Abdul Rahim Bin Mohamad Nor C 111 10 871: Prof - Dr.Peter Kabo, PHD, SPFK, SPJP (K), Fiha, Fascc

Abdul Rahim Bin Mohamad Nor
C 111 10 871
SUPERVISOR
Prof.dr.Peter Kabo,PhD,SpFK,SpJP(K),FIHA,FASCC
PATIENTS IDENTITY
Name : Mrs. S
Age : 58 y.o.
MR : 049115
Admitted : November 24th , 2015
HISTORY TAKING
Chief complaint
Swelling on the right leg
Present illness history
Occurs since one week ago, the patient
complained of right leg slowly beginning to swell
with pain and cramps. No cyanosis, patients can
still feel if his feet touched. No SOB, no DOE, no
orthopnea and no Paroxysmal Nocturnal Dyspnea.
HISTORY TAKING
Past medical history
2010 patient were diagnosed with hypertension
and regularly control with drugs.
History of heart disease denied.
History DM denied
History of malignant diseases: Carcinoma Cervix
History of the same disease in the family does not
exist.
RISK FACTOR
Aging
Malignancy
PHYSICAL EXAMINATION
General state :
Moderate illness/well nourished/ conscious
Vital status
Blood Pressure : 130/80 mmHg
Pulse Rate : 90 bpm (regular)
Respiratory Rate : 20 tpm
Temperature : 36,5 0C (axilla)
BW : 50kg
BH : 151cm
IMT : 21.91
Head : anemic (-) icteric (-)
Neck : JVP R+1 cmH2O (300)
Chest :
Inspection : symmetry left = right
Palpation : mass (-), no tenderness
Percussion : sonor left = right
Auscultation : vesicular, ronchi -/- wheezing -/-
Cor :
Inspection : ictus cordis not visible
Palpation : ictus cordis not palpable, thrill (-)
Percussion :
dull, Upper border 2nd ICS linea parasternalis sinistra,
Right border 4th ICS linea parasternalis dextra, Left
border 5th ICS linea medioclavicularis sinistra
Auscultation : heart sound I/II pure, regular, murmur (-)
Abdomen :
Inspection : flat, follows breath movement
Auscultation : peristaltic (+), normal
Palpation : liver and spleen not palpable
Percussion : tympani
Extremities :
Swelling on the right leg with pain
Pitting Edema
Warm(+)
Homans sign positif
LABORATORIUM (November, 1 st , 2015 )
HEMATOLOGY RESULT NORMAL VALUE
WBC 19,29 x 103 /mm3 4.0-10.0 x 103
RBC 3,96 x 106/mm3 4.0-6.0x106
HGB 10,5 g/dL 12-16
MCH 21,5 pg 26,5-33,5
MCHC 31,7 gr/dL 31,5-35
HCT 31,4 37-48
PLT 486 x 103/mm3 150-400 x 103
Ureum 54 10-50 md/dL
Creatinin 1,2 <1.3
Na 137 136-145 mmol/l
K 4,1 3.5-5.1 mmol/l
Cl 110 97-111 mmol/l
PT 17,4 10-14 detik
INR 1,45 -
APTT 36,5 22.0-30.0 detik
D Dimer 3,98 < 0,5

ELECTROCARDIOGRAPHY
(November 1st 2015)
Rhythm: Sinus rhytme
Frequence: 76 bpm
Axis: normoaxis
P wave: 0.04 sec
P-R interval: 0.1 sec
QRS interval: 0.1 sec
ST segment: normal
Conclusion : Sinus rhytme, normoaxis, heart rate 76 bpm.
ECG NORMAL
Echovascular
Blood flow from
distal to proximal is
not flowing well with
thrombus in
Common Femoral
Vein and Right
Popliteal vein.
CONCLUSION:
Deep Vein
Thrombosis
Resume
Women 58 yo came with Edema on right leg occurs since one
week ago, the right leg slowly beginning to swell, pain(+) and
cramps(+). History of hypertension(+) on treatment,
Malignancy(+): Carcinoma Cervix. Physical examination on
lower extremities: Edema on the right leg, warmt(+). Homans
sign(+). Risk factor: Carcinoma Cervix, Wells Score: +2
Laboratory finding: WBC: 19,29, PLT: 429000 , PT: 17,4, APTT:
36,5, INR: 1.45, D-Dimer: 3,98.
Echo vascular: Blood flow from distal to proximal is not flowing
well with thrombus in Common Femoral Vein and Right Popliteal
vein
DIAGNOSIS
Deep Vein Thrombosis
TREATMENT
IVFD NaCl 0.9% 500cc/24h/intravena
Alpentin 100 mg/24h/oral
Simarc 2 mg/24h/oral
MST 15 mg/24h/oral
DEFINITION
Deep vein thrombosis (DVT) refers to
the formation of one or more blood clots
in one of the bodys large veins, most
commonly in the lower limbs. The clot
can cause partial or complete blocking
of circulation in the vein
ANATOMY OF DEEP AND
SUPERFICIAL VEINS
ETIOLOGY / RISK FACTOR
PATHOGENESIS
Three mechanisms are involved in
the pathogenesis of venous
thrombosis (Virchows triad), they
are:
venous stasis,
injury to the venous wall,
hypercoagulable states.
Stasis disrupts laminar ow and brings platelets into
contact with the endothelium. This allows coagulation
VENOUS STASIS factors to accumulate and retards the inux of clotting
inhibitors. Factors that slow venous ow and induce
stasis include immobilization
HYPERCOAGULABLE including resistance of coagulation factor V to activated

protein C, a prothrombin gene mutation, and inherited
STATES deciencies of antithrombin, protein C, and protein S.
Vascular damage, either by external injury or by

intravenous catheters, can denude the endothelium and
INJURY TO THE expose subendothelial collagen. Exposed collagen acts
VENOUS WALL as a substrate for the binding of von Willebrand factor
and platelets and initiates the clotting cascade, leading
to clot formation.
CLINICAL FEATURES
A DVT most commonly develops in a deep
vein below the knee in the calf. Typical
DVT symptoms include:
Pain and tenderness of the calf.
Swelling of the calf.
Colour and temperature changes of the calf.
Blood that would normally go through the
blocked vein is diverted to outer veins. The calf
may then become warm and red.
Sometimes there are no symptoms and a DVT
is only diagnosed if a complication occurs, such
as a pulmonary embolus.
o Edema, principally unilateral, is the most
specific symptom.
o Leg pain occurs in 50% of patients, but
this is entirely nonspecific. Pain can
occur on dorsoflexion of the foot
(Homans sign).
o Pratt's sign: Squeezing of posterior calf
elicits pain.
DIAGNOSIS
Well score
D-Dimer
D-Dimer, a byproduct of brin degradation that can be
measured in a peripheral blood sample, is highly sensitive

for the diagnosis of DVT and/or acute PE.
Because D-dimer may also be elevated in many other
conditions (such as cancer, inammation, infection and

necrosis), a positive test result is not specic for DVT.
Thus, a normal D-dimer value can help exclude the
presence of DVT, but an elevated level does not conrm

the diagnosis.
Venous compression duplex
that is 95% sensitive for the diagnosis of
symptomatic DVT in a proximal vein but
only.
This technique uses real-time ultrasound
scanning to image the vein and pulsed
Doppler ultrasound to assess blood ow
within it.
Criteria used for diagnosis of DVT with
duplex ultrasonography include the inability
to compress the vein with direct pressure,
direct visualization of the thrombus, and
absence of blood ow within the vessel.
ALGORITHMA OF DIAGNOSIS
TREATMENT
The aim of treatment of VTE is to reduce
morbidity and mortality.
This is achieved by optimal therapy to
prevent thrombus extension and
embolisation.
The mainstay of therapy is
pharmacological.
Adjunct therapies include mechanical
devices like filters and stents.
INITIAL TREATMENT OF DVT
In clinically suspected DVT, treatment with UFH or
LMWH should be given until the diagnosis is
excluded by objective testing
The regimen for the administration of iv UFH is as
follows
Baseline APTT, PT, FBC, renal profile, liver function test
and thrombophilia screen
Initial dose of iv bolus UFH 80 IU/kg followed by
maintenance infusion at 18 IU/kg/hr.
Check APTT at 6, 12 and 24 hours. The target APTT ratio
is 1.5 to 2.5. This must be achieved in the first 24 hours
and maintained thereafter.
Start warfarin therapy at 5 mg on the first 2 days.
Thereafter adjust daily dose according to INR.
Check platelet count from day 3 till the end of second
week.
Discontinue heparin once target INR (2.0 - 4.0) is
achieved on 2 consecutive days.
MANAGEMENT OF IV UFH
Initial dose 80 IU/kg bolus, then 18 IU/kg/hr
APTT < 35 s (<1.2x control) 80 IU/kg bolus, then increase

rate by 4 IU/kg/hr
APTT 35 to 45 s (1.2 to 1.5x 40 IU/kg bolus, then increase
control) Infusion rate by 2 IU/kg/hr
APTT 46 to 70 s (1.5 to 2.3x No change

control)
APTT 71 to 90 s (2.3 to 3x Decrease infusion rate by 2

control) IU/kg/hr
APTT >90 s (>3x control) Hold infusion for 1 hour, then
decrease
Infusion rate by 3 IU/kg/hr
SUBCUTANEOUS UFH
effective alternative to intravenous UFH for the
initial management of DVT
The regimen for the administration of
subcutaneous, UFH includes an
Initially, intravenous bolus of 5000 IU followed by
subcutaneous injections of 15,000 to 20,000 IU 12 hourly
This is monitored by the APTT with the mid-interval APTT
maintained between 1.5-2.5 times the control
LMWH recommended
LMWH recommended Treatment
Enoxaparin (Clexane) 1 mg/kg twice

daily
Nadroparin (Fraxiparine) 0.1 ml/kg twice
daily
Nadroparin (Fraxiparine 0.1 ml/kg once

Forte) daily
Tinzaparine (Innohep) 175 units/kg once
daily
MAINTENANCE TREATMENT OF
DVT
Following initial heparinisation in patients with
DVT, maintenance of anticoagulation with oral
anticoagulants is recommended
Following discharge-followed up within a week
with a repeat INR.
If the INR remains within therapeutic range, the
same dose is maintained and the next follow-up
will be 2 weeks later
More frequent visits are required if therapeutic INR
is not achieved
DURATION OF THERAPY
Time Event
3 to 6 months first event with reversible or

time-limited risk factor (Surgery,
trauma, immobility, oestrogen
use)
= 6 months idiopathic VTE, first event
12 months to lifetime - anticardiolipin antibody

- first event with cancer - antithrombin deficiency
- recurrent event, idiopathic or
until resolved with thrombophilia

Abdul Rahim Bin Mohamad Nor C 111 10 871: Prof - Dr.Peter Kabo, PHD, SPFK, SPJP (K), Fiha, Fascc

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Abdul Rahim Bin Mohamad Nor

WBC 19,29 x 103 /mm3 4.0-10.0 x 103

RBC 3,96 x 106/mm3 4.0-6.0x106

HGB 10,5 g/dL 12-16

MCH 21,5 pg 26,5-33,5

MCHC 31,7 gr/dL 31,5-35

HCT 31,4 37-48

PLT 486 x 103/mm3 150-400 x 103

Ureum 54 10-50 md/dL

Creatinin 1,2 <1.3

Na 137 136-145 mmol/l

K 4,1 3.5-5.1 mmol/l

Cl 110 97-111 mmol/l

PT 17,4 10-14 detik

APTT 36,5 22.0-30.0 detik

D Dimer 3,98 < 0,5

Alpentin 100 mg/24h/oral

HYPERCOAGULABLE including resistance of coagulation factor V to activated

Vascular damage, either by external injury or by

measured in a peripheral blood sample, is highly sensitive

Because D-dimer may also be elevated in many other

conditions (such as cancer, inammation, infection and

Thus, a normal D-dimer value can help exclude the

presence of DVT, but an elevated level does not conrm

APTT < 35 s (<1.2x control) 80 IU/kg bolus, then increase

APTT 46 to 70 s (1.5 to 2.3x No change

APTT 71 to 90 s (2.3 to 3x Decrease infusion rate by 2

Enoxaparin (Clexane) 1 mg/kg twice

Nadroparin (Fraxiparine 0.1 ml/kg once

3 to 6 months first event with reversible or

12 months to lifetime - anticardiolipin antibody

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