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Laporan PBL Modul Vaskular Blok Kardiovaskular
Laporan PBL Modul Vaskular Blok Kardiovaskular
OLEH:
KELOMPOK 15
M. Farizan Atjo (11020160032)
Ainunnisa Muhammad (11020170003)
Miftahul Janna (11020170042)
Moh. Yusril (11020170052)
Muhammad Fakhri (11020170069)
Muh. Fadil Asrar (11020170055)
Jihan Adjdjibiyan S. Azzubaidi (11020170105)
Indah Setiyani Ulum (11020170134)
Andi Bau Syatirah Ninnong M (11020170138)
Hernita (11020170152)
TUTOR: dr. Farah Ekawati
FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2019
SCENARIO 3
A 42 year old man came to the Public Health Service with complaint of swelling
in the left leg with severe redness on the last 1 day. Patient often feel cramps and
sometimes feel numb and accompanied by pain. The patient’s occupational
history is an expedition driver between provinces.
On physical examination blood pressure was 120/80 mmHg. Pulse 92x/minute,
respiratory rate 20x/minute, temperature: 36,80C. Examination of the extremities
found redness as high as 1/3 proximal tibia with erythema accompanied by pitting
edema. Normal popliteal arterial pulsation
Keywords
1. 42 years old man
2. Swelling in the left leg with severe redness on the last 1 day
3. Feel cramps and feel numb
4. Patient is an expedition driver between provinces
5. Blood pressure: 120/80 mmHg, Pulse: 92x/minute, RR: 20x/minute,
Temperature: 36,80C
6. Extremities found Redness as high as 1/3 proimal tibia with erythema and
pitting edema. Normal A. Popliteal Pulsation
Question :
1. How is the mechanism of Edema?
2. How to difference disease cause by Artery and Vein?
3. What is relation between activity and swelling in the leg?
4. Why the patient feel cramp and numb?
5. How to diagnose the patient based on scenario?
6. What is the differential diagnose in the scenario?
7. What is the first treatment based on the scenario?
Answer :
1. How is the mechanism of Edema?
Edema is excessive fluid accumulation between body cells or in
various body cavities, this condition is often encountered in daily clinical
practice that occurs as a result of imbalance of factors that control the
transfer of body fluids, including the capillary hemodynamic system
causing sodium and water retention, kidney disease and the transfer of
water from intervascular to intertitial.
Edema occurs in conditions where there is an increase in
hydrostatic capillary pressure, increased capillary permeability or
increased intertial osmotic pressure, or a decrease in plasma osmotic
pressure. The kidneys have a central role in maintaining body fluid
homeostasis by controlling the volume of extracellular fluid through
regulation of sodium and water excretion. Antidiuretic hormones are
secreted in response to changes in blood volume, tonicity and blood
pressure to maintain balance of body fluids.1
Vein
Deep vein thrombosis can appear with the first symptoms found,
namely edema that is more often unilateral, then can be accompanied by
pain and itching or ulcers which improve with elevation of the foot
position, in some patients it is found that symptoms can be aggravated
during activities.4
Numb
Numbness is most often caused by damage, irritation or
compression of nerves. A single nerve branch, or several nerves, may be
affected, as with a slipped disc in the back or carpal tunnel syndrome in
the wrist. Certain diseases, such as diabetes, which can damage the
longest, most sensitive nerve fibers (such as those going to your feet), can
also cause numbness.
Usually, the affected nerves are located on the periphery of your
body. Only rarely is numbness caused by problems in your brain or spinal
cord. Numbness alone is only rarely associated with potentially life-
threatening disorders, such as strokes or tumors.7
Scenario:
A 42-year-old man came to the public health with a complaint
swelling in the left foot with redness weighing in the last 1 day. Frequent
patients feel cramps and sometimes like numbness and pain. History the
patient's job was an expedition driver between provinces.
PHYSICAL EXAMINATION
1. Vital signs: blood pressure 120/80 mmHg, pulse 92x / minute,
breathing 20x / minute, temperature: 36.8 0 C.
2. Inspection: symmetry, changes in skin appearance and edema, skin
color (on examination of extremities found redness as high as 1/3
proximal tibia with erythema accompanied by pitting edema.)
3. Palpation: pulsations in the upper and lower limbs. Asymmetricity,
intensity pressure suppression and weakening of the pulse can lead to
peripheral arterial disease
a. Examination of Allen
b. Thoracic outlet maneuver
c. Signs of homan: an examination is performed by bending the
patient's knee and forcibly pushing the ankle into a dorsiflexion
position. The presence of calf pain with this maneuver indicates
thrombosis in the vein.
Normal popliteal arterial pulsation.
SUPPORTING INVESTIGATION
Duplex examination of the extremity veins can evaluate the
presence of non-invasive thrombosis in the deep vein
Magnetic resonance angiography (MRA)8
Etiology
The veins function to drain blood from the entire body back to the
heart. To reach the heart, the muscles of the lower extremities must
contract to squeeze and pump blood from the lower extremity veins back
towards the top (heart) against the effects of gravity. Veins have many
one-way valves to prevent blood from returning down (reflux). If the
venous valve is damaged so that the blood pumped from the lower
extremity to the heart partially returns to the bottom and accumulates
causing venous pressure to increase.
Lower extremity venous damage resulting in backflow or reflux as a
result of:
a. Venous hypertension
b. Deep vein thrombosis
c. Obesity
d. Leg immobility
e. Pregnancy
f. Often standing or sitting for long periods of time due to lifestyle or
profession
g. The aging process
Pathogenesis
Valve failure in the superficial vein is most commonly caused due
to increased pressure in the blood vessels by venous insufficiency.
Another possible cause of venous valve failure is the direct trauma to the
vein in the presence of a valve abnormality due to thrombosis. If the
superficial vein is exposed in the presence of high pressure in the blood
vessels, these veins will be dilated and then continue to enlarge until the
vein valves from one another cannot meet each other. Failure in one vein
valve will trigger failure of the other valves. An increase in excessive
pressure in the superficial venous system will cause dilatation of the vein
local. After several venous valves fail, the function of the vein to drain
blood up and into the deep vein will be disrupted. Without functional
valves, venous blood flow will flow due to pressure and gravity gradients.
Clinical features
Varicose veins are classified as:
a. Primary varicose veins, due to superficial venous abnormalities of the
lower extremities
b. Secondary varicose veins, due to abnormal venous insufficiency,
which includes edema, skin pigmentation, and ulcers.
Physical examination:
a. Crash at night lower limb muscles (legs)
b. The legs get tired quickly when walking
c. Swelling and heaviness in the legs
d. Clinical features of venous insufficiency (edema, pain, discoloration,
to ulcers)
e. Itching of the legs
f. Tingling in the legs
g. Widening of the blue or dark purple veins that appear on the skin
Supporting investigation
• Brodie-Tredelenburg test
Shows back blood flow through the incompetence of superficial
venous valves and branches associated with veins in the legs. The patient
is lying down, the affected limb is elevated 45 ° to empty the vein. Then
tourniquet is placed around the upper limb and the patient is asked to
stand. If venous filling is <30 seconds distal to tourniquet, the perforator
vein and vein are incompetent. If when the tourniquet is released, blood
will fill and flow quickly from the top to the superficial vein, meaning the
superficial vein valve is incompetent.
• Test Perthes
A tourniquet is placed in the middle of the thigh in a standing
position. If the varicose vein disappears after 5 minutes of walking, the
inner vein and perforator vein are competent. If the blood vessels are not
able to empty themselves but instead pain and distension when walking,
meaning there is incompetence or obstruction.
• Venous Duplex Imaging
Can detect reflux in the superficial vein, perforator vein or deep
vein.
• Venous plestimography
To detect changes in venous blood volume in the limbs, normal
<2mL / s,> 4mL / s is abnormal.
• Computed Tomographic or Magnetic Resonance Venography
Can be used to assess venous anatomy, blockage of veins.
• Venography
Contrast is injected into the venous system to identify reflux in the
venous flow system.
Governance
1. MPFF (Micronized Purified Flavonoid Fraction)
Dosage of 1000 mg / day for 6 weeks
To improve venous vascular tone, improve microcirculation
and lymphatic flow thereby reducing swelling.
Reducing leukocyte adhesion thereby reducing inflammation
2. Compression stocking
It is useful to press the edge of the vein wall towards the lumen
so that the center of the valve approaches and reflux decreases
in addition to increasing the pressure of the paravascular tissue
and muscle contraction, thereby increasing venous tone.
Stocking is used while on the move, and released during sleep
Use of stockings below the knee
3. Treatment of venous sclerosing.
4. Endovenous radiofrequency or laser ablation therapy.
5. Surgery by means of ligation or vein stripping9
Epidemiology
The importance of CVI is related to the number of persons afflicted
and the socioeconomic impact of its more severe manifestations.
Varicose veins have an estimated prevalence between 5% and 30%
in the adult population, with a female:male predominance of 3:1, although
a more recent study supports a higher male prevalence. CVI was more
common with increasing age; however, there was no significant sex
difference. The rate of varicose vein development may be estimated from
the Framingham Study, which found an annual incidence of 2.6% in
women and 1.9% in men. The prevalence of varicose veins is higher in
developed, industrial countries than in underdeveloped countries. Risk
factors found to be associated with CVI include age, sex, a family history
of varicose veins, obesity, pregnancy, phlebitis, and previous leg
injury.9 There are also environmental or behavioral factors associated with
CVI, such as prolonged standing and perhaps a sitting posture at work.
The overall prognosis of venous ulcers is poor, because delayed
healing and recurrent ulceration are very common. The socioeconomic
impact of venous ulceration is dramatic because of an impaired ability to
engage in social and occupational activities, reducing the quality of life
and imposing financial constraints.
Venous Pathophysiology
Normal Venous Anatomy and Function
The peripheral venous system functions as a reservoir to store
blood and as a conduit to return blood to the heart. Proper functioning of
the peripheral venous system depends on patency of vessels containing a
series of 1-way valves and muscle pumps. In the erect position, blood that
enters into the lower extremity venous system must travel against gravity
and other pressures to return to the central circulation.
The veins of the lower extremity are divided into superficial, deep,
and perforator veins. The superficial venous system is located above the
muscular fascial layer. It is composed of an interconnecting network of
veins and several truncal superficial veins, including the great saphenous
vein (GSV) and small saphenous vein, as well as several accessory veins,
which may develop pathology contributing to CVI. The deep venous
system is located below the muscular fascia and serves as collecting veins
and the outflow from the extremity. The deep veins of the lower extremity
consist of axial veins, which follow the course of the major arteries, and
intramuscular veins, including venous sinusoids and plexi. The perforating
veins traverse the anatomic fascial layer to connect the superficial to the
deep venous system.
The valves within the veins are essential in assuring that blood
flows in the correct direction, particularly while in the upright posture.
There is a series of 1-way bicuspid valves located throughout the deep and
superficial veins that open to allow flow toward the heart but close to
prevent the return of blood toward the feet. There are 4 phases of valve
function which include opening, equilibrium, closing, and closed. The
critical factors to valve function are axial vertical of blood flow opening
the valve and vertical velocity in the valve cups that increases mural
pressure relative to the luminal pressure leading to valve closure. The
frequency of these venous valves increases from the proximal to distal leg
to prevent an increase pressure within the distal veins because of
gravitational effects. In addition, perforating veins also contain valves that
only allow blood flow from the superficial to the deep veins.
The valves function in concert with venous muscle pumps to allow
the return of blood against gravity to the heart. Contraction of the muscle
pumps, primarily in the calf, force blood out of the venous plexi to ascend
up the deep venous system. The valves prevent blood from being forced
more distally within the deep system or through perforator veins into the
superficial system. Immediately after ambulation, the pressure within the
veins of the lower extremity is normally low because the venous system
has been emptied by the muscle pump action (Figure 1). Relaxation of the
muscle pump then allows blood to refill to the deep venous system. With
prolonged standing, the veins become distended as the vein fills via
antegrade flow, allowing the valves to open and pressure to increase.
Contraction of the muscle pump will again empty the veins and reduce
venous pressure.
Clinical Manifestations
CVD represents a spectrum of conditions ranging from simple
telangiectases or reticular veins to more advanced stages, such as skin
fibrosis and venous ulceration. It is important to realize that the same
clinical manifestations may result from different pathogenic mechanisms,
including incompetent valves, venous obstruction, muscle pump
dysfunction, or a combination. The major clinical features of CVI are
dilated veins, edema, leg pain, and cutaneous changes in the leg. Varicose
veins are dilated superficial veins that become progressively more tortuous
and enlarged (Figure 2A). They may develop bouts of superficial
thrombophlebitis, recognized by painful, indurated, inflamed areas along
the varicose vein. Edema begins in the perimalleolar region and ascends
up the leg with dependent fluid accumulation. Leg discomfort is often
described as heaviness or aching after prolonged standing and is relieved
by elevation of the leg. This discomfort is thought to be produced by
increased intracompartmental and subcutaneous volume and pressure.
There may also be tenderness along varicose veins because of venous
distention. Obstruction of the deep venous system may lead to venous
claudication (or intense leg discomfort with ambulation). Cutaneous
changes include skin hyperpigmentation because of hemosiderin
deposition and eczematous dermatitis (Figure 2B). A fibrotic process may
occur in the dermis and subcutaneous fat termed “lipodermatosclerosis.”
There is an increased risk of cellulitis, leg ulceration, and delayed wound
healing (Figure 2C). In addition, protracted CVI may also contribute to the
development of lymphedema, representing a combined process.
Figure 2. Manifestations of chronic venous insufficiency. A,
Extensive varicose veins involving the thigh and leg. B,
Hyperpigmentation and severe lipodermatosclerosis with leg edema.
Notice healed ulcers in the gaiter region of the medial leg. C, Medial
malleolar venous ulcers. Notice concomitant eczema and
lipodermatosclerotic skin.
Diagnosis of CVI
A complete history and physical examination are important to
establish a proper diagnosis of CVI and may be assisted by noninvasive
testing. Invasive testing may also be used to establish the diagnosis but is
typically reserved for assessing disease severity or if surgical intervention
is being contemplated. The methods used to assess CVI are described
below, but comprehensive overviews have been published previously.
Physical Examination
The physical examination not only aids in establishing a diagnosis
but plays an important role in helping to guide therapy in CVI. Visual
inspection and palpation may reveal evidence of venous disorders. The
skin is examined for prominent, dilated superficial venous abnormalities,
such as telangiectasis, reticular veins, or varicose veins. The surface is
inspected for irregularities or bulges to suggest the presence of dilated
tortuous veins. The distribution of these varicose veins may follow the
course of the affected superficial vein, such as the GSV and small
saphenous vein. This evaluation should include positioning in the upright
posture to allow for maximal distention of the veins. Additional skin
findings may be seen, such as hyperpigmentation, stasis dermatitis,
atrophie blanche (or white scarring with a paucity of capillaries), or
lipodermatosclerosis. The presence of edema and its severity is assessed.
The edema seen in CVI is dependent and usually pitting; however, it may
become more resilient to palpation if protracted. There is often relative
sparing of the forefoot to help distinguish the etiology of other causes of
edema, such as lymphedema. An early finding of venous congestion
includes calf fullness or increased limb girth, so the calf muscle
consistency should be assessed, and measurement of the limb girth should
be performed. There is no universally agreed on scale for grading the
severity of edema. Palpation along the course of dilated veins may reveal
tenderness. The presence of active or healed ulcers, typically in a
distribution near the medial aspect of the ankle with GSV reflux or lateral
aspects of the ankle with small saphenous vein reflux, may be seen with
more advanced disease.
Differential Diagnosis
There is a broad differential for the most common presenting
symptoms of limb swelling and discomfort that are seen in CVI. The
initial task is to exclude an acute venous problem, such as deep vein
thrombosis. Then, systemic causes of edema need to be considered, such
as heart failure, nephrosis, liver disease, or endocrine disorders.
Importantly, adverse effects of medication should be considered, such as
those with calcium channel blockers, nonsteroidal anti-inflammatory
agents, or oral hypoglycemic agents. Critical disorders to consider are
lymphedema, lipedema, and the combined disorder of lipolymphedema.
Lymphedema because of obstruction of lymphatic drainage leads to fluid
accumulation that extends into the foot and toes, in contrast with CVI,
which relatively spares the foot. The edema may be pitting early in the
course of the disease but as the disease progresses becomes nonpitting. In
contrast, lipedema is characterized by fatty tissue accumulation rather than
fluid, thus, it is not pitting. It usually spares involvement of the feet, often
with a cuff of tissue at the ankle. Finally, other regional considerations
should be made, such as ruptured popliteal cyst, soft tissue hematoma or
mass, exertional compartment syndrome, or gastrocnemius tear. The use of
examination findings and noninvasive testing should allow for the proper
diagnosis to be established.
Noninvasive Testing
Treatment of CVI
Conservative Management
The initial management of CVI involves conservative measures to
reduce symptoms and prevent development of secondary complications
and progression of disease. The use of compressive stockings is the
mainstay of conservative management and is further described below. If
conservative measures fail or provide an unsatisfactory response, further
treatment should be considered on the basis of anatomic and
pathophysiologic features (Figure 7).
Pharmacologic Therapy
Four groups of drugs have been evaluated in the treatment of CVI,
including coumarins (α-benzopyrenes), flavonoids (γ-benzopyrenes),
saponosides (horse chestnut extracts), and other plant extracts. These drugs
with venoactive properties are widely used in Europe but are not approved
in the United States. The principle for using these venoactive drugs is to
improve venous tone and capillary permeability, although a precise
mechanism of action for these drugs has not been full elucidated. It is
thought that the flavonoids act on leukocytes and endothelium to modify
the degree of inflammation and reduce edema. A micronized purified
flavonoid fraction has been shown to reduce edema-related symptoms as
either primary treatment or in conjunction with surgical therapy. A
combination of coumarin and troxerutin (a flavonoid), with compression
garments, was shown to reduced edema and pain compared with placebo
at 12 weeks. In addition, a meta-analysis found that micronized purified
flavonoid fraction added to compression therapies aided in venous ulcer
healing. Horse chestnut seed extract has been found to be as effective as
compression stockings in the short term at reducing leg edema and pain
from CVI, but the long-term safety and efficacy have not been established.
In general, venoactive drugs, which provide relief of pain and swelling or
accelerate venous ulcer healing, carry a moderate recommendation in the
CPG when used in conjunction with compression therapy but are not
approved by the US Food and Drug Administration.
There have been several trials to suggest that pentoxifylline may
improve healing rates of venous ulcers, although the magnitude of the
effect appears to be small, and its role in patient management is unclear.
The use of pentoxifylline in conjunction with compression therapy is also
recommended in the CPG, although it is not approved by the US Food and
Drug Administration for this purpose. The use of other agents, such as
aspirin and platelet-derived growth factor, has been reported to promote
healing or prevent the recurrence of venous ulceration, but no large
randomized studies have been conducted. It should also be mentioned that
there have been data to support the use of aspirin in the prevention of
recurrent thromboembolic events in those with unprovoked thrombosis.
Sulodexide has been used in Europe to treat venous ulcers with relative
success and has a modest recommendation by the CPG, but further studies
are required to determine its clinical efficacy long term.11
Deep Vein ThrombosisDeep Vein Thrombosis
A. Definition of
(DVT) is a blood clot that occurs in the veins (veins) inside. The
inhibition of the return of arterial flow is the cause that often initiates
TVD. The causes can be heart disease, infection, or long
immobilization of the limbs.
B. Epidemiology
The incidence of DVT in the United States is 159 per 100 thousand
or around 398 thousand per year. The fatality rate of TVD is largely
due to pulmonary embolism of 1% in young patients to 10% in older
patients. Without prophylaxis, the incidence of TVD obtained in
hospitals is 10-40% in medical and surgical patients and 40-60% in
major orthopedic surgery. Of the approximately 7 million patients who
were treated in 944 hospitals in America, venous thromboembolism
was the second most medical complication, the cause of increased
length of stay, and the third leading cause of death.
C. Pathogenesis
The main cause of venous thrombosis is unclear, but there are three
groups of supporting factors that are considered to play an important
role in the formation known as TRIAS VIRCHOW namely abnormal
blood flow, blood vessel walls and coagulation factor components
Venous
stasis Stasis of venous blood flow, occurs when blood flow
slowing down, as in heart failure or shock; when the vein is dilated, as
a result of drug therapy, and if the skeletal muscle contractions are
reduced, such as at long rest, limb paralysis or anesthesia. These
things eliminate the effect of peripheral venous pumps, increasing
stagnation and collecting blood in the lower extremities. TVD in
stroke patients occurs in the limbs that have paralysis.
Hypercoagubility
The balance between natural coagulation factors, fibrinolysis and
its inhibitors serves to maintain the balance of normal hemostasis.
Hypercoagulability of blood, occurs most often in patients with
sudden cessation of anticoagulant drugs, use of oral contraceptives
and replacement hormone estrogen and cancer, especially types of
adenocarcinoma can activate clotting factors thereby increasing the
risk of TVD.
D. Risk Factors
TVD sometimes occurs in normal veins, however risk factors that
can cause TVD are:
Immobility (lack of movement)
Immobility will cause slowing of blood flow to the veins and
increase the occurrence of blood clots. For example:
1. Post-surgery for more than 30 minutes, because during anesthesia
the venous blood flow decreases. Therefore postoperatively,
injections of heparin are usually given to prevent the occurrence of
TVD.
2. Pain and care can cause immobilization such as stroke
3. pregnancy, including 6-8 weeks post partumLong
4. Obesity
5. trips by train or plane can increase the risk of TVD
Hypercoagulability
In this condition blood clots are faster than normal as in:
1. Treatment (family planning pills, estrogen)
2. Cancer
3. Smoking
4. Polycytha
E. Diagnosis
The standard gold standard for the diagnosis of TVD is intravenous
venography, where contrast material is injected into the vein then
photographed x-ray to see where there is venous obstruction. This is
invasive so it is rarely done.
Symptoms and signs
Symptoms and signs on TVD are associated with the obstruction of
blood flow back to the heart which causes blood to collect in the arms
or legs. Classic symptoms and signs:
1. Tenderness in the legs or calves if they occur in the limbs and arms
or neck when it comes to the upper extremities.
2. Swelling is localized to the affected area accompanied by edema.
For TVD distal swelling to below the knee and TVD proximal to
the buttocks area.
3. Warming and redness of the skin around the TVD area, especially
in the back and knees, there is superficial venous dilation and
severe obstruction of the skin appears cyanosis.
4. Sometimes TVD does not provide real symptoms, symptoms occur
after complications such as emboli into the lungs.
1. Compression Ultrasonography
CU is the preferred non-invasive examination to help
establish a diagnosis of suspected TVD clinically. This procedure
is quite thorough for detecting symptomatic proximal TVD
(femoral, popliteal, calf bifurcation) with a sensitivity of 97% and
specificity 94% .12. If the results are abnormal, a diagnosis of
venous thrombosis can be made, if normal results are repeated the
following week. Conversion from normal to abnormal at repeated
CU examination is in 2% of patients. CU is less sensitive for distal
TVD, asymptomatic TVD and recurrent TVD.
2. D-dimer
Examination of d-dimer levels (the result of the breakdown
of crosslinked fibrin broken down by plasmin), is an additional
examination of CU to improve the accuracy of the diagnosis of
TVD. D-dimer levels usually increase in TVD and / or EP
(Pulmonary Embolism). Increased ddimer levels indicate
abnormally high levels of fibrin degradation products. This
increase in levels means that there has been a meaningful thrombus
and solution in the body, but it has not been able to show
location13. Normal levels can help to get rid of TVD, but elevated
levels are not specific and have a low positive predictive value.
Increased levels of d-dimer can be a non-specific response to the
disease that occurs together.
3. Venography
Venography is the gold standard inspection of TVD. The
advantage of venography is being able to detect proximal
thrombosis and isolated calf veins. The disadvantages of this
examination are:
a. Invasive
b. Cause pain
c. Expensive and requires special expertise in the technique
d. Takes a long time
e. Possible thrombotic complications
f. Allergies and renal impairment due to contrast fluids
For this reason, non-invasive examinations such as CU and d-
dimer, combined with physical examination, are widely used
instead of venography.
F. Management
Management of TVD is to prevent increased clot size, prevent
pulmonary embolism, post thrombosis syndrome and recurrent TVD.