artery


In extraperitoneal approach, to left sympathectomy the following may be injured –

a) Ureter b) Gonadal vessels

c) A+B d) IVC


Lumbar sympathectomy is indicated in – (TN 90)

a)Intermittent claudication

b)TAO with skin changes

c)Burger’s disease

d)Raynaud’s disease


Commonest site of throboangitis obliterans is –

a) Femoral artery b) Popiteal artery (A190)

c) iliac artery d) Pelvic vessels



Treatment of acute femoral embolus is- (AIIMS 91)



c)Immediate embolectomy

d)Embolectomy after 5 days bed rest


Ganglion which is spared in Lumbar sympathetomy is – (JIPMER 92)

a) Ll b) L2

c) L3 d) L4


Surgical lumbar sympathectomy may be indicated in arterial disease. Surgical or chemical (phenol injection) sympathectomy may be used to treat rest pain or other troublesome sensory symptoms in arterial disease or in causalgia. The segment of the chain including the second and third lumbar ganglia is removed: preservation of the first lumbar ganglion is said to lessen the risk of ejaculatory problems



Vessels most commonly involved in thrombo angitis obliterans – (AIIMS 92)



c)Femora popliteal

d)Arterior and Posterior tibial


Following are used in treatment of Buergers disease except – (Al 93)

a) Trental b) Anticoagulation

c) Sympathectomy d) Antiplatelets


Buerger’s disease affects all except – (PGI 01)

a) Small arteries b) Small veins

c) Medium -size arteries d) Multiparity

e) First pregnancy after 30 years


Buerger’s disease is associated with – (rGI 02)

a) smoking b) Poor nutrition

c) Alcohol d) Prolonged standing

e) Superficial thrombophlebitis


The most common cause of peripheral limb ischaemia in India is – (AIIMS NOV 05)

a) Trauma b) Altherosclerosis

c) Buerger’s disease d) Takayastu’s disease



A 45-year-old male having a long history of cigarette smoking presented with gangrene of left foot. An amputation of the left foot was done. Representative sections from the specimen revealed presence of arterial thrombus with neutrophilic infiltrate in the arterial wall. The inflammation also extended into the neighbouring veins and nerves. The most probably diagnosis is – (AIIMS 06)

a)Takayasu arteritis

b)Giant cell arteritis

c)Hypersensitivity angiitis

d)Thromboangiitis obliterans


Ans. is ‘d’ i.e., Thromboangiitis obliterans [Ref: Hariison 166/e p. 1487; Schwartz 86/e p. 792]


THROMBOANGIITIS OBLITERANS :- Thromboangiitis obliterans (Buerger’s disease) is an inflammatory occlusive vascular disorder involving small and medium-sized arteries and veins in the distal upper and lower extremities. Cerebral, visceral, and coronary vessels may be affected rarely. This disorder develops most frequently in men <40 years. The prevalence is higher in Asians and individuals of eastern European descent. While the cause of thromboangiitis obliterans is not known, there is a definite relationship to cigarette smoking in patients with this disorder. In the initial stages of thromboangiitis obliterans, polymorphonuclear leukocytes infiltrate the walls of the small and medium-sized arteries and veins. The internal elastic lamina is preserved, and a cellular, inflammatory, thrombus develops in the vascular lumen. As the disease progresses, mononuclear cells, fibroblasts, and giant cells replace the neutrophils. Later stages are characterized by perivascular fibrosis, organized thrombus, and recanalization. The clinical features of thromboangiitis obliterans often include a triad of claudication of the affected extremity, Raynaud’s phenomenon, and migratory superficial vein thrombophlebitis. Claudication is usually confined to the calves and feet or the forearms and hands because this disorder primarily affects distal vessels. In the presence of severe digital ischemia, trophic nail changes, painful ulcerations, and gangrene may develop at the tips of the fingers or toes. The physical examination shows normal brachial and popliteal pulses but reduced or absent radial, ulnar, and/or tibial pulses. Arteriography is helpful in making the diagnosis. Smooth, tapering segmental lesions in the distal vessels are characteristic, as are collateral vessels at sites of vascular occlusion. Proximal atherosclerotic disease is usually absent. The diagnosis can be confirmed by excisional biopsy and pathologic examination of an involved vessel. There is no specific treatment except abstention from tobacco. The prognosis is worse in individuals who continue to smoke, but results are discouraging even in those who do stop smoking. Arterial bypass of the larger vessels may be used in selected instances, as well as local debridement, depending on the symptoms and severity of ischemia. Antibiotics may be useful; anticoagulants and glucocorticoids are not helpful. If these measures fail, amputation may be required.


Lumbar sympathectomy:- Operative method. Using a transverse loin incision, an extraperitoneal approach is used in which the colon and peritoneum, to which the ureter clings, are stripped medially so as to expose the inner border of the psoas muscle .The sympathetic trunk lies on the sides of the bodies of the lumbar vertebrae; on the right side it is overlapped by the vena cava. Lumbar veins are apt to cross the trunk superficially. The sympathetic trunk is divided on the side of the body of the fourth lumbar vertebra. It is then traced upwards to be divided above the large second lumbar ganglion, which is easily recognised by the number of white rami which join it. Care should be taken not to mistake small lymph nodes, lymphatics, the genitofemoral nerve or the occasional tendinous strip of the psoas minor for the sympathetic chain. It is possible to perform the operation via an endoscope after the creation of a suitably expanded retroperitoneal tissue plane. Along with a decline in the recognised indications for sympathectomy there has been a move away from the operative approach in favour of the less hazardous chemical (phenol) sympathectomy.

Chemical method. This is contraindicated in patients taking anticoagulants. Under radiographic fluoroscopic control, with the patient in the lateral position, local anaesthetic is injected. A long spinal needle is then inserted to seek the side of the vertebral body and to pass alongside it to reach the lumbar sympathetic chain. After confirming the needle position by injection of contrast agent, approximately 5 ml of phenol in water is injected. This is usually done at two sites: beside the bodies of the second and fourth lumbar vertebrae. Great care is needed to avoid penetrating the aorta, cava or ureter; the plunger of the syringe must always be drawn back before injection to exclude the presence of blood.


In a lumbar sympathectomy the sympathetic chain in its usual position is likely to confused with the – (pal 81, AIIMS 80, 82)


a) Ureter b) Psoas minor

c) Genitofemoral nerve d) Ilioinguinal nerve e) Lymphatics


The commonest cause of aneurysm formation

is – (JIPMER 80, Delhi 89)

a) Gun shot injury b) Syphilis

c) Congenital factors d) Atherosclerosis


Bullet wounds near major blood vessels should

be explored only if- (PGI 81, AMC 85)

a)The extremity is cold

b)The fingers or toes are paralysed

c)The pulse is weakened

d)There in no pulse

e)In all cases regardiess of physical findings


A knitted Dacron artery graft (PGI 99, AIIMS 84)

a)Is not porous

b)Is eventually dissolived by tissue reaction

c)Never gets infected

d)Can be easily incised and the opening resutured


The sequence of symptoms in pulmonary embolism is – (JIPMER 89, DNB 90)

a)Fever, pain, dyspnoea

b)Fever, dyspnoea

c)Dysponea, pain, haemoptysis

d)Dysponea, cough, purulent sputum


A useful through temporary improvement in a patient’s ischaemic foot can be attained by giving intravenously – (PGI 79, Delhi 84)

a) 10% Mannitol b) 10% Dextrose

c) Dextran 40 d) Dextran 100


Diabetic gangrene is due to – (Kerala 94)


b)Increased blood glucose

c)Altered defence by host and neuropathy

d)All of the above


All are true about Embolic Arterial occlusion except-

a)No previous history (JIPMER 95)

b)Muscles are unaffected

c)Pulse is absent

d)Anaesthesia is present


All are true about Raynauds phenomena except-

a)Exposure to cold aggravate (Kerala 95)

b)Spasm of vessels

c)More common is females

d)Atherosclerosis of vessels


The commonest site of iodgement of a pulmonary embolus is in the territory at – (UPSC 95)

a) Rt. lower lobe b) Rt. upper lobe

c) Lt. lower lobe d) Lt. upper lobe


Kaposi sarcoma is commonly seen in – (AMU 95)

a) Upper limbs b) Lower limbs

c) Head and Neck d) Trunk


Which of the following causes meximum bleeding-

a)Partial arterial severing (PGI 95)

b)Complete arterial severing

c)Artery caught between fractured ends of bones

d)Intimal tear


In a 40 years old male thrombus in the common femoral artery is because of – (AIIMS 97)


b)Thrombangits obliterans

c)Reynauds disease

d)Abdominal mass


One of the following is not indicated for arterial

leg ulcer – (PGI 96)

a) Debridement b) Elevation of limb

c) Head end of bed is raised d) Low dose aspirin


Not used as graft material in peripheral vascular disease – (PGI 97)

a) Dacron graft b) Vein

c) PTFE d) PVC


The commonest cause of arterio-venous fistula is-

a)Penetrating injury (MP 97)


c)Neoplasmic invasion of an artery and adjacent vein

d)Aneurysm of the artery eroding a vein


AV fistula leads to all except – (AIIMS 98)

a)Sinus tachycardia

b)Increased preload

c)Cardiac arrythm ias

d)Increased cardiac output


Commonest peripheral aneurysm is – (SCTIMS 98) a) Popliteal b) Femoral

c) Carotid d) iliac


Popliteal aneurysm-All are true except-

a)Presents as a swelling (SCTIMS 98) behind the knee

b)Presents with symptoms due to complication

c)Surgery is indicated in case of complication

d)Uncommon among peripheral aneurysm


Graft used in infra inguinal by pass is 4Jipmer 2K)

a) PTFE b) Dacron

c) Autologous vein d) Autologous artery


True about Erythrocyanosis except — (A.P 96)

a)Affects young girls

b)Cold peripheries

c)Palpable pulses

d)Ulceration & gangrene of fingers


Diabetic gangrene is due to AfE (TN 86)



c)Peripheral neuritis

d)Increased sugar in blood


Pseudo aneurysms are most commonly due- (Jipmer a) Atherosclerosis b) Trauma 93)

c) Congenital deficiency d) Infections


Bilateral pulseless disease in upper limbs in caused

by- (PGI 97)

a) Aortoarteritis b) Coarctation of aorta

c) Fibromuscular dysplsia d) Buerger’s disease


Abdominal Aneurysm is characterized by all except – (PGI 2000)

a)Elective surgery complication should be < 5%

b)Emergency surgery complication < 10%

c)Rarely asymptomatic before rupture

d)Bigger the size it is more prone to rupture


Dissection of which artery is seen in pregnancy –

a) Carotid artery b) Aorta (PGI 2000)

c) Coronary A d) Femoral artery


Peripheral arterial occlusion (Sudden onset) is characterized all except – (PGI 2000)

a) Paresthesia b) Rubor

c) Pallor d) Pain


In which one of the following conditions Dactylitis CANNOT be seen- (UPSC 02)

a) Sickle – cell anemia b) Beta thalassemia

c) Congenital syphilis d) Tuberculosis

e) Sarcoidosis


Not seen in sudden onset peripheral arterial occlusion – (Kerala 04)

a) Pain b) Rubor

c) Pallor d) Anesthesia


Drug used for Burger’s disease – (MAHE 05)

a) Xanthinol micotinate b) Propranolol

c) GTN d) All the above


Pseudoarterial aneurysm in drug abuser’s seen in -a) Radial b) Brachial (PGI June 05)

c) Femoral d) Carotid

e) Pedal


Syndrome of internal iliac artery occlusion manifested by – (PGI June 05)

a)Pain in calf

b)Absent pulse at the dorsalis pedis artery

c)Intermittent claudication



The most common cause of peripheral limb ischaemia in India is – (AIIMS NOV 05)

a) Trauma b) Altherosclerosis

c) Buerger’s disease d) Takayastu’s disease


Lumbar sympathectomy is of value in the management of- (AI 05)

a)Intermittent claudication

b)Distal ischaemia affecting the skin of the toes

c)Arteriovenous Fistula

d)Back pain


The most common cause of acquired arteriovenous fistuala is – (Al 06)

a) Bacterial infection b) Fungal infection

c) Blunt trauma d) Penetrating trauma


Etiopathogenesis of diabetic foot include the following except- (UPSC 07)






Fogarty’s catheter is used for – (UPSC 07)

a)Drainage of urinary bladder

b)Parenteral hyperalimentation

c)Removal of embolus from blood vessels

d)Ureteric catheterisation


Pseudoaneurysms in IV drug abusesrs seen commonly in – (PGI June 07)

a)Brachial artery

b)Radial artery

c)Femoral artery


Treatment of femoral artery naeurysm –

a)Ultrasound guided compression of the neck of aneurysm (PGI June 07)

b)Thrombin injection

c)Bypass graft repair



Venous Disorders:-


Bailey & Love,Gray, Sabiston




Perforators are not present at – (AIIMS Nov 07)

a) Ankle b) Medial calf

c) Distal to calf d) Below inguinal ligament



The superficial veins are in the subcutaneous connective tissue and are interconnected with and ultimately drain into the deep veins. The superficial veins form two major channels-the great saphenous vein and the small saphenous vein. Both veins originate from a dorsal venous arch in the foot:


the great saphenous vein originates from the medial side of the dorsal venous arch, and then ascends up the medial side of the leg, knee, and thigh to connect with the femoral vein just inferior to the inguinal ligament;

the small saphenous vein originates from the lateral side of the dorsal venous arch, ascends up the posterior surface of the leg, and then penetrates deep fascia to join the popliteal vein posterior to the knee; proximal to the knee, the popliteal vein becomes the femoral vein.

The superficial and deep veins join at a number of points. The short saphenous vein terminates at the saphenopopliteal junction (SPJ) and the long saphenous vein at the saphenofemoral junction (SFJ) in the groin. Here the flow in the superficial veins joins that in the deep veins. There is, in addition, a number of places in the calf and thigh where flow in the superficial veins may also join that in the deep veins. These is the ankle, calf and thigh communicating or perforating veins (Fig. 16.3). The names of these veins come from their course from the superficial to the deep venous system in which they perforate the deep fascia of the leg. Near the ankle are the Cockett perforating veins, near the knee the Boyd perforators and in the thigh the Hunterian perforating vein. All veins in the upper and lower limbs contain valves every few centimetres which ensure that blood flows towards the heart.


Multiple perforator veins traverse the deep fascia to connect the superficial and deep venous systems. Clinically important perforator veins are the Cockett and Boyd perforators. The Cockett perforator veins drain the medial lower leg and are relatively constant. They connect the posterior arch vein (a tributary to the GSV) and the posterior tibial vein. They may become varicose or incompetent in venous insufficiency states. The Boyd perforator veins connect the GSV to the deep veins approximately 10 cm below the knee and 1 to 2 cm medial to the tibia.


Earliest sign of deep vein thrombosis is(AIIMS 87) a) Calf tenderness b) Rise in temperature c) Swelling of calf muscle d) Homan’s sign


Injection sclerotherapy for varicose veins is by using – (PGI 88)

a) Phenol b) Absolute alcohol

c) 70% alcohol d) Ethanolamine oleate


Sclerotherapy acts by destroying the venous endothelium. Sclerosing agents include hypertonic saline, sodium tetradecyl sulfate, and polidocanol. Concentrations of 11.7 to 23.4% hypertonic saline, 0.125 to 0.250% sodium tetradecyl sulfate, and 0.5% polidocanol are used for telangiectasias. Larger varicose veins require higher concentrations: 23.4% hypertonic saline, 0.50 to 1% sodium tetradecyl sulfate, and 0.75 to 1.0% polidocanol.83 Elastic bandages are wrapped around the leg after injection and worn continuously for 3 to 5 days to produce apposition of the inflamed vein walls and prevent thrombus formation. After the bandages are removed, elastic compression stockings should be worn for a minimum of 2 weeks. Complications from sclerotherapy include allergic reaction, pigmentation, thrombophlebitis, DVT, and possible skin necrosis.


White leg is due to – (TN 90)

a)Femoral vein thrombosis and lymphatic obstruction

b)Deep femoral vein thrombosis

c)Lymphatic obstruction only

d)None of the above


All of the following are seen in deep vein thrombosis except – (Al 90)

a) Pain b) Discolouration

c) Swelling d) Claudication


The following is the commonest site for venous ulcer- (A IIMS 91)

a)Instep of foot

b)Lower 1/3 leg and ankle

c)Lower 2/3 of leg

d)middle 1/3 of leg


The most important perforator of the Lower limb is between – (ALL INDIA 92 )

a)Long saphenous and posterior tibial vein

b)Short saphenous and posterior tibial vein

c)Short saphenous and popliteal vein

d)Long saphenous and femoral vein


Best method for diagnosis of Deep vein thromvosis is – (JIPMER 92)

a)Doppler examination


c)Contrast phlebography

d)1131 Fibrinogen studies


Commonest complication varicose vein stripping is-

a) Thrombo embolism b) Hemorrhage

c) Ecchymosis d) Infection


Investigation of choice for diagnosis of deep vein thrombosis – (AIIMS 92)

a) Venogram b) Doppler

c) Isotope scan d) Homans sign


Pulsating varicose vein in ayoung adult is due to-

a)Arteriovenous fistula (AIIMS 92)

b)Sapheno femoral incompetence

c)Deep vein thrombosis

d)Abdominal tumour


Which is not used in treatment of Superficial venous thrombosis – (AIIMS 92)

a)Immediate anticoagulation

b)Rest and elevation


d)Treat assosiated malignancy


Most common complication of varicose vein stripping is – (JIPMER 78, AIMS 79,92)

a) Infection b) Haemorrhage

c) Ecchymosis d) Thrombo embolism


An operated case of varicose veins has a recurrence rate of – (AIIMS 80, AP 89)

a) About 10% b) About 25%

c) About 50% d) Over 60%


What is acceptable in the management of femoral vein thrombosis – (AIIMS81, PGI 86)

a)Bed rest and spiral elastic bandages

b)A venogram



e)A mobin udin umbrella inserted into the vein


Operative Venous Thrombectomy



In patients with acute iliofemoral DVT, surgical therapy is generally reserved for patients who worsen with anticoagulation therapy and those with phlegmasia cerulea dolens and impending venous gangrene. If the patient has phlegmasia cerulea dolens, a fasciotomy of the calf compartments is first performed. In iliofemoral DVT, a longitudinal venotomy is made in the common femoral vein and a venous balloon embolectomy catheter is passed through the thrombus into the IVC and pulled back several times until no further thrombus can be extracted. The distal thrombus in the leg is removed by manual pressure beginning in the foot




Operations for varicose veins are best accomplished by – (PGI 81, AIIMS 84, 86)


b)Multiple subcutaneos ligatures

c)Subfascial ligatures

d)Division and ligation at the superficial venous system


A 60-years old male has been operated for carcinoma of caecum and right hemicolectomyhas been done. On the fourth post – oprative day, the patient develops fever and pain in the legs. The most important clinical entity one should lookfor is – (UPSC 96)

a)Urinary tract infection

b)Intravenous line infection

c)Chest infection

d)Deep vein thrombosis


All of following may be predisposing factors for deep vein thrombosis except – (AIIMS 95)

a) Oral contrceptives b) Nephrotic syndrome

c) Sickle cell anemia d) Thrombocytosis


The duration of heparin therapy in deep vein thrombosis is – (CUPGEE 96)

a) 7 – 10 days b) 15-20 days

c) 3-4 days d) 1 month


Cocket & Dodd’s operation is for (AP 96)

a)Saphenofemoral flush ligation

b)Subfascial ligation

c)Deep vein thrombosis

d)Diabetic foot


In obstruction of inferior vena cava there is -(A197)

a)Prominent thoraco epigastric vein

b)Caput medusa


d)Esophageal varices


Most accurate & non invasive method for diagnosing deep vein thrombosis – (JIPMER 98)

a)Doppler duplex


c)Radioactive labelled fibrinogen



Most common site for venous thrombosis -(JIPMER a) Popliteal vein b) Soleal vein 98)

c) Femoral vein d) Internal iliac vein


Deep vein thrombosis is caused by all except –

a)Lower limb trauma (AIIMS 98)

b)Hip and pelvic surgery

c)Subungual melanoma

d)Cushing’s syndrome


Which of the following test is used to detect perforator incompetence in varicose- (JIPMER 2K)

a) Trendelenberg test b) Fegan’s test- (localise)

c) Morissey’s test d) Homan’s test













The deficiency of all of the following factors increases the incidence of thrombus formation except – (UPSC 2K)

a) Lipoprotein A b) Protein – C

c) Anti – thrombin III d) Protein – S


The most common vein to get thrombosed is the – (AIIMS 99)

a) Long saphenous b) Short saphenous

c) Both d) Posterior tibial


Brodie -Trendlenburg test demonstrates-

a)Mid – thigh perforation (ORRISA 98)

b)Deep vein thrombosis

c)Sapheno — femoral incompetence

d)Calf perforators


An intern was doing saphenous cannulation for a burns patient. Then the patient developed sudden onset of pain along the medial border of the correponding foot. Which nerve must have been accidentally ligated – (AIIMS 2K)

a) Sural nerve b) Deep peroneal nerve

c) Saphenous nerve d) Genicular nerve


In DVT all are seen except (CMC 2001)

a)High fever

b)Increased temperature at site




Low Grade Pyrexia is seen not High.


An obese patient develops acute oedematous lower limb following a Pelvic surgery. Deep vein thrombosis is suspected . The most useful investigation in this case would be – (UPSC 2002)

a) Doppler imaging b) Fibrinogen uptake

c) Venography d) Plethysmography


In a patient on anticoagulant therapy, the INR is maintained at – (UPSC 2002)

a)1.5 to 2.5 times the normal

b)2.5 to 3.5 times the normal

c)3.5 to 4.5 times the normal

d)4.5 to 5.5 times the normal


DVT, investigation of choice is – (PGI 97)

a) Doppler b) Plethysmography

c) Venography d) X-ray


In diabetic ulcer, following site is involved-(PGI 97)

a) Heel b) Head of metatarsal

c) Webs d) Tips of toes


For prophylaxis of deep vein thrombosis used is –

a)Warfarin (PGI 97)


c)Pneumatic shock garment

d)Graded stocking


Effective methods of VTE prophylaxis involve the use of one or more pharmacologic or mechanical modalities. Currently available pharmacologic agents include low-dose UFH, LMWH, synthetic pentasaccharides, and vitamin K antagonists. Mechanical methods include intermittent pneumatic compression (IPC) and graduated compression stockings. Aspirin therapy alone is notadequate for DVT prophylaxis. These prophylaxis methods vary with regard to their efficacy, and the 2008 ACCP Clinical Practice Guidelines stratify their uses according to the patient’s level of risk.









Thromboembolism Risk and Recommended Thromboprophylaxis in Surgical Patients




Level of Risk Approximate DVT Risk without Thromboprophylaxis (%) Suggested Thromboprophylaxis Options

Low risk:- <10 No specific thromboprophylaxis

Minor surgery in mobile patients Early and "aggressive" ambulation

Moderate risk:- 10–40 LMWH (at recommended doses), LDUH bid or tid, fondaparinux

Most general, open gynecologic, or urologic surgery Mechanical thromboprophylaxis

Moderate VTE risk plus high bleeding risk

High risk:- 40–80 LMWH (at recommended doses), fondaparinux, oral vitamin K antagonist (INR 2–3)

Hip or knee arthroplasty, hip fracture surgery

Major trauma, spinal cord injury Mechanical thromboprophylaxis

High VTE risk plus high bleeding risk


DVT = deep vein thrombosis; INR = International Normalized Ratio; LDUH = low-dose unfractionated heparin; LMWH = low molecular weight heparin; VTE = venous thromboembolism.





Deep vein thrombosis is best diagnosed by-(PGI 97)

a) Plethysmography b) Duplex ultrasound

c) Radionuclide scan d) CT scan


Which is true regarding Trendelenburg operation – (PGI 01)

a)Sripping of the superficial varicose vein

b)Flush ligation of the superficial varicose vein

c)Ligation of the perforators

d)Ligation of small tributaries at the distal end of superficial varicose vein

e)Ligation of short saphenous vein


Surgical treatment of varicose veins

Surgical treatment of varicose veins is widely used and is effective in removing varicose veins of the main saphenous trunks, as well as their tributaries, down to a size of about 3 mm. Veins smaller than this are best treated by sclero­therapy. Surgical removal of varices is inappropriate where these form a major part of the venous drainage of the limb, for example where a deep vein thrombosis has destroyed the main axial limb veins and the patient relies on the superficial veins. This possibility may be suggested by the patient’s medical history and can be confirmed by duplex ultrasonography or venography.

The main principles of surgical treatment are to ligate the source of the venous reflux (usually the SFJ or the SPJ) and to remove the incompetent saphenous trunks and the associated varices. Sapheno-femoral ligation alone, sometimes referred to as a ‘Trendelenburg procedure’, is associated with a high rate of recurrence of varices. Recent research has shown that it is necessary to remove the long saphenous vein to ensure that as much venous reflux as possible is eliminated. Similarly, communications between the many deep veins in the popliteal fossa and the short saphenous vein mean that some patients develop recurrences in the short saphenous vein due to the re-establishment of reflux from these veins. This problem may be eliminated by removing the short saphenous vein. Removal of the saphenous veins has the disadvantage that both veins are accompanied by a nerve that may be damaged in the vein stripping operation. To avoid nerve injury the long saphenous vein should not be removed below mid-calf level and great care should be exercised in removing the short saphenous vein.


Sensory nerve injury is seen occasionally after removal of varicose veins. The saphenous nerve and its branches accompany the long saphenous vein in the calf, the sural nerve accompanies the short saphenous vein. Damage to the main part of these nerves occurs in about 1 per cent of operations, but small areas of anaesthesia may occur more frequently (in up to 10 per cent of patients). The adoption of inverting stripping techniques and avoidance of stripping the long saphenous vein below mid-calf level have reduced the risk of damage to these nerves. All patients should be warned before surgery that they may experience small areas of numbness and tingling after the operation. These changes are usually reversible but can be quite persistent.




For which of the following venous abnormality is surgery indicated – (PGI 01)

a)Deep vein incompetence with DVT

b)Deep vein incompetence without DVT

c)Varicosity > 3 cm

b) Varicosity < 3 cm

e) Saphenofemoral incompetence


Imp:- Surgical treatment of varicose veins is widely used and is effective in removing varicose veins of the main saphenous trunks, as well as their tributaries, down to a size of about 3 mm. Veins smaller than this are best treated by sclero­therapy. Surgical removal of varices is inappropriate where these form a major part of the venous drainage of the limb, for example where a deep vein thrombosis has destroyed the main axial limb veins and the patient relies on the superficial veins. This possibility may be suggested by the patient’s medical history and can be confirmed by duplex ultrasonography or venography

Saphenous vein ligation and stripping is still the more commonly performed procedure worldwide, and it may be the preferred therapy for patients with GSVs of very large diameter (>2 cm).


Migratory thrombophlebitis is seen most commonly with- (PGI 02)

a) Pancreatic ca b) Testicular ca

c) Gastric ca d) Breast ca

e) Liver ca


Brodie-Tredenlenburg test is positive in – (PGI 02)

a)Sapheno-Femoral incompetence

b)Perforator competence above knee

c)Deep vein incompetence

d)Perforator competence below knee



Varicose veins are seen in – (PGI 02)

a) DVT

b) Superficial venous thrombosis


c)AV fistula

d)Prolonged standing



Gold standard diagnostic test in varicose veins is

a)Photoplethysmography (Jipmer 03)

b)Duplex imaging


d)Radio – labeled fibrinogen study


The initial therapy of documented deep venous thrombosis in a post operative case is –

a)Subcutaneous heparin therapy (Karnataka 03)

b)Intravenous heparin therapy

c)Thropmbolytic therapy with urokinase

d)Aspirin therapy


Which one of the following reagents is not used as sclerosant in the treatment of bleeding varices –

a) Ethyl alcohol .b) Ethanolamine oleate (ICS 05)

c) Phenol d) Sodium morrhuate


Site of diabetic for ulcer – (PGI June 05)

a) Medial malleolus b) Lateral malleolus

c) Heel d) Head of metatarsal

e) Head of toes


Harrison:-Approximately 15% of individuals with DM develop a foot ulcer (great toe or MTP areas are most common), and a significant subset will ultimately undergo amputation (14–24% risk with that ulcer or subsequent ulceration). Risk factors for foot ulcers or amputation include: male sex, diabetes >10 years’ duration, peripheral neuropathy, abnormal structure of foot (bony abnormalities, callus, thickened nails), peripheral arterial disease, smoking, history of previous ulcer or amputation, and poor glycemic control. Large callouses are often precursors to or overlie ulcerations.


Which of the following statements is true regarding fat embolism – (AJIMS NOV 05)

a)Most patients with major trauma involving long bones have urinary fat globules

b)All patients with urinary fat globules develop fat embolism

c)Peak incidence of respiratory insufficiency for pulmonary fat embolism is around day 7 after injury

d)Heparin as an anticoagulant decreases mortality and morbidity in fat embolism syndrome


Fat Embolism::- A certain degree of lung dysfunction occurs in all patients after long bone fractures, but clinically significant fat embolism syndrome as such develops in only 10 to 15 percent of these patients. Signs include hypoxia, tachycardia, mental status changes, and petechiae on the conjunctiva, axilla, or upper thorax. Fat globules in the urine are nondiagnostic, but lung infiltrates seen on chest radiograph confirm the presence of lung injury.

The pathophysiology of fat embolism represents capillary endothelial breakdown causing pericapillary hemorrhagic exudates most apparent in the lungs and brain. Pulmonary edema and hypoxemia occur as a result of pulmonary exudates. Hypoxia and areas of cerebral edema may account for the variable neurologic abnormalities seen.

The more severe cases of fat embolism involve fractures of the femur and tibia. Delays in fixation of bones and extensive reaming of the medullary canals contribute to perioperative morbidity and to the severity of fat embolism syndrome. Efforts to surgically correct fractures early and minimize trauma to the bone marrow lessen the degree of fat/bone marrow embolism. Patients with coexisting lung injury are at additional risk of fat embolism. Evidence suggests that fat may pass to the systemic circulation through a patent foramen ovale or by transpulmonary passage.The chemical composition of the fat may even contribute to this process. For this reason, it is preferable to minimize pulmonary artery hypertension to reduce transpulmonary passage of fat and limit pulmonary endothelial transudation of fluid.

Treatment includes early recognition, oxygen administration, and judicious fluid management. Corticosteroids in large doses shortly after major trauma have been found to minimize the clinical presentation of fat embolism but are probably not necessary in most cases if oxygen therapy is administered. With appropriate fluid management, adequate ventilation, and the prevention of hypoxemia, outcome is usually excellent.




Which of the following is true about varicocele except ? (Manipal 06)

a)Incompetent valves of testicular vein are responsible for varicocele

b)90% are on the left side

c)Asymptomatic cases require surgery

d)Femoral catheterization with spermatic vien ablation is done in recurrence


Which one of the following is the investigation of choice for suspected deep vein thrombosis of the lower extremity ? (UPSC 07)

a)Radioactive labelled fibrinogen uptake

b)Ascending contrast phlebography

c)D-dimer estimation

d)Duplex ultrasonography


With reference to varicocele, which one of the following is not true of it ? (UPSC 07)

a)Varicosity of cremastric veins

b)Left side is affected usually

c)Feels like a bag of worms

d)May lead to infertility



All are done for a case of deep vein thrombosis except – (MAHE 07)

a) Thrombolytic therapy b) Bandage

c) Heparin d) Bed rest


The practice of having a patient “out of bed into a chair” is one of the most thrombogenic positions that one could order a patient into. Sitting in a chair with the legs in a dependent position causes venous pooling, which in the postoperative milieu could easily be a predisposing factor in the development of thromboembolism


Treatment regimens may include antithrombotic therapy, vena caval interruption, catheter-directed or systemic thrombolytic therapy, and operative thrombectomy


studies, as well as the current ACCP guidelines, suggest that catheter-directed thrombolysis (with adjunctive angioplasty, venous stenting, and pharmacomechanical fragmentation and extraction) may be useful in selected patients with extensive iliofemoral DVT. Patients should have a recent onset of symptoms (<14 days), good functional status, decent life expectancy, and low bleeding risk.


Table 24-2 Risk Factors for Venous Thromboembolism




Acquired Inherited

Advanced age Factor V Leiden

Hospitalization/immobilization Prothrombin 20210A

Hormone replacement therapy and oral contraceptive use Antithrombin deficiency

Protein C deficiency

Pregnancy and puerperium Protein S deficiency

Prior venous thromboembolism Factor XI elevation

Malignancy Dysfibrinogenemia

Major surgery Mixed Etiology

Obesity Homocysteinemia

Nephrotic syndrome Factor VII, VIII, IX, XI elevation

Trauma or spinal cord injury Hyperfibrinogenemia

Long-haul travel (>6 h) Activated protein C resistance without factor V Leiden

Varicose veins

Antiphospholipid antibody syndrome

Myeloproliferative disease


Early in the course of DVT development, venous thrombosis is thought to begin in an area of relative stasis, such as a soleal sinus vein or immediately downstream of the cusps of a venous valve in the axial calf veins. Isolated proximal DVT without tibial vein thrombosis is unusual. Early in the course of a DVT, there may be no or few clinical findings such as pain or swelling. Even extensive DVT may sometimes be present without signs or symptoms. History and physical examination are therefore unreliable in the diagnosis of DVT. In addition, symptoms and signs generally associated with DVT, such as extremity pain and/or swelling, are nonspecific. In large studies, DVT has been found by venography or DUS in ≤50% of patients in whom it was clinically suspected.Objective studies are therefore required to confirm a diagnosis of DVT or to exclude the presence of DVT.


Investigation of Choice-Duplex USG


With major advances in technology of imaging, magnetic resonance venography has come to the forefront of imaging for proximal venous disease. The cost and the issue of patient tolerance due to claustrophobia limit the widespread application, but this is changing. It is a useful test for imaging the iliac veins and the IVC, an area where duplex ultrasound is limited in its usefulness.


Gold standard:-Injection of contrast material into the venous system is obviously and understandably the most accurate method of confirming DVT and the location.Not used usually.



Clinical symptoms may worsen as DVT propagates and involves the major proximal deep veins. Massive DVT that obliterates the major deep venous channel of the extremity with relative sparing of collateral veins causes a condition called phlegmasia alba dolens or white leg .This condition is characterized by pain, pitting edema, and blanching. There is no associated cyanosis. When the thrombosis extends to the collateral veins, massive fluid sequestration and more significant edema ensues, resulting in a condition known as phlegmasia cerulea dolens.Phlegmasia cerulea dolens is preceded by phlegmasia alba dolens in 50 to 60% of patients. The affected extremity in phlegmasia cerulea dolens is extremely painful, edematous, and cyanotic, and arterial insufficiency or compartment syndrome may be present. If the condition is left untreated, venous gangrene can ensue, leading to amputation




Superficial vein thrombophlebitis (SVT) most commonly occurs in varicose veins but can occur in normal veins. When SVT recurs at variable sites in normal superficial veins, it may signify a hidden visceral malignancy or a systemic disease such as a blood dyscrasia and/or a collagen vascular disease. This condition is known as thrombophlebitis migrans. SVT also frequently occurs as a complication of indwelling catheters, with or without associated extravasation of injected material. Upper extremity vein thrombosis has been reported to occur in 38% of patients with peripherally inserted central catheters; 57% of these developed in the cephalic vein . Finally, suppurative SVT may occur in veins with indwelling catheters and may be associated with generalized sepsis.


Rx of SVT by schwartz:- In patients with SVT not within 1 cm of the saphenofemoral junction, treatment consists of compression and administration of an anti-inflammatory medication such as indomethacin. In patients with suppurative SVT, removal of any existing indwelling catheters is mandatory, and excision of the vein may be necessary. If the SVT extends proximally to within 1 cm of the saphenofemoral junction, extension into the common femoral vein is more likely to occur. In these patients, anticoagulation therapy for 6 weeks and GSV ligation appear equally effective in preventing thrombus extension into the deep venous system.


Rx of SVT by Harrisons:- Treatment is primarily supportive. Initially, patients can be placed at bed rest with leg elevation and application of warm compresses. Nonsteroidal anti-inflammatory drugs may provide analgesia but may also obscure clinical evidence of thrombus propagation. If a thrombosis of the greater saphenous vein develops in the thigh and extends toward the saphenofemoral vein junction, it is reasonable to consider anticoagulant therapy to prevent extension of the thrombus into the deep system and a possible pulmonary embolism.






Elastic compression stocking with zippered side to facilitate treatment of chronic venous insufficiency


Compression therapy is most commonly achieved with graduated elastic compression stockings. Graduated elastic compression stockings, initially developed by Conrad Jobst in the 1950s, were made to simulate the gradient of hydrostatic forces exerted by water in a swimming pool. Elastic compression stockings are available in various compositions, strengths, and lengths, and can be customized for a particular patient.


To improve compliance, patients should be instructed to wear their stockings initially only as long as it is easily tolerated and then gradually to increase the amount of time the stockings are worn. Alternatively, patients can be fitted with lower-strength stockings initially followed by introduction of higher-strength stockings over a period of several weeks. Many commercially available devices, such as silk inner toe liners, stockings with zippered sides,and metal fitting aids ,are available to assist patients in applying elastic stockings.




Metal fitting aid to assist in placement of elastic compression stockings


Lymphatic Disorders



Lymphedema is extremity swelling that results from a reduction in lymphatic transport, with resultant pooling of lymph within the interstitial space. It is caused by anatomic problems such as lymphatic hypoplasia, functional insufficiency, or absence of lymphatic valves.



The original classification system, described by Allen, is based on the cause of the lymphedema.


Primary lymphedema is further subdivided into


1. Congenital lymphedema may involve a single lower extremity, multiple limbs, the genitalia, or the face. The edema typically develops before 2 years of age and may be associated with specific hereditary syndromes (Turner syndrome, Milroy syndrome, Klippel-Trénaunay-Weber syndrome).The familial version of congenital lymphedema is known as Milroy’s disease and is inherited as a dominant trait


2.Lymphedema praecox is the most common form of primary lymphedema, accounting for 94% of cases. Lymphedema praecox is far more common in women, with the gender ratio favoring women 10:1. The onset is during childhood or the teenage years, and the swelling involves the foot and calf. The familial version of lymphedema praecox is known as Meige’s disease.


3.Lymphedema tarda is uncommon, accounting for <10% of cases of primary lymphedema. The onset of edema is after 35 years of age.



Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption. Axillary node dissection leading to lymphedema of the arm is the most common cause of secondary lymphedema in the United States. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. Globally, filariasis (caused by Wuchereria bancrofti, Brugia malayi, and Brugia timori) is the most common cause of secondary lymphedema.In developed countries, the most common causes of secondary lymphedema involve resection or ablation of regional lymph nodes by surgery, radiation therapy, tumor invasion, direct trauma, or less commonly, an infectious process.


Lymphoscintigraphy has emerged as the test of choice in patients with suspected lymphedema.It cannot differentiate between primary and secondary lymphedemas; however, it has a sensitivity of 70% to 90% and a specificity of nearly 100% in differentiating lymphedema from other causes of limb swelling.


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Malignant cell in Hodgkin’s lymphoma is –


a) Reed sternberg cell b) Lymphocytes 85)

c) Histiocyte d) Reticulum cells


Chronic lymphedema predisposes to all except – (PGI 89)

a) Lymphangiosarcoma b) Marjolins ulcer

c) Recurrent infections d) Thickening of skin

In the lower extremity the swelling involves the dorsum of the foot, and the toes have a squared-off appearance. In advanced cases, hyperkeratosis of the skin develops, and fluid weeps from lymph-filled vesicles


Recurrent cellulitis is a common complication of lymphedema. Repeated infection results in further lymphatic damage, worsening existing disease. The clinical presentation of cellulitis ranges from subtle erythema and worsening of edema to a rapidly progressive soft tissue infection with systemic toxicity


Commonest cause of unilareral pedal edema in india is – (A190)

a) Filariasis b) Post traumatic

c) Post irradiation d) Milroy’s disease


All are true about congenital lymphedema except-

a)It is bilateral (AI 91)

b)Involve lower limb

c)Almost always manifests before puberty

d)Acute lymphangitis may occur

All are true?


The commonest cause for lymphedema of upper limb is – (AI 91)

a) Filariasis b) Congenital

c) Neck surgery d) Post mastectomy irradiation


Commonest cause of upper limb lymphedema is –

a) Congenital b) Filariasis (AI 92)

c) Post mastectomy d) Irradiation




ANS given in all guides is Filariasis but it should be Post Mastectomy.


Secondary lymphedema, more common than the primary form, usually develops following disruption or obstruction of lymphatic pathways associated with a disease process, or following surgery or radiotherapy. Worldwide, filariasis is the most common cause of secondary lymphedema usually affecting lower limbs.In the United States, the most common secondary lymphedema develops in the upper extremity following axillary lymph node dissection.The incidence varies considerably, depending on the definition of edema. Results of one series of published reports reveal a 14 percent rate of secondary lymphedema in postmastectomy patients who also had undergone irradiation therapy.


Milroys disease is – (JIPMER 92)

a)Edema due to filareasis

b)Post cellulitic lymphedema

c)Congenital lymphedema

d)Lymphedema following surgery

Reasons that during transposition of basilic vein its better to reanastomose compared to using the native anastomosis

Posted by [email protected] on April 27, 2018 at 12:20 AM Comments comments (0)

Reasons that during transposition of basilic vein (matured) its better to reanastomose compared to using the native anastomosis.


1. It will be easy to reposition to desired place, can be done by tunellation technique.

2. Can improve on anastomosis shape, can increase the anastomosis site as the vein is much dilated.

3. Angle of anastomosis will be as desired.

4. Preservation of a branch of musculocutaneous nerve is possible.

5. In case the length of the vein is excess, trimming of the vein can be done to desired length.


LEAD important questions (Part 1)

Posted by [email protected] on August 1, 2017 at 12:55 AM Comments comments (0)

LEAD important questions (Part 1):

1) ABI normal values:

a. 1-1.4 is normal. 0.9-1 is borderline. Less than 0.9 and more than 1.4 is abnormal. Non compressible vessel is when ABI >1.4.

2) Prognostic value of ABI:

a. Not related with symptoms, even asymptomatic has poor prognosis. Values other than normal predicts poor prognosis.

3) Risk factors for Intermittent Claudications.

a. Hypertension, 2.5times in male 3.9times in female.

b. Diabetes. Prevalence 25% higher.

c. Diabetes. More likely to have symptoms, 3.5times in male and 8.6times in female.

d. Metabolic syndrome: 25% of Intermittent Claudication patients have this problem.

i. Three or more of high BP, TG high or HDL low, FBS high, Abdominal obesity.

e. Cigarette smoking more than 25pack years has LEAD risk 2.72times.

4) Impact of female gender in LEAD.

a. Faster functional decline in relation to 6minute walk test.

5) Conversion of IC to CLI if risk factors are controlled.

a. About 8% in first year, followed by 2% per annum.

i. E.g. IC if stops smoking, 8% develops CLI in 6 years, but 80% develops CLI if continues smoking.

b. Risks of major amputation is 5% per year.

6) Quality of life measurement in IC.

a. SF-36 measures physical and emotional quality of life and correlates with 6minute walk test.

7) Based on history how to differenciate with neurogenic claudication from vascular claudication?

a. In NC no pain on climbing stair (flexed waist relieves pain).

8) Any newer biochemical test to know likelihood of PAD?

a. Homocysteine level. Elevated level has likelyhood of PAD by 7folds.

b. Hypercoagulable states increase likelihood. Like fibrinogen level.

9) Risk stratification for patients with CLI.

a. Outcome is amputation free survival.


c. All independently predicts.

d. Major predictors like Diabetes, gangrene, CAD, need of surgery, dialysis, age >75, BMI, ABI, Smoking, Bollinger Score etc.

10) Bollinger scoring:

a. Arterial tree from Common iliac to plantar vessel into 16 segments, One point for each segment. Less score signifies poor prognosis.

11) Scopes in vascular lab for diagnosis of LEAD and knowing of severity.

a. Segmental arterial pressure, ABI, Doppler waveform analysis, toe pressure measurement, transcutaneous oxygen pressure.

12) Stages of PAD classifications.

a. Fontaine Grade: I Asymptomatic, IIaMild claudication, IIb Moderate to severe claudication, III Rest pain, IVAmputation

b. Rutherford category: 1asymp.2Mild claudication.3Mod claud.4Severe claud.5Minor tissue loss.6 Major tissue loss.

13) Imaging modalities for PAD.

a. Conventional angiogram, CT Angiogram, MR Angiogram.

b. Each has own advantages and disadvantages.

14) Treatment (Medical management).

a. Antiplatelet.

b. Smoking cessation

c. Treatment of hyperlipidemia

d. Treatment of hypertension

e. Treatment of diabetes.



LEAD important questions (Part 1)

Posted by [email protected] on August 1, 2017 at 12:55 AM Comments comments (0)

LEAD important questions (Part 1):

1) ABI normal values:

a. 1-1.4 is normal. 0.9-1 is borderline. Less than 0.9 and more than 1.4 is abnormal. Non compressible vessel is when ABI >1.4.

2) Prognostic value of ABI:

a. Not related with symptoms, even asymptomatic has poor prognosis. Values other than normal predicts poor prognosis.

3) Risk factors for Intermittent Claudications.

a. Hypertension, 2.5times in male 3.9times in female.

b. Diabetes. Prevalence 25% higher.

c. Diabetes. More likely to have symptoms, 3.5times in male and 8.6times in female.

d. Metabolic syndrome: 25% of Intermittent Claudication patients have this problem.

i. Three or more of high BP, TG high or HDL low, FBS high, Abdominal obesity.

e. Cigarette smoking more than 25pack years has LEAD risk 2.72times.

4) Impact of female gender in LEAD.

a. Faster functional decline in relation to 6minute walk test.

5) Conversion of IC to CLI if risk factors are controlled.

a. About 8% in first year, followed by 2% per annum.

i. E.g. IC if stops smoking, 8% develops CLI in 6 years, but 80% develops CLI if continues smoking.

b. Risks of major amputation is 5% per year.

6) Quality of life measurement in IC.

a. SF-36 measures physical and emotional quality of life and correlates with 6minute walk test.

7) Based on history how to differenciate with neurogenic claudication from vascular claudication?

a. In NC no pain on climbing stair (flexed waist relieves pain).

8) Any newer biochemical test to know likelihood of PAD?

a. Homocysteine level. Elevated level has likelyhood of PAD by 7folds.

b. Hypercoagulable states increase likelihood. Like fibrinogen level.

9) Risk stratification for patients with CLI.

a. Outcome is amputation free survival.


c. All independently predicts.

d. Major predictors like Diabetes, gangrene, CAD, need of surgery, dialysis, age >75, BMI, ABI, Smoking, Bollinger Score etc.

10) Bollinger scoring:

a. Arterial tree from Common iliac to plantar vessel into 16 segments, One point for each segment. Less score signifies poor prognosis.

11) Scopes in vascular lab for diagnosis of LEAD and knowing of severity.

a. Segmental arterial pressure, ABI, Doppler waveform analysis, toe pressure measurement, transcutaneous oxygen pressure.

12) Stages of PAD classifications.

a. Fontaine Grade: I Asymptomatic, IIaMild claudication, IIb Moderate to severe claudication, III Rest pain, IVAmputation

b. Rutherford category: 1asymp.2Mild claudication.3Mod claud.4Severe claud.5Minor tissue loss.6 Major tissue loss.

13) Imaging modalities for PAD.

a. Conventional angiogram, CT Angiogram, MR Angiogram.

b. Each has own advantages and disadvantages.

14) Treatment (Medical management).

a. Antiplatelet.

b. Smoking cessation

c. Treatment of hyperlipidemia

d. Treatment of hypertension

e. Treatment of diabetes.



Varicose vein information

Posted by [email protected] on March 15, 2015 at 5:30 AM Comments comments (0)


What are varicose veins?

Varicose veins are the visible and large, bulging, surface

veins, felt under the skin. They generally are larger than

one eighth inch in width, and are usually located along the

inside part of the calf or thigh. Varicose veins develop due

to weakness of the vein wall and because the valves of the

veins no longer work. Under the pressure of gravity these

veins can continue to expand and, in time, they may become

longer, twisty, pouched, thickened and painful.

Other veins often mistaken for varicose veins are spider

veins and reticular veins, which are the visible purple or

greenish-blue veins that appear in our legs. Spider veins or

teleangiectesias are tiny veins that you can easily see, but

cannot feel, and are usually located at the surface skin layers.

Reticular veins are larger than spider veins but smaller than

varicose veins and may cause symptoms. Spider veins typically

do not cause symptoms, and treatment for these is

frequently cosmetic unless symptoms are present.

Vein problems are among the most common chronic

conditions in North America. In fact, more people lose work

time from vein disorders than from artery disease. Varicose

veins affect up to 25 percent of women and 15 percent of men.

By the age of 50, nearly 40 percent of women and 20 percent

of men have significant leg vein problems. Spider veins occur

much more frequently in women. It is estimated that at

least 20 to 25 million Americans have varicose veins.


Who is at risk?

The most important factors leading to the development

of varicose veins include:

• Family history of varicose veins

• Prolonged standing

• Increasing age

• Heavy lifting

• Prior blood clots in superficial or deep veins

• Multiple pregnancies

Limited physical activity, high blood pressure and obesity

have also been linked with the presence of varicose veins

in women.

What are the signs and symptoms?

Varicose veins may be entirely symptom-free and cause

no immediate health problems. Treatment in such cases

is usually considered cosmetic. When symptoms are

present, the most common are ankle and leg swelling,

heaviness or fullness, aching, restlessness, fatigue, pain,

cramps and itching. Varicose veins can also be associated

with ulcers (sores) of the legs. In the most severe cases,

varicose veins may lead to thickening and discoloration

of the skin of the legs, eczema and non-healing sores

around the ankle area. Varicose veins, especially when

they are very large, are at risk of forming a blood clot,

a condition known as superficial thrombophlebitis. If

you experience any of these of varicose veins symptoms,

talk with your doctor. Don’t ignore leg pains.


What are the causes?

The causes of varicose veins are related to non-functioning

vein valves. Vein valves are designed to allow blood to

flow from the legs toward the heart against gravity, while

preventing reverse flow back down the legs. Reverse flow

is called venous reflux. Vein valves may fail to close due

o either, 1) vein wall weakness that causes the vein to

enlarge and the valves to leak; 2) a history of blood clots

in the vein that damage the valves; or 3) an absence of

vein valves since birth. Varicose veins can be hereditary,

often occurring in several members of the same family.

Varicose veins can also develop after trauma or injury.

Regardless of cause, defective valves cause venous

blood to stagnate (pool) in the legs, leading to high

blood pressure in the leg veins. This may result in further

enlargement of the varicose veins, increasing the likelihood

of advanced symptoms such as skin changes and

ulcers at the ankles. Reflux in the largest superficial veins,

such as the saphenous veins, is often an underlying cause

of painful varicose veins. Venous reflux is a condition

that can be progressive. If left untreated, it can worsen

and cause more advanced symptoms. In addition, blockage

of the veins in the pelvis may severely aggravate the

symptoms of varicose veins, requiring separate treatment.

To find out more about the Vascular Disease Foundation, call 888.833.4463 or visit us online at www.vasculardisease.org

What you need to know about risk factors,

symptoms, and treatment

Focus on

Varicose Veins

How are varicose veins diagnosed?

The diagnosis of varicose veins is made primarily by

physical examination. The accuracy of physical examination

is further improved with the aid of a hand-held Doppler

(ultrasound) instrument, which allows the examiner to

listen to the blood flow. The most accurate and detailed test

is a duplex ultrasound exam, which provides an ultrasound

image of the vein to detect any blockage caused by blood

clots, and to determine whether the vein valves are working

properly or have evidence of reflux. Measurement of

the venous function of the leg may also be obtained with

other tests such as plethysmography. These diagnostic tests

are non-invasive and painless.

How are varicose veins treated?

Varicose veins are always a sign of an underlying venous

insufficiency disorder, whether symptomatic or not. Traditional

treatments include making

life-style modifications, wearing

compression stockings and taking

some medications. Patients with

varicose veins are encouraged to

lose weight, exercise and elevate

their legs. Compression stockings

are effective in reducing swelling

and pain. Low-dose diuretics (water

pills) reduce swelling in the short

term, topical steroid creams reduce

inflammation, and antibiotics treat

cellulitis (skin infection). Horse

chestnut seed extract is an herbal

remedy taken to reduce short-term

swelling, but this preparation has not

been approved by the FDA.

If these traditional treatments are not successful, then

endovascular procedures or surgery is recommended.

Catheter-directed (endovascular) techniques have revolutionized

the treatment of varicose veins, with reduced

complications and time away from work. Vein stripping

was the traditional treatment for bad values in the veins

however it is rarely used today due to the advancement of

less invasive procedures.

Here are the most common treatments:

• Prescription compression stockings to reduce the

symptoms of varicose veins, prevent and reduce

leg swelling and decrease the risk of blood clots.

Prescription stockings offer appropriate counter-

compression and are more effective than the over

the counter stockings.

• Sclerotherapy (injections of the veins) involves

njecting a sclerosing solution into spider, reticular

or varicose veins. This is a minimally invasive office

procedure. This blocks the veins that are unsightly or

not working well. Injection of sclerosing solutions

slowly eliminates the unsightly skin veins to improve

appearance. Patients typically receive multiple treat-

ments and most see significant improvement over

the course of several months of treatment.

• Ambulatory phlebectomy is also a minimally invasive

procedure that can be performed under local, epidura

or general anesthesia in an outpatient setting. Varicose

veins are removed with

small hooks through tiny

skin incisions. Stitches

are not used, and the tiny

incisions are pulled together

with sterile paper-tape. Recovery

is generally brief.

To find out more about the Vascular Disease Foundation, call 888.833.4463 or visit us online at www.vasculardisease.org

• Laser treatments use a fine optical fiber, which is

advanced through a catheter into the saphenous vein.

Laser energy is then delivered through the fiber. The

fiber makes contact with the blood and inner wall of

the vein and, as the fiber is slowly withdrawn, the

laser energy is absorbed by the blood and vein tissue,

sealing it shut. The procedure can be performed in the

outpatient setting. Recovery time is usually fast with

positive short and mid-term results.

• RF treatment involves controlled delivery of radio-

frequency (RF) energy directly to a vein wall by a

thin catheter causing collagen in the vein wall to

shrink and the vein to close. Once the vein is closed,

blood is naturally rerouted by the body to other

healthy veins. It has good results at two years with

similar post-procedure pain, bruising, tenderness and

recovery compared to other endovascular treatments.

RF treatment is most commonly performed in a

doctor’s office or outpatient setting.

Other complications:

Without treatment, varicose veins may cause pain or

aching, leg swelling, skin color changes,hardened skin

and subcutaneous tissue (lipodermatosclerosis),and eczema.

In advanced cases, breakdown of the skin may causebleeding

from varicose veins, and large varicosities may developblood

clots, a condition called superficial phlebitis or

thrombophlebitis. Patients with varicose veins may also

eventually develop chronic skin ulceration around the ankle.

© 2012 VASCULAR DISEASE FOUNDATION 8206 Leesburg Pike, Suite 301 • Vienna, VA 22182 31vdf2012

The Vascular Disease Foundation

Established in 1998, The Vascular Disease Foundation (VDF) develops

educational information and initiatives for patients, their families

and friends, and health care providers regarding often ignored, but

serious vascular diseases. In fact, VDF is the only multidisciplinary

national public 501(c)(3) non-profit organization focused on providing

public education and improving awareness about vascular diseases.

For more information, visit vasculardisease.org.

Help the Vascular Disease Foundation continue to make this critical educational

information available. Your contribution will make saving lives a greater reality.

Make a donation today at: contact.vasculardisease.org/donate

What you can do!

You can’t do anything about your heredity, age, or gender.

However, you can help delay the development of varicose

veins or keep them from progressing. Some things you

can do:

• Be active. Moving leg muscles keeps the blood flowing.

• Work with your doctor to keep your blood pressure

under control.

• To temporarily relieve symptoms, lie down and raise

your legs at least six inches above the level of your

heart. Do this for at least 10 minutes a few times

each day.

• Strive for a normal weight.

• Wear your prescription compression stockings as

specified by your doctor.

• See a qualified doctor who can diagnose the cause of

your varicose veins, the sources of venous reflux in

your legs, and offer a variety of treatment options.

To find out more about the Vascular Disease Foundation, call 888.833.4463 or visit us online at www.vasculardisease.org

Radiofrequency ablation for varicose vein

Posted by [email protected] on March 11, 2015 at 7:05 AM Comments comments (0)


Varicose veins

Radiofrequency ablation is a minimally invasive procedure used in the treatment of varicose veins. It is an alternative to the traditional stripping operation. Under ultrasound guidance, a radiofrequency catheter is inserted into the abnormal vein and the vessel treated with radio-energy, resulting in closure of the involved vein. Radiofrequency ablation is used to treat the great saphenous vein, the small saphenous vein, and the perforator veins. The latter are connecting veins that transport blood from the superficial veins to the deep veins. Branch varicose veins are then usually treated with other minimally invasive procedures, such as ambulatory phlebectomy, sclerotherapy, or foam sclerotherapy. Currently, the VNUS ClosureRFS stylet is the only device specifically cleared by FDA for endovenous ablation of perforator veins.[14]


It should be pointed out that the possibility of skin burn during the procedure is very small, because the large volumes (500 cc) of dilute Lidocaine (0.1%) tumescent anesthesia injected along the entire vein prior to the application of radiofrequency provide a heat sink that absorbs the heat created by the device. Early studies have shown a high success rate with low rates of complications.


In comparision to conservative surgery for varicose vein (also known as Trendelenberg's operation), Radiofrequency ablation of Varicose vein has been found to have advantage specifically with lower postoperative pain, earlier recovery, earlier discharge, earlier return to work, less bruise, more cosmetically appealing, less number of phlebectomy required. (http://ctvsdh.webs.com/)

Contact details of Surgeon

Posted by [email protected] on March 2, 2015 at 4:30 AM Comments comments (1)

Dr. R. M. Karmacharya,

Office: 011-490497,

Mobile no: 9801002478

Viber: 9818729013

Surgery OPD 

OPD days:

Monday/ Wednesday


Deep vein thrombosis review in Merck manual

Posted by [email protected] on February 27, 2015 at 4:15 AM Comments comments (0)

From Merck manual


Deep venous thrombosis (DVT) is clotting of blood in a deep vein of an extremity (usually calf or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. DVT results from conditions that impair venous return, lead to endothelial injury or dysfunction, or cause hypercoagulability. DVT may be asymptomatic or cause pain and swelling in an extremity; pulmonary embolism is an immediate complication. Diagnosis is by history and physical examination and is confirmed by objective testing, typically with duplex ultrasonography. d-Dimer testing is used when DVT is suspected; a negative result helps to exclude DVT, whereas a positive result is nonspecific and requires additional testing to confirm DVT. Treatment is with anticoagulants. Prognosis is generally good with prompt, adequate treatment. Common long-term complications include venous insufficiency with or without the postphlebitic syndrome.


DVT occurs most commonly in the lower extremities or pelvis (Fig. 1: Deep veins of the legs.). It can also develop in deep veins of the upper extremities (4 to 13% of DVT cases).


Fig. 1

Deep veins of the legs.


Lower extremity DVT is much more likely to cause pulmonary embolism (PE), possibly because of the higher clot burden. The superficial femoral and popliteal veins in the thighs and the posterior tibial and peroneal veins in the calves are most commonly affected. Calf vein DVT is less likely to be a source of large emboli but can propagate to the proximal thigh veins and from there cause PE. About 50% of patients with DVT have occult PE, and at least 30% of patients with PE have demonstrable DVT.


Pearls & Pitfalls

About 50% of patients with DVT have occult pulmonary emboli.


Many factors can contribute to DVT (see Table 1: Risk Factors for Venous Thrombosis). Cancer is a risk factor for DVT, particularly in elderly patients and in patients with recurrent thrombosis. The association is strongest for mucin-secreting endothelial cell tumors such as bowel or pancreatic cancers. Occult cancers may be present in patients with apparently idiopathic DVT, but extensive workup of patients for tumors is not recommended unless patients have major risk factors for cancer or symptoms suggestive of an occult cancer.


Table 1

Open table

Risk Factors for Venous Thrombosis

Age > 60 yr




Cigarette smoking (including passive smoking)


Estrogenreceptor modulators (eg, tamoxifen



, raloxifene





Heart failure


Hypercoagulability disorders:


Antiphospholipid antibody syndrome

Antithrombin deficiency

Factor V Leiden mutation (activated protein C resistance)




-induced thrombocytopenia

Hereditary fibrinolytic defects


Increase in factor VIII

Increase in factor XI

Paroxysmal nocturnal hemoglobinuria

Protein C deficiency

Protein S deficiency

Prothrombin G-A gene variant



Indwelling venous catheters


Limb trauma


Myeloproliferative disease (hyperviscosity)


Nephrotic syndrome




Oral contraceptives or estrogen therapy


Pregnancy and postpartum


Prior venous thromboembolism


Sickle cell anemia


Surgery within the past 3 mo





Lower extremity DVT most often results from impaired venous return (eg, in immobilized patients), endothelial injury or dysfunction (eg, after leg fractures), or hypercoagulability.


Upper extremity DVT most often results from endothelial injury due to central venous catheters, pacemakers, or injection drug use. Upper extremity DVT occasionally occurs as part of superior vena cava (SVC) syndrome or results from a hypercoagulable state or subclavian vein compression at the thoracic outlet. The compression may be due to a normal or an accessory first rib or fibrous band (thoracic outlet syndrome) or occur during strenuous arm activity (effort thrombosis, or Paget-Schroetter syndrome, which accounts for 1 to 4% of upper extremity DVT cases).


DVT usually begins in venous valve cusps. Thrombi consist of thrombin, fibrin, and RBCs with relatively few platelets (red thrombi); without treatment, thrombi may propagate proximally or travel to the lungs.


Complications: Common complications include


Chronic venous insufficiency (see Chronic Venous Insufficiency and Postphlebitic Syndrome)

Postphlebitic syndrome

Pulmonary embolism (see Pulmonary Embolism)

Much less commonly, acute DVT leads to phlegmasia alba dolens or phlegmasia cerulea dolens, both of which, unless promptly diagnosed and treated, can result in venous gangrene.


In phlegmasia alba dolens, a rare complication of DVT during pregnancy, the leg turns milky white. Pathophysiology is unclear, but edema may increase soft-tissue pressure beyond capillary perfusion pressures, resulting in tissue ischemia and wet gangrene.


In phlegmasia cerulea dolens, massive iliofemoral venous thrombosis causes near-total venous occlusion; the leg becomes ischemic, extremely painful, and cyanotic. Pathophysiology may involve complete stasis of venous and arterial blood flow in the lower extremity because venous return is occluded or massive edema cuts off arterial blood flow. Venous gangrene may result.


Rarely, venous clots can become infected. Jugular vein suppurative thrombophlebitis (Lemierre syndrome), a bacterial (usually anaerobic) infection of the internal jugular vein and surrounding soft tissues, may follow tonsillopharyngitis and is often complicated by bacteremia and sepsis. In septic pelvic thrombophlebitis, pelvic thromboses develop postpartum and become infected, causing intermittent fever. Suppurative (septic) thrombophlebitis, a bacterial infection of a superficial peripheral vein, comprises infection and clotting that usually is caused by venous catheterization.


Symptoms and Signs

DVT may occur in ambulatory patients or as a complication of surgery or major medical illness. Among high-risk hospitalized patients, most deep vein thrombi occur in the small calf veins, are asymptomatic, and may not be detected.


When present, symptoms and signs (eg, vague aching pain, tenderness along the distribution of the veins, edema, erythema) are nonspecific, vary in frequency and severity, and are similar in arms and legs. Dilated collateral superficial veins may become visible or palpable. Calf discomfort elicited by ankle dorsiflexion with the knee extended (Homans sign) occasionally occurs with distal leg DVT but is neither sensitive nor specific. Tenderness, swelling of the whole leg, > 3 cm difference in circumference between calves, pitting edema, and collateral superficial veins may be most specific; DVT is likely with a combination of ≥ 3 in the absence of another likely diagnosis (see Table 2: Probability of Deep Venous Thrombosis Based on Clinical Factors).


Low-grade fever may be present; DVT may be the cause of fever without an obvious source, especially in postoperative patients. If PE occurs, symptoms may include shortness of breath and pleuritic chest pain (see Symptoms and Signs).


Table 2

Open table

Probability of Deep Venous Thrombosis Based on Clinical Factors


Tenderness along distribution of the veins in calf or thigh


Swelling of entire leg


Calf swelling (> 3 cm difference in circumference between calves, measured 10 cm below tibial tuberosity)


Pitting edema greater in affected leg


Dilated collateral superficial veins


Cancer (including cases in which treatment was stopped within 6 mo)


Immobilization of lower extremity (eg, due to paralysis, paresis, casting, or recent long-distance travel)


Surgery leading to immobility for > 3 days within the past 4 wk



Probability equals the number of factors, subtracting 2 if another diagnosis is as likely as or more likely than DVT.


High probability: ≥ 3 points


Moderate probability:1–2 points


Low probability: ≤ 0 points


Based on data from Anand SS, Wells PS, Hunt D, et al: Does this patient have deep vein thrombosis? Journal of the American Medical Association 279 (14):1094–1099, 1998.

Common causes of asymmetric leg swelling that mimic DVT are soft-tissue trauma, cellulitis, pelvic venous or lymphatic obstruction, and popliteal bursitis (Baker cyst) that obstructs venous return. Abdominal or pelvic tumors that obstruct venous or lymphatic return are less common causes. Use of drugs that cause dependent edema (eg, dihydropyridine Ca channel blockers, estrogen, high-dose opioids), venous hypertension (usually due to right heart failure), and hypoalbuminemia typically cause symmetric bilateral leg swelling; however, swelling may be asymmetric if venous insufficiency coexists and is worse in one leg.


Common causes of calf pain that mimic acute DVT include venous insufficiency and postphlebitic syndrome; cellulitis that causes painful erythema of the calf; ruptured popliteal (Baker) cyst (pseudo-DVT), which causes calf swelling, pain, and sometimes bruising in the region of the medial malleolus; and partial or complete tears of the calf muscles or tendons.




Sometimes d-dimer testing

History and physical examination help determine probability of DVT before testing (see Table 2: Probability of Deep Venous Thrombosis Based on Clinical Factors). Diagnosis is typically by ultrasonography with Doppler flow studies (duplex ultrasonography). The need for additional tests (eg, d-dimer testing) and their choice and sequence depend on pretest probability and sometimes ultrasonography results. No single testing protocol is best; one approach is described in Fig. 2: One approach to testing for suspected deep venous thrombosis..



Clinical Calculator


Fig. 2

One approach to testing for suspected deep venous thrombosis.


Ultrasonography: Ultrasonography identifies thrombi by directly visualizing the venous lining and by demonstrating abnormal vein compressibility or, with Doppler flow studies, impaired venous flow. The test is >90% sensitive and > 95% specific for femoral and popliteal vein thrombosis but is less accurate for iliac or calf vein thrombosis.


d-Dimer: d-Dimer is a byproduct of fibrinolysis; elevated levels suggest recent presence and lysis of thrombi. d-Dimer assays vary in sensitivity and specificity; however, most are sensitive and not specific. Only the most accurate tests should be used. For example, a highly sensitive test is enzyme-linked immunosorbent assay (ELISA), which has a sensitivity of about 95%.


If pretest probability of DVT is low, DVT can be safely excluded in patients with a normal d-dimer level on a sensitive test. Thus, a negative d-dimer test can identify patients who have a low probability of DVT and do not require ultrasonography. However, a positive test result is nonspecific; because levels can be elevated by other conditions (eg, liver disease, trauma, pregnancy, positive rheumatoid factor, inflammation, recent surgery, cancer), further testing is necessary.


If pretest probability of DVT is moderate or high,d-dimer testing can be done at the same time as duplex ultrasonography. A positive ultrasound result confirms the diagnosis regardless of the d-dimer level. If ultrasonography does not reveal evidence of DVT, a normal d-dimer level helps exclude DVT. Patients with an elevated d-dimer level should have repeat ultrasonography in a few days or additional imaging, such as venography, depending on clinical suspicion..


Venography: Contrast venography was the definitive test for the diagnosis of DVT but has been largely replaced by ultrasonography, which is noninvasive, more readily available, and almost equally accurate for detecting DVT. Venography may be indicated when ultrasonography results are normal but pretest suspicion for DVT is high. The complication rate is 2%, mostly because of contrast dye allergy.


Other testing: Noninvasive alternatives to contrast venography are being studied. They include MRI venography and direct MRI of thrombi using T1-weighted gradient-echo sequencing and a water-excitation radiofrequency pulse; theoretically, the latter test can provide simultaneous views of thrombi in deep veins and subsegmental pulmonary arteries (for diagnosis of PE).


If symptoms and signs suggest PE, additional imaging (eg, ventilation/perfusion [V/Q] scanning or CT pulmonary angiography) is required.


Determination of cause: Patients with confirmed DVT and an obvious cause (eg, immobilization, surgical procedure, leg trauma) need no further testing. Testing to detect hypercoagulability is controversial but is sometimes done in patients who have idiopathic (or unprovoked) DVT or recurrent DVT, in patients who have a personal or family history of other thromboses, and in young patients with no obvious predisposing factors. Some evidence suggests that presence of hypercoagulability does not predict DVT recurrence as well as clinical risk factors.


Screening patients with DVT for cancer has a low yield. Selective testing guided by complete history and physical examination and basic "routine" tests (CBC, chest x-ray, urinalysis, liver enzymes, and serum electrolytes, BUN, creatinine) aimed at detecting cancer is probably adequate. In addition, patients should have any age- and gender-appropriate cancer screening (eg, mammography, colonoscopy) that is due.



Without adequate treatment, lower extremity DVT has a 3% risk of fatal PE; death due to upper extremity DVT is very rare. Risk of recurrent DVT is lowest for patients with transient risk factors (eg, surgery, trauma, temporary immobility) and greatest for patients with persistent risk factors (eg, cancer), idiopathic DVT, or incomplete resolution of past DVT (residual thrombus). A normal d-dimer level obtained after warfarin



is stopped may help predict a relatively low risk of DVT or PE recurrence. Risk of venous insufficiency is difficult to predict. Risk factors for postphlebitic syndrome include proximal thrombosis, recurrent ipsilateral DVT, and body mass index (BMI) ≥ 22 kg/m2.



Anticoagulation with an injectable heparin



followed by an oral anticoagulant (warfarin



, or a factor Xa or direct thrombin inhibitor)

Treatment is aimed primarily at PE prevention (see also Prevention) and secondarily at symptom relief and prevention of DVT recurrence, chronic venous insufficiency, and postphlebitic syndrome. Treatment of lower and upper extremity DVT is generally the same.


All patients with DVT are given anticoagulants, initially an injectable heparin



(unfractionated or low molecular weight) for a brief period, followed by longer term treatment with an oral drug (eg, warfarin



) started within 24 to 48 h. Select patients may continue treatment with a low molecular weight heparin



rather than switching to an oral drug. Inadequate anticoagulation in the first 24 to 48 h may increase risk of recurrence or PE. Acute DVT can be treated on an outpatient basis unless severe symptoms require parenteral analgesics, other disorders preclude safe outpatient discharge, or other factors (eg, functional, socioeconomic) might prevent the patient from adhering to prescribed treatments.


General supportive measures include pain control with analgesics, which may include short (3- to 5-day) courses of an NSAID. Extended treatment with NSAIDs and aspirin



should be avoided because their antiplatelet effects may increase the risk of bleeding complications. In addition, elevation of legs (supported by a pillow or other soft surface to avoid venous compression) is recommended during periods of inactivity. Patients may be as physically active as they can tolerate; there is no evidence that early activity increases risk of clot dislodgement and PE and may help to reduce the risk of the postphlebitic syndrome.


Anticoagulants: The anticoagulants most often used are the following:


Low molecular weight heparins (LMWHs)

Unfractionated heparin













oral anticoagulants: factor Xa inhibitors (eg, rivaroxaban



, apixaban



), direct thrombin inhibitors (dabigatran)

LMWHs (eg, enoxaparin



, dalteparin



, tinzaparin



—see Table 3: Some Low Molecular Weight Heparin* Options in Thromboembolic Disease) are the initial treatment of choice because they can be given on an outpatient basis. LMWHs are as effective as UFH for reducing DVT recurrence, thrombus extension, and risk of death due to PE. Like UFH, LMWHs catalyze the action of antithrombin (which inhibits coagulation factor proteases), leading to inactivation of coagulation factor Xa and, to a lesser degree, factor IIa. LMWHs also have some antithrombin–mediated anti-inflammatory properties, which facilitate clot organization and resolution of symptoms and inflammation.


LMWHs are typically given sc in a standard weight-based dose (eg, enoxaparin



1.5 mg/kg sc once/day or 1 mg/kg sc q 12 h or dalteparin



200 units/kg sc once/day). Patients with renal insufficiency may be treated with UFH or with reduced doses of LMWH. Monitoring is not reliable because LMWHs do not significantly prolong the results of global tests of coagulation. Furthermore, they have a predictable dose response, and there is no clear relationship between the anticoagulant effect of LMWH and bleeding. Treatment is continued until full anticoagulation is achieved with warfarin



(typically about 5 days). However, evidence suggests that LMWH is effective for long-term DVT treatment in high-risk patients, such as those with cancer. Thus, LMWH may become an acceptable alternative to warfarin



for some patients, although warfarin



is likely to be the treatment of choice for most patients because of its low cost and oral route of administration.


UFH may be used instead of LMWH for hospitalized patients and for patients who have renal insufficiency or failure (creatinine clearance 10 to 30 mL/min) because UFH is not cleared by the kidneys. UFH is given as a bolus and infusion (Fig. 2: Weight-based heparin dosing.) to achieve full anticoagulation, (eg, activated PTT [aPTT] 1.5 to 2.5 times that of the reference range). For outpatients, UFH 333 units/kg initial bolus, then 250 units/kg sc q 12 h can be substituted for IV UFH to facilitate mobility; the dose does not appear to need adjustment based on aPTT. Treatment is continued until full anticoagulation has been achieved with warfarin





Complications of heparins include bleeding, thrombocytopenia (less common with LMWHs), urticaria, and, rarely, thrombosis and anaphylaxis. Long-term use of UFH causes hypokalemia, liver enzyme elevations, and osteopenia. Rarely, UFH given sc causes skin necrosis. Inpatients and possibly outpatients should be screened for bleeding with serial CBCs and, where appropriate, testing for occult blood in stool.


Bleeding due to overheparinization can be stopped with protamine



sulfate. The dose is 1 mg protamine



for each milligram of LMWH given as 1 mg in 20 mL of normal saline infused slowly over 10 to 20 min. If a 2nd dose is required, it should be one half the first dose. However, the precise dose is undefined because protamine



only partially neutralizes LMWH inactivation of factor Xa. During all infusions, patients should be observed for hypotension and a reaction similar to an anaphylactic reaction. Because UFH given IV has a half-life of 30 to 60 min, protamine



is not given to patients receiving UFH (eg, if UFH was given > 60 min beforehand) or is given at a dose based on the amount of heparin



estimated to be remaining in plasma, based on the half-life of UFH.


Fondaparinux, a parenteral selective factor Xa inhibitor, may be used as an alternative to UFH or LMWH for the initial treatment of DVT or PE. It is given in a fixed dose of 7.5 mg sc once/day (10 mg for patients > 100 kg, 5 mg for patients < 50 kg). It has the advantage of fixed dosing and is less likely to cause thrombocytopenia.


Parenteral direct thrombin inhibitors (argatroban



, bivalirudin



, desirudin



) are available but do not have a role in treatment of prevention of DVT or PE. Argatroban



may be useful to treat DVT in patients with heparin



-induced thrombocytopenia.


Vitamin K antagonists, including warfarin



, are the drugs of choice for long-term anticoagulation for all patients except pregnant women (who should continue to take heparin



) and patients who have had new or worsening venous thromboembolism during warfarin



treatment (who may be candidates for an inferior vena cava filter). Warfarin



5 to 10 mg can be started immediately with heparin



because it takes about 5 days to achieve desired therapeutic effect. The elderly and patients with a liver disorder typically require lower warfarin



doses. Therapeutic goal is an INR of 2.0 to 3.0. INR is monitored weekly for the first 1 to 2 mo of warfarin



treatment and monthly thereafter; the dose is increased or decreased by 0.5 to 3 mg to maintain the INR within this range. Patients taking warfarin



should be informed of possible drug interactions, including interactions with foods and nonprescription medicinal herbs (see Table 4: Drug, Herbal Preparation, and Food Interactions With Warfarin).


Non-warfarin oral anticoagulants, also called direct oral anticoagulants (DOACs), are available as alternatives to warfarin



as a 1st-line treatment for the treatment of DVT and PE; not all DOACs are currently FDA-approved for this indication (see Table 6: Some Anticoagulation Options Other Than Heparin in Thromboembolic Disease). Drugs include factor Xa inhibitors (rivaroxaban



, apixaban



) and a direct thrombin inhibitor (dabigatran). Compared to warfarin



, these drugs have been shown to give similar protection against recurrent DVT and have similar (or with apixaban



, perhaps lower) risk of serious bleeding. Their advantages are that they are effective within several hours (thus, except for dabigatran, do not require parenteral bridging treatment with a heparin



), and they are given as a fixed dose (thus do not require ongoing laboratory testing). Their disadvantages are that they are expensive, and currently there are no available antidotes to reverse their anticoagulant effect in patients with major bleeding or who need urgent surgery. If used, rivaroxiban 15 mg po bid is started immediately upon diagnosis and given for 3 wk followed by 20 mg po once/day for 9 wk. Apixaban



10 mg po bid is started immediately upon diagnosis and given for 7 days followed by 5 mg po bid for 6 mo. Dabigatran 150 mg po bid is given only after an initial 5 to 7 days of treatment with LMWH. If major bleeding occurs, prothrombin complex concentrate (PCC) may be tried to decrease the anticoagulant effect of rivaroxaban



and apixaban



, and activated PCC may be used for dabigatran. Rarely, hemodialysis or hemoperfusion may help decrease the anticoagulant effect of dabigatran, which is not highly protein bound; such measures are not effective on rivaroxaban



and apixaban



. None of these treatments for DOAC-associated bleeding are clearly effective; many experts recommend only supportive care with fluids and packed RBC transfusions. Antidotes for DOACs are currently being developed.


Duration of treatment varies. Patients with transient risk factors for DVT (eg, immobilization, surgery) can usually stop taking warfarin



after 3 to 6 mo. Patients with nonmodifiable risk factors (eg, hypercoagulability), idiopathic (or unprovoked) DVT with no known risk factors, or recurrent DVT should take warfarin



for at least 6 mo and, in selected patients, probably for life unless complications occur.


Bleedingis the most common complication. Risk factors for severe bleeding (defined as life-threatening hemorrhage or loss of ≥ 2 units of blood in ≤ 7 days) include age ≥ 65; history of prior GI bleeding or stroke; recent MI; and coexisting anemia (Hct < 30%), renal insufficiency (serum creatinine > 1.5 mg/dL), or diabetes. In patients who are actively bleeding or may be at increased risk of bleeding, anticoagulation can be reversed with vitamin K; the dose is 1 to 2.5 mg po if INR is 5 to 9, 2.5 to 5 mg po if INR is > 9, and 5 to 10 mg IV (given slowly to avoid anaphylaxis) if hemorrhage occurs. If hemorrhage is severe, a transfusion of coagulation factors, fresh frozen plasma, or prothrombin complex concentrate should also be given. Selected patients with overanticoagulation (INR 5 to 9) who are neither actively bleeding nor at increased risk of bleeding can be managed by omitting 1 or 2 warfarin



doses and monitoring INR more frequently, then giving warfarin



at a lower dose. Rarely, warfarin



causes skin necrosis in patients with protein C or S deficiency or factor V Leiden mutations.


Inferior vena cava filter (IVCF): An IVCF may help prevent PE in patients with lower extremity DVT who have contraindications to anticoagulant therapy or in patients with recurrent DVT (or emboli) despite adequate anticoagulation. An IVCF is placed in the inferior vena cava just below the renal veins via catheterization of an internal jugular or femoral vein. Some IVCFs are removable and can be used temporarily (eg, until contraindications to anticoagulation subside or resolve). IVCFs reduce risk of acute embolic complications but can have longer-term complications (eg, venous collaterals can develop, providing a pathway for emboli to circumvent the IVCF, and increased risk of recurrent DVT). Also, IVCFs can dislodge or become obstructed by a clot. Thus, patients with recurrent DVT or nonmodifiable risk factors for DVT may still require anticoagulation despite the presence of an IVCF. A clotted filter may cause bilateral lower extremity venous congestion (including acute phlegmasia cerulea dolens), lower body ischemia, and acute renal failure. Treatment for a dislodged filter is removal, using angiographic or, if necessary, surgical methods. Despite widespread use of IVCFs, efficacy in preventing PE is unstudied and unproved. IVCFs should be removed whenever possible.


Thrombolytic (fibrinolytic) drugs: Streptokinase



, urokinase, and alteplase



lyse clots and may be more effective to prevent postphlebitic syndrome than heparin



alone, but the risk of bleeding is higher than with heparin



. Their use is under ongoing study, especially in patients with PE and right ventricular dysfunction and in combination with percutaneous mechanical thrombectomy for extensive proximal DVT. Thrombolytic therapy alone may be indicated for large proximal thrombi, especially those in the iliofemoral veins, and for phlegmasia alba or cerulea dolens. Local administration of thrombolytic therapy with an indwelling catheter (during percutaneous thrombectomy) may be preferable to IV administration.


Surgery: Surgery is rarely needed. However, thrombectomy, fasciotomy, or both are mandatory for phlegmasia alba dolens or phlegmasia cerulea dolens unresponsive to thrombolytics to try to prevent limb-threatening gangrene.



Prevention of immobility

Assessment of risk

Anticoagulation (eg, LMWH, fondaparinux



, adjusted-dose warfarin




Intermittent pneumatic compression


Patients at low risk of DVT (eg, those who are undergoing minor surgery but have no clinical risk factors for DVT, those who must be temporarily inactive for long periods, as during an airplane flight) should be encouraged to walk or otherwise move their legs periodically; no medical treatment is needed. Dorsiflexion 10 times/h is probably sufficient.


Patients at higher risk of DVT include those undergoing minor surgery if they have clinical risk factors for DVT; those undergoing major surgery, especially orthopedic surgery, even without risk factors; and bedbound patients with major medical illnesses (eg, most critical care unit patients, other patients with heart failure, COPD, chronic liver disease, stroke). These patients require additional preventive treatment (see Table 3: Risk of Deep Venous Thrombosis and Pulmonary Embolism in Surgical Patients). Most of these patients can be identified and should receive DVT prophylaxis; in-hospital thrombosis may be responsible for > 50,000 deaths/yr in the US. Hospitalization itself is not considered a risk factor, and hospitalized patients not in one of these categories do not require routine DVT prophylaxis.


After surgery, elevating the legs and avoiding prolonged immobility, which places the legs in a dependent position thereby impeding venous return, can help. Additional treatment may involve low-dose UFH, LMWH, warfarin



, fondaparinux



, new oral anticoagulants, compression devices or stockings, or a combination, depending on patient's risk level, type of surgery (if applicable), projected duration of preventive treatment, contraindications, adverse effects, relative cost, ease of use, and local practice. Low-dose UFH 5000 units sc is given 2 h before surgery and q 8 to 12 h thereafter for 7 to 10 days or until patients are fully ambulatory. Bedbound patients who are not undergoing surgery are given 5000 units sc q 12 h until risk factors are reversed.


LMWHs are more effective than low-dose UFH for preventing DVT and PE, but widespread use is limited by cost. Enoxaparin



30 mg sc q 12 h, dalteparin



5000 units sc once/day, and tinzaparin



4500 units sc once/day appear to be are equally effective. Fondaparinux



2.5 mg sc once/day is at least as effective as LMWH in patients who are undergoing nonorthopedic surgery and is possibly more effective than LMWHs after orthopedic surgery.





, using a target INR of 2.0 to 3.0, is proven to be effective in orthopedic surgery but is being used less frequently because alternative anticoagulants such as LMWHs and new oral anticoagulants are easier to administer.


New oral anticoagulants (eg, dabigatran, rivaroxaban



, apixaban



) are at least as effective and safe as LMWH for preventing DVT and PE after hip or knee replacement surgery but are more expensive than warfarin



, and their cost-effectiveness requires further study. Aspirin



is better than placebo but likely worse than LMWH and warfarin



for preventing DVT and PE and is not recommended as the first-line method of prevention in most patients (see Table 5: Risk of Deep Venous Thrombosis and Pulmonary Embolism in Surgical Patients).


Intermittent pneumatic compression (IPC) uses a pump to cyclically inflate and deflate hollow plastic leggings, providing external compression to the lower legs and sometimes thighs. IPC may be used instead of or in combination with anticoagulants after surgery. IPC is recommended for patients undergoing surgery associated with a high risk of bleeding in whom anticoagulant use may be contraindicated. IPC is probably more effective for preventing calf than proximal DVT. IPC is contraindicated in some obese patients who may be unable to apply the devices properly.


The benefit of graded compression stockings is questionable except for low-risk surgical patients and selected hospitalized medical patients. However, combining stockings with other preventive measures may be more protective than any single approach.


For elective neurosurgery, spinal cord injury, or multiple trauma, low-dose UFH (eg, 5000 units sc q 8 h), LMWH, or adjusted-dose warfarin



is recommended. For hip and other lower extremity orthopedic surgery, LMWH, fondaparinux



, or adjusted-dose warfarin



is recommended. For patients undergoing total knee replacement and some other high-risk patients, IPC is also beneficial. For orthopedic surgery, preventive treatment may be started before or after surgery and continued for at least 14 days. Fondaparinux



2.5 mg sc once/day appears to be more effective to prevent DVT than LMWH for orthopedic surgery but may be associated with an increased risk of bleeding. For neurosurgery patients, physical measures (IPC, elastic stockings) have been used because intracranial bleeding is a concern; however, LMWH appears to be an acceptable alternative. Limited data support the combination of IPC, elastic stockings, and LMWH in patients with spinal cord injury or multiple trauma.


For patients who are at very high risk of venous thromboembolism and bleeding (eg, after major trauma) IPC is recommended until the bleeding risk subsides and anticoagulants can be given. The use of IVCF should be avoided unless DVT has been confirmed, except in highly selected patients.


Preventive treatment is also indicated for patients who have a major medical illnesses requiring bed rest (eg, MI, ischemic stroke, heart failure). Low-dose UFH or LMWH is effective in patients who are not already receiving IV heparin



or thrombolytics; IPC, elastic stockings, or both may be used when anticoagulants are contraindicated. After a stroke, low-dose UFH or LMWH can be used; IPC, elastic stockings, or both may be beneficial.


In patients with symptomatic DVT who develop symptoms of postphlebitic syndrome (eg, leg swelling, pain, aching), the use of knee-high compression stockings providing 30 to 40 mm Hg pressure is recommended, although stockings with lower tension (20 to 30 mm Hg) can be considered if patients are unable to tolerate the higher tension stockings. However, the routine use of stockings in all patients who have had a DVT has been questioned by a recent study which randomly allocated patients with a DVT to receive knee-high compression stockings or sham-compression stockings. This study failed to show any decrease in postphlebitic syndrome with use of compression stockings.


Table 3

Open table in new window

Risk of Deep Venous Thrombosis and Pulmonary Embolism in Surgical Patients

Risk Category


Preventive Measures

Risk of DVT/PE (%)




Fatal PE



Nonmajor surgery* in patients < 40 yr with no clinical risk factors


Early and aggressive ambulation












Nonmajor surgery in patients with risk factors


Minor surgery in patients 40–60 yr with no clinical risk factors


Major surgery in patients < 40 yr with no other clinical risk factors


Immobilized patients with major medical illnesses


LDUH q 12 h, LMWH, fondaparinux



, or IPC, with or without elastic stockings












Nonmajor surgery in patients > 60 yr or 40–60 with risk factors


Major surgery in patients > 40 yr or with other clinical risk factors


LDUH q 8 h, LMWH, fondaparinux



, or IPC










Very high


Major surgery in patients > 40 yr who have had a previous venous thromboembolic, malignant, or hypercoagulability disorder


In patients of any age:


Hip or knee arthroplasty

Hip fracture surgery

Elective neurosurgery

Multiple trauma

Spinal cord injury

LMWH, oral anticoagulation, IPC, or elastic stockings plus either LDUH q 8 h or LMWH





if patients have had orthopedic, abdominal, or thoracic surgery or have an acute, severe illness










*Nonmajor surgery is defined here as an operation that does not involve general anesthesia or respiratory assistance.

DVT = deep venous thrombosis; PE = pulmonary embolism; LDUH = low-dose unfractionated heparin



; LMWH = low molecular weight heparin



; IPC = intermittent pneumatic compression.

Adapted with permission from Geerts WH, Heit JA, Clagett GP, et al: Prevention of venous thromboembolism. Chest 119:132S–175S, 2001.

Key Points

Symptoms and signs are nonspecific, so clinicians must be alert, particularly in high-risk patients.

Low-risk patients may have d-dimer testing, as a normal result essentially excludes DVT; others should have ultrasonography.

Treatment initially is with an injectable heparin



(unfractionated or LMWH) followed by oral warfarin



or perhaps a LMWH; the role of oral factor Xa inhibitors is evolving.

Duration of treatment is typically 3 or 6 mo depending on the presence and nature of risk factors; certain patients require lifelong treatment.

Preventive treatment is required for bedbound patients with major illness and/or those undergoing certain surgical procedures.

Early mobilization, leg elevation, and an anticoagulant are the recommended preventive measures; patients who should not receive anticoagulants may benefit from intermittent pneumatic compression devices, elastic stockings, or both.

Last full review/revision May 2014 by James D. Douketis, MD

Content last modified May 2014

Patient stories on treatment of Varicose veins

Posted by [email protected] on February 27, 2015 at 1:15 AM Comments comments (0)

Story of Mrs. Thapa

Varicose veins: Prominent dilated veins


Mrs. Thapa, a 45 year old female from Banepa came to Dhulikhel hospital with history of non healing wound in left leg since two years. Since two years she was on different oral antibiotics, local antibiotics, pain killers from different hospitals. Despite these treatment the 4*4 cm wound in foot was never completely cured. She was in immense emotional stress as her friends and family members thought that she was suffering from cancer. On examining her, prominent dilated veins could be seen in left leg. On doing Doppler examination, there was an incompetent perforator in above ankle region of left leg and multiple varicosities in leg region. As the non healing ulcer was due to this imcompetent perforator, an operation was advised to ligate it. Following operation, she was completely fine and within two weeks, the ulcer completely healed and hasn’t recurred since four months.


What Mrs. Thapa was suffering was due to condition of vein called as varicose vein. The venous system in lower limb comprises of three systems as deep veins, superficial veins and communicating veins (perforators). Superficial veins communicate with deep veins via perforator veins which have valves to prevent back flow. When there is disease in valves of these perforator veins there is back flow of blood from deep to superficial system resulting in abnormal dilatation of these superficial veins. Also the superficial veins such as long saphenous vein, short saphenous vein finally drain into deep system (femoral and popliteal veins respectively). When there is incompetence in these junction, this can also cause varicose veins.


Occupations requiring prolonged standing, lifting heavy loads, prolonged walking predispose this condition. Also, pregnancy, deep vein thrombosis can also cause varicose veins. Nursing profession also requires prolonged standing, and this can also predispose this condition. Avoiding prolonged standing, use of crepe bandaging in calf and thigh, use of graduated stocking help in prevention of this disease.


When already diagnosed, the main aim is to stop the progression of the disease by above mentioned techniques. Medications donot help to treat this condition. If there is pain, if the veins are cosmetically unsightly, if there are skin changes (like erythema, ulcers), we should proceed with surgical treatment. Surgically, there are multiple options but most commonly we ligate the junction such as saphenofemoral/ saphenopopliteal junction, we remove the segment of superficial vein in thigh (called as stripping of the vein), we ligate the incompetent perforators and we do multiple phlebectomy. Choice of different procedures depends upon the individual cases. Now a days, newer surgical treatments like Endo Venous Laser Treatment (EVLT), Radio Frequency Ablation (RFA) are also available which are associated with very good outcome and early recovery.


Department of surgery in Dhulikhel hospital is regularly performing surgeries for varicose vein. We have already started newer modalities of treatment for varicose vein like Radiofrequency ablation in more than 150 cases. With good cooperation from Nursing faculties, we have been able to provide good service to patients with this condition. We hope there will not be other people like Mrs Thapa waiting for proper treatment for years for a condition known to have easy remedy.

Dr. Robin Man Karmacharya,

Department of Surgery,

Dhulikhel hospital