Friday, May 30, 2014

Varicose Vein and Examination

Normal Venous Circulation in Leg

Two venous systems are found in the lower extremity, the deep and superficial, as depicted in the image below. The deep system ultimately leads backs to the inferior vena cava, then to the heart. The superficial system is found above the deep fascia of the lower extremity, within the subcutaneous tissue. Many superficial veins exist, but they all drain into the 2 largest superficial veins, the greater saphenous vein (GSV) and the short saphenous vein (SSV), formerly called the lesser saphenous vein.



The superficial venous system is connected to the deep system at a number of the following locations:


  • Perforator veins: These veins traverse the deep fascia of the lower extremity. A number of named perforators are found at the thigh, knee, and leg.






  • Saphenofemoral junction (SFJ): This is located proximally at the groin where the GSV meets the femoral vein, as depicted in the images below.










  • Saphenopopliteal junction (SPJ): This is located behind the knee where the SSV joins with the popliteal vein.


In healthy veins, the flow of venous blood is through the superficial system into the deep and up the leg and toward the heart. One-way venous valves are found in both systems and the perforating veins. Incompetence in any of these valves can lead to a disruption in the unidirectional flow of blood toward the heart. In 53% of patients only superficial venous reflux was found, in 15% isolated deep venous reflux was found, and in 32% a combination of deep and superficial venous reflux was found.

Incompetence in the superficial venous system alone usually results from failure at valves located at the SFJ and SPJ. The gravitational weight of the column of blood along the length of the vein creates hydrostatic pressure, which is worse at the more distal aspect of the length of vein.

Incompetence of the perforating veins leads to hydrodynamic pressure. The calf pump mechanism helps to empty the deep venous system, but if perforating vein valves fail, then the pressure generated in the deep venous system by the calf pump mechanism are transmitted into the superficial system via the incompetent perforating veins.




Once venous hypertension is present, the venous dysfunction continues to worsen through a vicious cycle. Pooled blood and venous hypertension leads to venous dilatation, which then causes greater valvular insufficiency. Over time, with more local dilatation, other adjacent valves sequentially fail, and after a series of valves has failed, the entire superficial venous system is incompetent.





The clinical finding of varicose veins, reticular veins, and telangiectasia are due to the hypertension in the superficial venous system that spreads to collateral veins and tributary veins.

In contrast to the superficial veins, the deep veins do not become excessively distended. They can withstand the increased pressure because of their construction and the confining fascia.


Examination of Varicose Vein

Perthes maneuver/Linton test: This is a physical examination technique in which a tourniquet is placed over the proximal part of the leg to compress any superficial varicose veins while leaving deep veins unaffected. The patient walks or performs toe-stands to activate the calf-muscle pump which normally causes varicose veins to be emptied. However, if obstruction of the deep system exists, then activation of the calf-muscle pump causes a paradoxical congestion of the superficial venous system and engorgement of varicose veins resulting in a positive test. To verify, the patient is then placed supine, and the leg is then elevated (Linton test). If varices distal to the tourniquet fail to drain after a few seconds, again deep venous obstruction must be considered.





Once the dilated veins of the leg are marked, the Brodie-Trendelenburg test can be performed. With the patient in the supine position and the leg elevated 60°, emptying the varices of blood by stroking distally to proximally is performed, and a tourniquet is placed around the proximal thigh. The patient then stands up, and the leg is observed for 30 s with the tourniquet in place. The following responses can be seen:




  • “Nil” test: (Competent valves of the deep and perforating veins and at the saphenofemoral junction): No distention of the veins for 30 s both with the tourniquet in place and after removal
  • “Positive” test: (Incompetent valve at the saphenofemoral junction): Distention of the veins only after release of the tourniquet
  • “Double” positive test: (Incompetent deep and perforating veins, with reflux through the saphenofemoral junction): Distention of veins with the tourniquet in place and further distention after release
  • “Negative” test: (Deep and perforating valvular insufficiency): Distention of veins within 30 s of the tourniquet in place, and no increased filling after release of the tourniquet. However, filling of the vein(s) after 30 s of tourniquet placement does not imply competence of perforating veins.


The percussion/Schwartz test is performed by placing one hand over the saphenofemoral junction or the saphenopopliteal junction while the other hand is used to tap lightly on a distal portion of the long or short saphenous vein. The presence of an impulse implies valvular insufficiency in the segment between the two hands.




Morrisey’s Cough Impulse test

  1. Ask patient to stand.
  2. Use finger to held over patient's saphenofemoral opening [5cm below and medial to femoral pulse].
  3. Ask patient to cough.
  4. If saphenofemoral junction is incompetent, there is presence of fluid thrill.


Fegan’s test




Pratt test
The Pratt Test is a simple test to check for Deep Vein Thrombosis in the leg. It involves having the patient lie supine with the leg bent at the knee, grasping the calf with both hands and pressing on the popliteal vein in the proximal calf. If the patient feels pain, it is a sign that a DVT exists.


Multiple Tourniquet Test




*Do not confuse Trendelenburg Test with Multiple Tourniquet Test

Trendelenburg test is to apply one tourniquet below (for example SFJ). If during the tourniquet is applied, there is filling of varicose vein(which you had just emptied before the test), it means the pt’s perforating vein is incompetent, blood flow from deep vein to superficial vein. If after applied, no filling, and when you release the tourniquet and there is filling, it means the SFJ above your tourniquet is incompetent and cause downward flow of blood because of the gravity. However,

For multiple tourniquet test, it is simply used to test perforating veins, so don’t think about the superficial vein. Multiple tourniquets are applied to occlude the superficial vein at different area. For example one at the mid thigh and one above the knee. So normally when without tourniquet, if blood flow from the incompetent perforating vein to superficial vein, it might flow downward when it’s in the superficial vein(if there is further incompetent valve), or it will be carried upward to the SFJ and so on…

So applying tourniquet is to occlude the superficial vein above and below the area which the perforator vein has problem. So that we can see the pooling of blood at the varicose vein there(remember that you already empty the varicose vein before the test by elevate leg and also rub the veins).


So for multiple tourniquet, the result is not to be acquired by releasing the tourniquet, but is during which the tourniquets are applied. So, for my personal opinion, it doesn’t matter whether you remove them from bottom to above or from above to bottom.


The purpose of doing all these tests is to determine the area so as to perform surgery on the problem veins. But these tests are not so important nowadays provided that technology such as colour flow imaging, magnetic resonance venography can already help to give a better image. Varicose veins can cause complications such as ulcers beside just comestically undesirable. So, sometimes surgery to take out the varicose vein is necessary. However, nowadays, other methods such as sclerotherapy is also used.

Adapted from: Medscape and Some old surgery books

Ankle Brachial Index (Mr.Foot and Mrs.Arm has different opinions on SBP)

What is Ankle Brachial Index?

The Ankle Brachial Index (ABI or ABPI) is the ratio of the blood pressure in the lower legs to the blood pressure in the arms. Compared to the arm, lower blood pressure in the leg is an indication of blocked arteries (peripheral vascular disease or PVD). The ABI is calculated by dividing the systolic blood pressure at the ankle by the systolic blood pressures in the arm.

ABPI_{Leg} = \frac { P_{Leg} }{ P_{Arm} }

risk factor for atherosclerosis:

Etiology:



Causes of Peripheral Vascular Disease:
1. Artheriosclerosis (also will develop in carotid or coronary artery, increase risk for stroke or heart attack)
Known first for pain in leg when exercising or walking(Intermittent claudication)

2. Diabetes Mellitus (There are FIVE pathway for pathogenesis of Macro and Microvascular diseases)

Treatment of PVD:
1. Cessation of smoking
2. Controlling high BP
3. Statins/Lipid level control
4. Dietary changes
5. Exercise
6. Diabetic control
7. Surgery

Pain of PVD can range from mild pain when exercise to severe pain even at rest. PVD limit the ability to exercise. Also can leads to sores and ulcers at leg that do not heal in critical limb ischemia that cause gangrene and require of amputation.

Stroke and heart attack are the most serious and common complication.

Over 5 years period, PVD sufferers
20% sustain stroke
30% fatal event

Critical Limb Ischaemia
30%- amputations
20%-dead

How to perform ABI test?
Things you need:
Doppler, Sphygmomanometer, Gel
Makes sure patient is warm and rest 10-15mins before begin
Measure all the 4 limbs SBP(posterior tibialis and brachial), take the highest reading

See here: http://www.youtube.com/watch?v=LvHeMiCaUdw

AHA ABI Interpretation:
Greater than 1.3, noncompressible arteries, obtain toe pressure
1.00-1.29, normal
0.91-0.99, appears normal, but exercise reveals low degree of obstruction
0.41-0.90, mild to moderate PAD (will experience intermittent claudication when they walk or exercise)
0.00-0.40, rest pain, failure for healing of injury to foot or toe

ABI provides 3 info:
1. Doppler sound
2. Index
3. Waveform

Normal young healthy have triphasic waveform
Biphasic: mildly abnormal
Monophasic progressive disease







People particularly at risk for PAD:
-->less than 50 years of age with DM and one other risk factor for atherosclerosis: HPT, Dyslipidemia, Smoking or Hyperhomocysteinemia

-->age 50-69, hx of diabetes or smoking

-->70 or older

-->leg symptoms upon exertion, intermittent claudication/ischemic rest pain

-->abnormal leg, ankle or foot pulse examination

-->known atherosclerotic carotid, coronary or renal artery disease

-->Psoriasis increase risk of PAD, MI or CVA

Not all people with PAD are symptomatic, only 10 percent have the classic symptoms of intermittent claudication

Adapted from:
Youtube; Vascular Hokanson Channel; How to do ABI
http://360woundcare.wordpress.com/category/uncategorized/
Netter Cardiology Images














Thursday, May 29, 2014

The Police Officer-Neutrophil (some patrol in the blood, some guard at the vessel)

Neutrophil is an amazing cell inside our body. In fact every cell is. AT first I always thought neutrophil is an agent of inflammation. Talking about inflammation made me thought of neutrophil. BUT here I read something about neutrophil today and I felt that the way it works is amazing!

Adapted from Haematology ICT WH120 H849h pg6

The blood neutrophil is the end product of an orchestrated sequence of differentiation in the myeloid cells of the bone marrow. (revise haemopoiesis!).


The mature cell has a multi-lobed nucleus and four different type of granules in the cytoplasm. (Hmm...any application of this?) They have limited lifespan of 5-6 days. Approximately half the cells are included in a normal blood count (revise what is absolute count for WBC here!), the remainder being in the marginal pool.

so, what is the marginal pool mentioned here?
Neutrophils released from the marrow enter the blood where they distribute into two compartments of approximately equal size: the circulating and the marginal pools. Neutrophils in the former compartment are freely circulating, whereas those in the marginal compartment are temporarily adherent to endothelial cells, generally in the postcapillary venules. In normal adult humans, the total of these two compartments (termed the total blood neutrophil pool) contains about 0.6 × 109 cells/kg body weight; with about one half of the cells (0.3 × 109 cells/kg) in each (circulating and marginal) pool.
In the marrow, the proportion of band to segmented neutrophils is much higher than in the blood. On that basis, it is likely that a selective release of segmented neutrophils occurs from the marrow, whereas band neutrophils generally remain behind to mature.
from this website: http://www.expertconsultbook.com/expertconsult/ob/book.do?method=display&type=bookPage&decorator=none&eid=4-u1.0-B978-1-4160-3479-7..10143-0--s0025&isbn=978-1-4160-3479-7

From CLINICAL HAEMATOLOGY, BARNARD, pg3
After about 10 days of maturation and differentiation in the marrow,the mature neutrophil polymorph has a circulating lifespan of only a few hours.The marrow storage pool of neutrophils is approx. 12 times that present in the blood. Whilst a vernous blood sample can measure the circulating neutrophil pool, there is a further marginating neutrophil pool in close proximity to blood vessel wall. the normal fate is attraction to tissue sites by inflammatory mediators or excretion in body secretions. In response to the stimulus of infection or inflammation, large no. of neutrophils maybe relesed into the circulating pool from the marrow and marginating pool to give the neutrophil leucocytosis characteristics of such states. Less mature form with unsegmented nuclei maybe prematurely liberated from the marrow to produce a 'left shift' in the differential white cell count.

That's means when released into the blood, half is circulating and half is marginating due to adhesion molecules.

Notes to come: Hypersegmented neutrophil, neutropenia, acute inflammation














Blood Group and HDN

Adapted from Haematology, an illustrated color text

The blood groups

Antigen exits on RBC membrane
Numerous blood group systems encoded by genes on different chromosomes
highly variable in their polymorphonism and clinical significance
most important is ABO system, the genes encodingis located on chromosome 9 and inherited in autosomal dominant fashion
Each antigen is a sugar residue made by a specific glucosyl transferase


This is an example of antigen H. which means no extra added residue, and this is antigen for blood group type O.




This is example of antigen A, which has added N-acetylgalactosamine to the original template antigen H. This is antigen for the blood group type A.


This is antigen B on surface of rbc blood group type B. It has another added galactos on the template antigen H.

Person who has blood group type AB is having both antigen A and antigen B on their RBC surface.

The ABO SYSTEM is crucial in blood transfusion. As the antibody against ABO antigen is naturally occuring. For example, if you are blood group type A, this means that you have antigen A on your red cell, but you do not have antigen B on your red cell, so your body will naturally have antibody against B, which we called it as anti-B.


These naturally occurring antibodies(anti-A and anti-B) are of IgM type and if the blood transfusion is not compatible, the patient serum which contains this IgM will attacks donor's red cell and will induce fatal hemolytic transfusion reaction.

So test must be done before blood transfusion. We will discuss this later on.


Another type of antigens are minor antigens. ABO is considered as major but our RBC surface might also have other antigens namely Rhesus, Duffy, Lewis, Kell etc. The antibody against these antigens are not naturally occurring, they are called 'immune antibodies' as they will only be produced when your body's immune system is sensitized by these antigens. The strongest antigen D(Rhesus), for example, can be induced through previous blood transfusion or pregnancy. In pregnancy, if the mother is Rhesus -ve but baby is Rhesus +ve(inherited from father), during first pregnancy, some of the fetal blood might leak into the mother during delivery and causes sensitization of the mother's immune system. Once mother's blood contains this antibody, the second baby which is also Rhesus +ve, the fetal antigen will be attacked by mother's developed antibody and thus develop hemolytic newborn disease(HDN). The HDN here must not be confused with Hemorrhagic Newborn Disease, which is increased risk of bleeding in newborn due to vit K deficiency which impaired the production of Factor 2, 7, 9, 10, C and S by the liver.


The reasons that being different in Rhesus grouping between mother and child has more consequences than ABO grouping is, 1) the rhesus antibody is lgG in nature and can cross placenta to reach the fetus whereas ABO antibody(IgM) can't 2) Fetus doesn't develop fully yet ABO antigen, so less likely to sensitize mother and cause an immune attack.


Notes to come: GSH, GXM, Blood Grouping, Coombs test