SCENARIO 2

A 38-year-old women presents with a complaint of swelling in the left leg that has
been experienced since 1 week prior. Complaints accompanied by cramps and
severe pain, especially at night. On this last 3 days have wounds on the ankle area.
The physical examination found redness on the left leg, accompanied by swelling and
a widening of the vein accompanied with a visible wound on the left dorsum pedis
area with a red surface and resonant edges.
History of hypertention and dyslipidemia. Currently the patient is still working
actively as a secretary on a company.
KEYWORD
A 38-year-old
Complain of swelling in the left leg since 1 week prior.
Complain accompanied by cramps and severe pain especially at night.
Last 3 days have wounds on the ankle area.
Physical examination found redness on the left leg.
A widening of the vein accompanied with a visible wound on the left dorsum pedis
area with a red surface and resonant edges.
History of hypertention and dyslipidemia.
Working actively as a secretary on a company.
QUESTIONS
1. What is Difference in arterial & venous disease?
2. What is are the risk factors for swelling in the legs?
3. How is the etiology and pathophysiology of complaints based on the scenario?
4. What causes pain to increase at night?
5. What is the difference between edema caused by vascular disease and heart disease?
6. What is the relationship between the history of hypertension and dyslipidemia in the scenario?
7. What is steps for diagnosis of vascular examination?
8. How is the initial handling related to the scenario?
9. What is different diagnose is involved in the scenario?
10. What is the Islamic perspective?
1. WHAT IS DIFFERENCE IN ARTERIAL & VENOUS DISEASE?

ARTERY
Artery diseases include many rare diseases, but also some more frequent such as
atherosclerosis, aneurysm or aortic dissection.

 Atherosclerosis :Atherosclerosis involves changes in the vessel wall

 Aortic aneurysm : Aortic aneurysm, or a bulge, is a sac-like extension that occurs most
frequently in the area of the abdominal aorta.
 Aortic dissection: Aortic dissection is a tear mostly in the ascending part of the aorta
from the heart. This creates a sac where blood accumulates
VEINS
Diseases of veins affect more and more young individuals. This is mainly due to lifestyle, lack of
exercise and bad nutrition. The most common diseases of veins are venous thrombosis, varicose veins
and inflammation of the veins.

 Venous thrombosis: Venous thrombosis is a condition that arises as a result of coagulation

disorders or deceleration of blood flow in the veins
 Varicose veins: Varicose veins are twisted, elongated, weakened veins in which blood can not
flow and thus leading to blood accumulation.
 Inflammation of the veins: Inflammation of the veins or phlebitis is a disease that mainly affects
the superficial veins of the lower extremities.
2. WHAT ARE THE RISK FACTORS FOR SWELLING IN THE LEGS?
Health condition,
chronic accumulation
of more generalized
edema.

Pregnancy, the
enlarged uterus can
Surgery history press on a vein known
as the inferior vena
cava

Problems with the

extremities (A blood
clot, varicose, a cyst, Drugs
growth, or
lymphedema)
3. HOW IS THE ETIOLOGY AND PATHOPHYSIOLOGY OF COMPLAINTS
BASED ON THE SCENARIO?
Pain & Cramps
Activation of
phospholipase A2, And local release of
Local Inflammatory proinflammatory
in turn, leads to the mediators
synthesis

It self is Such as bradykinin,

Local hypoxia associated responsible for an prostaglandins E2 and D2,
with capillary stasis increase in phospholipase platelet-activating factor
A2 activity (PAF), and leukotriene B4

The hypoxia induced Such activation is manifest

by capillary stasis has the by elevation of calcium
effect of activating concentrations in the
endothelial cells cytoplasm of endothelial
cells
 • It enhances local release of serotonin
PAF seems to and histamine
play a pivotal • It produces abnormal adherence of
neutrophils to the venous endothelium
role

• released locally as the result

Some • of hypoxia can activate nociceptors located in the venous wall
(between endothelial cells

proinflammatory
• smooth muscle cells of the media) and in the connective tissue that
forms the perivenous space, in close contact with the microcirculation.
Therefore, the study of the painful sensation evoked in healthy subjects

mediators by the intravenous or perivenous application of bradykinin

unambiguously demonstrates the role of this neuromediator in venous
pain
Ulcer
Arterial/venous
insufficiency

Blood pressure
Ulcer
↓

O2 ↓ & Damage of the

Nutrients in the Tissue
tissue
Oedema
4. WHAT CAUSES PAIN TO INCREASE AT NIGHT?

The “small fibers” without myelin sheaths (protective coating, like insulation that normally surrounds a
wire) include fiber extensions called axons that transmit pain and temperature sensations. Small-fiber
polyneuropathy can interfere with the ability to feel pain or changes in temperature. It is often difficult
for medical caregivers to control, which can seriously affect a patient’s emotional well-being and overall
quality of life. Neuropathic pain is sometimes worse at night, disrupting sleep. It can be caused by pain
receptors firing spontaneously without any known trigger, or by difficulties with signal processing in the
spinal cord that may cause you to feel severe pain (allodynia) from a light touch that is normally painless.
For example, you might experience pain from the touch of your bedsheets, even when draped lightly over
the body.
5. WHAT IS THE DIFFERENCE BETWEEN EDEMA CAUSED BY
VASCULAR DISEASE AND HEART DISEASE?
Edema is reduced by excessive accumulation of fluid in the interstitial space. Edema can
also affect through various ways, and simple classifications as below:
a. Generalized edema
b. Local edema
 Increased permeability of small blood vessels
 Edema caused by lymphatic obstruction
 Edema caused by venous obstruction
EDEMA CAUSED BY
HEART DISEASE

Cases of right heart failure, generally caused by indirect consequences and

left heart failure. In the process of right heart failure, the right ventricle is
unable to accept large amounts of blood volume which is not disserted with
sufficient pressure. Unlike left heart failure, pulmonary congestion is not found
in right heart failure. Symptoms and signs experienced by patients are portal
vein congestion with hepato and / or splenomegaly, peripheral edema,
pleural effusion, and ascites.
EDEMA CAUSED BY
VASCULAR DISEASE

 The increase in pressure inside the lumen is most often caused by the
occurrence of venous insufficiency in the presence of reflux which
passes through the incompetent venous valve both in the deep vein and
in the superficial vein.
 The damage caused by venous insufficiency is related to venous
pressure and venous blood volume that passes through the incompetent
valve.
6. WHAT IS THE RELATIONSHIP BETWEEN THE HISTORY OF
HYPERTENSION AND DYSLIPIDEMIA IN THE SCENARIO?
The opening of the endothelium will expose the
extracellular matrix -> Release the clotting factor
-> Platelet adhesion -> Thrombus

Endothelial dysfunction can be induced by a

variety of conditions including hypertension and
hypercholesterolemia
7.WHAT IS DIAGNOSE STEPS FOR PATIEN IN THE SCENARIO ?

• IDENTITY
HISTORY • MAIN COMPLAIN
• PAST MEDICAL HISTORY
• FAMILY HISTORY
DIAGNOSE PHYSICAL • CLINICAL PARAMETERS
STEPS EXAMINATION ACCORDING TO WELLS
CLINICAL SCORE

• D-DIMAR
SUPPORTING • GDS, FIBRINOGEN, PROTEIN
INVESTIGATION S AND PROTEIN C
• DOPPLER-DUPLEX
ARTERIOVENOUS
• PHLEBOGRAPHY AND MRI
 8. HOW IS THE INITIAL HANDLING RELATED TO THE SCENARIO?
Limb Elevation Stocking Compression
 Anticoagulant Irrigation of wound with tap water and saline

Topical Antibiotic
 WHAT IS DIFFERENT DIAGNOSE IS INVOLVED IN THE
9. SCENARIO?
Difference Chronic Venous Insufficiency
Epidemiology In the general population
between 1% to 17% of men
and 1% to 40% of women
may experience chronic venous
insufficiency.
Etiology can be caused by congenital
absence of or damage to
venous valves in the superficial
and communicating systems. It
can also be caused by venous
incompetence due to thrombus
formation as favored by the
Virchow triad (venous stasis,
hypercoagulability, and
endothelial trauma
Deep vein thrombosis
The incidence of DVT in the
United States is 159 per
100,000 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
3 factors for the formation of
thromboembolic stimuli, namely
vascular wall abnormalities,
changes in blood flow, and
changes in blood clotting
power. In addition to
stimulatory factors, there are
protective factors, namely
active coagulation factor
inhibitors.
Varicose Veins
epidemi: Serial examinations
of children aged 10-12 years
and again 4 and 8 years later
showed that symptoms are
experienced (and venous test
results are abnormal) before
any abnormal veins are visible
at the surface of the skin.
Venous reflux originates from
the failure of the venous valves
in the saphenous veins, which
results in retrograde flow and
stasis, or pooling, of venous
blood in the branches of the
saphenous veins.
 Difference Chronic Venous Insufficiency
Patomechanism either due to reflux (backward
flow) or obstruction of venous
blood flow. Chronic venous
insufficiency can develop from
the protracted valvular
incompetence of superficial
veins, deep veins or
perforating veins which connect
them. In all cases, the result is
venous hypertension of the
lower extremities. Superficial
incompetence is usually due to
weakened or abnormally
shaped valves or widened
venous diameter which
prevents normal valve
congruence
Deep vein thrombosis Varicose Veins
1. Venous stasis Elevated venous pressure
Venous blood flow tends to be slow, even stasis, most often is the result of
especially in areas that experience long venous insufficiency due to
immobilization. Venous stasis is a predisposing
valve incompetence in the
factor for the occurrence of local thrombosis,
because it can interfere with the mechanism of deep or superficial veins.
cleansing the activity of blood clotting factors so Varicose veins are the
as to facilitate the formation of thrombosis. for undesirable pathways by
the occurrence of local thrombosis, because it can which venous blood
interfere with the mechanism of cleansing the refluxes back into the
activity of blood clotting factors so as to facilitate congested extremity.
the formation of thrombosis. Ablation of the varicose
2. Damage to blood vessels
pathways invariably
Damage to blood vessels can play a role in the
process of forming venous thrombosis, through: improves overall venous
• Direct trauma resulting in clotting factors. circulation. Chronically
• Activation of endothelial cells by cytokines increased venous pressure
released as a result of tissue damage and can also be caused by
inflammatory processes. outflow obstruction, either
3. Changes in the power of frozen blood from intravascular
Under normal conditions there is a balance of the thrombosis or from
blood clotting system and fibrinolysis system. The
extrinsic compression.
tendency of thrombosis occurs when blood clotting
activity increases or fibrinolysis activity decreases
 Difference Chronic Venous Insufficiency Deep vein thrombosis Varicose Veins

Clinical Manifestation • a combination of dependent 1. Pain clinical manifestation: •

pitting edema, leg discomfort, Pain intensity does not depend on the size dilated visible veins at
and fatigue, and itching and extent of thrombosis the skin surface
• pain 2. Swelling (varicose veins, reticular
• cramping The onset of edema can be caused by veins, and
• Itching obstruction of the proximal vein and telangiectasias)
• itching inflammation of the perivascular tissue. • Swelling
• prickling 3. Change in skin color • Aching
• throbbing sensation Unspecified skin changes and not many • Heaviness
• improve with rest and leg found in deep vein thrombosis compared • skin discoloration
elevation, and with no association with arterial thrombosis, found only in 17% - • potential ulcer
for exercise 20% of cases. formation
Management The treatment goals include reducing Non-pharmacological management is Patients with milder
discomfort and edema, stabilizing skin primarily aimed at reducing morbidity in symptoms of venous
appearance, removing painful varicose acute attacks and reducing the incidence of reflux disease may
veins and healing ulcers. Most patients
post-thrombosis syndrome which is usually obtain adequate
should initially be treated
conservatively with leg elevation, characterized by pain, stiffness, edema, symptomatic relief with
exercise (which improves calf muscle paresthesia, erythema, and edema. compression stockings.
pump), weight management, and • Unfractionated Heparin Compression stockings
compression therapy. Ulcers are • Warfarin should at the minimum
treated best with compression • Thrombolytic therapy reach the level of the
bandaging systems. • Thrombectomy upper calf.
10. WHAT IS THE ISLAMIC PERSPECTIVE?
Surah Al Haqqah verses 45 and 46 Allah says:

ِ ‫اَم ْنهَُ ِب ْٱلي ِم‬

٤٥َ‫ين‬ ِ ‫أَخ ْذن‬
ْ ‫اَم ْنه‬
٤٦َ‫َُٱلوتِين‬ ِ ‫ث ُ َّمَلقط ْعن‬
"We surely hold him in his right hand. Then really we cut the veins of the heart."
The purpose of the verse is if the Prophet Muhammad lied against Allah, the sanction that would be
given was cutting the blood vessels coming out of his heart (aorta) so that death was the end result.
In addition to looking at the heart from the psychological side, Islam also views the heart in terms of
anatomy and physiology.
Remember, in the human body there is a lump of meat. If a lump of meat is good, the whole body
will be good. But, if it is damaged, the whole body will also be damaged. A lump of meat called qolbu!
- (Narrated by Bukhari and Muslim).