This document summarizes pulmonary embolism (PE), including its epidemiology, risk factors, pathophysiology, clinical features, diagnostic testing, and treatment. PE is the second most common cause of unexpected death, with risk factors including recent surgery, trauma, cancer, and inherited or acquired thrombophilias. Diagnosis involves assessing clinical probability then confirming with D-dimer, imaging like CT pulmonary angiogram, or lung scintigraphy. For acute PE, initial treatment is heparin or fondaparinux followed by long-term oral anticoagulation to prevent recurrence. New oral anticoagulants targeting factor Xa provide alternatives to warfarin.

1. Pulmonary Embolism
By
Eman mahmoud
M.D of chest diseases

2. Pulmonary Embolism
• Embolism : Impaction of a thrombus or
foreign matter in the pulmonary vascular
bed.

3. Epidemiology
• 2nd most common cause of unexpected death in
most age groups.
• present in 60-80% of patients with DVT, more
than 50 % them are asymptomatic.
• Account for 15 % of all postoperative deaths
• it is estimated that in the USA .100 000 people
• die each year of pulmonary embolism.

4. • Thrombotic
EMBOLUS
• Non-thrombotic : Fat, Air, Tumour ,
Amniotic fluid.

5. RISK FACTORS
• Bed rest
• Post-operative
• After severe blood
loss and trauma
• COPD
• CHF
• Varicose veins
• Advancing age
• Obesity
• Post-partum
• Malignancy
• Travel of 4 hours or
more
• Smoking
• 1ry polycythemia
• Oral contraceptives

6. THROMBOPHILIA
• Acquired thrombophilia
•
• Inherited thrombophilias

7. Hereditary factors
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Factor V Leiden (most common genetic
risk factor for thrombophilia)
• Plasminogen abnormality
• Plasminogen activator abnormality
• Fibrinogen abnormality
• Resistance to activated protein C

8. Acquired thrombophilia
• This is mostly associated with the
antiphospholipid syndrome (APS).
• APS is the combination of (LAC) with
or without, (ACA), with a history of
recurrent miscarriage and or
thrombosis.

9. Pathophysiology

10. Clinical Features
•Size of the embolus and blood
vessel occluded.
•State of the lung.
•Associated disease(s).

11. PE, Clinical Features
•dyspnea (75–85%)
• Pleuritic chest pain (57–87%)
• cough (40–53% )
• Hemoptysis
• Syncope.

13. Massive Pulmonary Embolism
MPE
•collapse/hypotension
•unexplained hypoxia
•engorged neck veins
•Acut right heart failure

14. Physical Signs
•Normal
•Tachypnea (respiratory rate >16/min) - 96%
•Rales - 58%
•Accentuated second heart sound - 53%
•Tachycardia (heart rate >100/min) - 44%
•Fever (temperature >37.8°C) - 43%
•Diaphoresis - 36%
•S3 or S4 gallop - 34%
•Clinical signs and symptoms suggesting thrombophlebitis -
32%
•Lower extremity edema - 24%
•Cardiac murmur - 23%
•Cyanosis - 19%

15. Clinical Probability of PE

16. D-Dimer
•Degradation product produced by plasmin-mediated
proteases of cross-linked fibrin.
•Blood D-dimer assay should only be considered following
assessment of clinical probability.
•D-dimer assay should not be performed in those
with high clinical probability of PE.

17. D-dimer
.Highly sensitive assays, such rapid ELISA assays,
have high false positive rates but safely rule out VTE
in outpatients presenting with a low clinical
probability of PE.
•A negative D-dimer test reliably excludes PE in
patients with low clinical probability; such patients
do not require imaging for VTE.

18. Ischemia-Modified Albumin
levels
•A potential alternative to D-dimer testing is assessment of the
ischemia-modified albumin (IMA) level.
• 93% sensitive and 75% specific for pulmonary embolism
• The positive predictive value of IMA, in particular, is better than
D-dimer. However, it should not be used alone.

19. Chest x-ray
•14% Normal
•68% Atelectasis
•48% Pleural Effusion
•35% Pleural based opacity
•24% Elevated diaphragm
•15% Prominent central pulmonary artery
•7% Westermark’s sign
•7% Cardiomegaly
•5% Pulmonary edema

20. Elevated L H.Diaph

21. Decreased vascularity (Westermark sign)

22. (Hampton hump)
•The classic radiographic findings of
pulmonary infarction
• a wedge-shaped, pleura-based
triangular opacity with an apex
pointing toward the hilus

23. Atelectic band

24. cardiac troponins
•Recently, cardiac troponins I and T have been
shown to be associated with early mortality and a
complicated hospital course in patients with PE.
The assessment of cardiac plasma troponin levels
revealed ventricular injury, especially in patients
with massive PE who had hypotension
or shock.

25. B Natriuretic Peptide (BNP)
•BNP is a neurohormone secreted from the cardiac
ventricles in response to dilatation or an increase
of pressure.
• BNP levels may increase with right ventricle
dysfunction when the patients is in bed and
decrease with treatment.
•Serum brain natriuretic peptide levels of > 90 pg/mL
have a sensitivity of 85% and a specificity of 75% for
predicting adverse clinical outcomes

26. Arterial blood gases
•Blood gases may increase the suspicion and
contribute to the clinical assessment, but they
are insufficient to permit proof or exclusion of
PE.

27. ECG
•In minor pulmonary embolism, the only finding is sinus
tachycardia.
•In massive pulmonary embolism, evidence of right heart
strain may be seen (rightward shift of the QRS axis,
transient RBBB, T-wave inversion, SIQIIITIII pattern, P-pulmonale),
but these signs are non-specific.
The main value of ECG is exclusion other diagnoses, such
as MI or pericarditis.

28. S1 Q3 T3 Pattern

29. Echocardiography
•RV dilatation
•RV size does not change from diastole to systole
= hypokinesis
•D-shaped LV
•40% of pts have RV abnormalities seen by
ECHO

30. Echocardiography
•Transthoracic echocardiography rarely enables direct
visualisation of the pulmonary embolus but may reveal
thrombus floating in the right atrium or ventricle.
• Transoesophageal echocardiography, it is possible to
visualise massive emboli in the central pulmonary arteries.

31. Lower extremity venous
ultrasonography
Advantages
Portability
May avoid further diagnostic imaging if positive
Limitations
Low sensitivity and risk of false positives
No consistent protocol for technique
Operator dependant

32. Venous Ultrasonography
Recommendations of Use
•First-line if radiographic imaging contraindicated or not
readily available
•Not likely required in patient with negative CT-PA.
•Helpful to rule out DVT in patient with non-diagnostic
V/Q scan.

33. Lung scintigraphy
•The lung scan is an indirect method of diagnosis
since it does not detect the embolus itself but only
its consequence, the perfusion abnormality.
•Used when CT scanning is not available or if the patient
has a contraindication to CT scanning or intravenous
contrast material.

34. The Lung Scan Perfusion
Perfusion
• IV injection of human serum albumin labelled w/ technetium-99m
•Particles are same size as pulmonary capillaries and become trapped
•Lung peripheral to a clot is not perfused and will show defect
Ventilation:
•Inhalation of xenon-133 radioactive gas
•Degree of ventilation of all lung areas can be assesed
•Pneumonia, emphysema, tumors can cause defects
•Pulmonary embolism does not cause ventilation defect
Patients w/ a perfusion defect w/out a ventilation defect is
suggestive of a pulmonary embolus.

36. VQ Scan results
Presence of several large focal perfusion defects not matched by
ventilation defects indicates a high probability of PE !!!!!
Normal scan basically excludes PE and indicates for other
explanations for the pts condition.
High probability – start Rx.
Low probability – withhold Rx – can do CT / angiogram.
Intermediate probability – can do CT / angio

37. V/Q Scan
Advantages
Excellent negative predictive value (97%)
Can be used in patients with contraindication to
contrast medium
Limitations
30-50% of patients have non-diagnostic scan
necessitating further investigation

38. CTPA
• CTPA studies using the multislice technique
showed a high sensitivity (96 to 100%) and
specificity (97 to 98%),
•CTPA is now the recommended
initial lung imaging modality for non-massive
PE.
•Patients with a good quality
negative CTPA do not require further
invest. or ttt for PE.
BTS (2003)

39. Multidetector helical CT
pulmonary angiography
Advantages
Diagnosis of alternative disease entities
Coverage of entire chest with high spatial
resolution in one breath hold
Availability
Improved depiction of small peripheral
emboli

40. Multidetector helical CT pulmonary angiography –
Limitations
Reader expertise required
Expense
Requires precise timing of contrast bolus
Radiation exposure
Not portable
Contraindications to contrast
Renal insufficiency
the radiation dose from 3 to 5 mSv, with an estimated cancer risk
of 150 excess cancer deaths per million

41. Multidetector-CT Findings
Partial or complete filling defects in lumen of pulmonary arteries
Most reliable sign is filling defect forming acute angle with vessel wall with defect
outlined by contrast material “polo mint” sign
“Tram-track sign” Parallel lines of contrast surrounding thrombus in vessel that travels
in transverse plane
“Rim sign” Contrast surrounding thrombus in vessel that travels orthogonal to
transverse plane
a right-to-left ventricular dimensional ratio of 0.9 or more at MDCTA, had 92%
sensitivity for right ventricular dysfunction

42. “railway track” sign on longitudinal images of the vessel

43. Arterial occlusion with failure to enhance the entire lumen due to a large filling defect

44. A peripheral intraluminal filling defect that forms acute angles with the arterial wall

45. A partial filling defect surrounded by contrast material, producing the
“polo mint” sign on images acquired perpendicular to the long axis of a
vessel

46. a peripheral, crescent-shaped intraluminal defect that forms obtuse angles with the
vessel wall

47. Pulmonary Angiography
•Was traditionally regarded as the reference test for PE.
• Due to the invasive character, including right heart
catheterization and injection of contrast material.
•The current availability of noninvasive diagnostic imaging
catheter pulmonary angiography now has an insignificant role.

48. Magnetic resonance angiography
(MRA)
MRA appears promising & avoids ionising radiation but has poor sensitivity for
subsegmental clot.

49. Further Alternative Imaging Tests
•Dual-energy CTPA
•Electrocardiographically gated CTPA
•Three-dimensional images acquired by single-photon
emission computed tomography (SPECT) using a
gamma-emitting radioisotope may improve V/Q
scintigraphy and has a lower radiation dose.

50. Dual-energy CTPA
Provides functional and anatomic lung imaging
Demonstrates perfusion defects beyond obstructive and non-obstructive
clots
Diagnostic accuracy requires further research
Advantages
Indirect evaluation of peripheral pulmonary arterial bed
Disadvantages
Longer data acquisition time
Increased radiation exposure

51. Dual-energy CTPA
[A] Axial reconstruction with color-coded
dual energy perfusion
information. Note the large perfusion
defects in both lungs.
[B] Coronal reconstruction.
Only the apical parts show a
normal perfusion.

52. Electrocardiographically gated
CTPA
•can differentiate between cardiac events and PE
• may be of use in patients presenting with thoracic pain and
suspected PE, cardiac events, or aorta dissection.
• More contrast material is needed, and the radiation dose is
higher compared with CTPA.

53. Three-dimensional images
•Single-photon emission computed tomography (SPECT) using a gamma-emitting
radioisotope may improve V/Q scintigraphy
• lower radiation dose.

54. Low dose MDCT
using ultra high pitch technique
Useful in patients who are unable to hold their breath

57. Treatment
•For acute PE, the ACCP guidelines recommend starting low–
molecular weight heparin (LMWH) or fondaparinux, preferred over
unfractionated heparin (UFH) or subcutaneous heparin
•Patients should have an oral anticoagulant (warfarin) initiated at
the time of diagnosis, and they should have UFH, LMWH, or
fondaparinux discontinued only after the international normalized
ratio (INR) is 2.0 for at least 24 hours but no sooner than 5 days
after warfarin therapy has been started

59. Heparin
•The initial treatment of PE is LMWH or UHF for at
least 5 days, followed by warfarin.
•Dose of UFH: 80 U/kg/h bolus followed by18 U/kg
. Monitoring by APTT(1.5-3)times normal.
•It binds to endogenous antithrombin, This heparin -
antithrombin complex catalyzes the inactivation of
factor Xa and IIa (thrombin).

60. Heparin
•Adverse drug reactions include bleeding, heparin-induced
thrombocytopenia, and osteoporosis .with
prolonged use .
•A platelet count should be obtained weekly for the
first month. If there is an abrupt decrease in the
platelet count (approx. 50%) or by skin lesions at
heparin injection sites or acute systemic reactions
(eg, chills, cardiorespiratory distress) after IV
heparin bolus administration consideration must be
given to the possibility of (HIT).

61. LMWH
•It should be used whenever possible for the initial
inpatient treatment of DVT & PE.
.
•Outpatient ttt of DVT, and possibly PE,is safe and
cost-effective for carefully selected patients.

62. Oral anticoagulant
Warfarin inhibits gamma-carboxylation of the
vitamin K-dependent coagulation factors II, VII, IX,
and X.
Warfarin and heparin can be started on the same
day, but concomitant administration of these drugs
for 4 or 5 days is recommended.

63. Oral anticoagulant
•Warfarin also inhibits carboxylation of natural anticoagulant
proteins C and S resulting in a rapid decline of their levels.
This poses a theoretical risk for a venous thromboembolic
events.
•Starting the patient on the expected daily dose (eg, 5mg)
rather than administering a loading dose can minimize
potential bleeding and avoid an extreme decline in protein C.
•Target international normalised ratio [INR], 2.0–3.0) for at
least 3–6 months.

64. Factor Xa inhibitors
•Rivaroxaban (Xarelto) is an oral factor Xa inhibitor
approved by the FDA in November 2012 for the
treatment of DVT or PE.
• Reduce risk of recurrent DVT and PE following initial
treatment.
•Associated with less bleeding, particularly in elderly
patients and those with moderate renal impairment.

65. Factor Xa inhibitors
•Apixaban was approved for treatment of PE in August 2014.
•This advance thus offers the prospect of a safe and effective
regimen of anticoagulation for patients with the advantages of
simplicity and cost-effectiveness in comparison to current
management strategies.

66. Fondaparinux
• Synthetic polysaccharide derived from the antithrombin binding
region of heparin. Catalyzes factor Xa inactivation by antithrombin
without inhibiting thrombin.
•In patients with acute PE, favored over IV UFH and over SC
UFH
• Once-daily fondaparinux was found to be similar as IV UFH.

67. Direct Thrombin Inhibitors
Argatroban (Novastan
)
approved in 2000: Anticoagulant for pts with HIT needing
prophylaxis or treatment for thrombosis
Ximelagatran (Exanta)
• have shown benefit over warfarin or LMWH

68. Duration of anticoagulation
•A patient with a first thromboembolic event occurring in the
setting of reversible risk factors, should receive warfarin therapy
for at least 3 months.
•The current ACCP guidelines recommend that all patients with
unprovoked PE receive three months of treatment with
anticoagulation and have an assessment of the risk-benefit ratio
of extended therapy at the end of three months .
patients with a second unprovoked episode of venous thromboembolism and
low or moderate risk of bleeding, extended anticoagulant therapy is
recommended
Patients who have pulmonary embolism and preexisting
irreversible risk factors should be placed on long-term
anticoagulation.

69. Heparin-induced
thrombocytopenia (HIT)
•Transient prothrombotic disorder initiated by heparin.
•The main features of HIT are (1) thrombocytopenia (2)
increased risk of venous and arterial thrombosis.
•The highest frequency , 5%, has been reported in post–
orthopedic surgery patients receiving up to 2 weeks of
unfractionated heparin

70. Heparin-induced
thrombocytopenia (HIT)
•should be suspected whenever the patient's platelet count falls to
less than 100,000/μL or less than 50% of the baseline value
•The treatment stop all heparin products, initiate an alternative,
nonheparin anticoagulant, even when thrombosis is not clinically
apparent. the use of lepirudin, argatroban, or danaparoid is
preferred over continued use of heparin, LMWH, or either initiation
or continuation of a vitamin K antagonist

71. Thrombolytic Therapy

72. Thrombolytic Therapy
•The ACCP guidelines recommend that thrombolytic therapy
should be used in
•patients with acute PE associated with hypotension (systolic BP<
90 mm HG) who do not have a high bleeding risk .
•select patients with acute PE not associated with hypotension
and with a low bleeding risk whose initial clinical presentation or
clinical course after starting anticoagulation suggests a high risk of
developing hypotension
•Tissue plasminogen activator (tPA) has a short infusion time
and has been recommended as the best agent for this
reason.

73. Major contraindications
•A history of intracranial hemorrhage
•Known intracranial aneurysm or arteriovenous
malformation
•Significant head trauma
•Active internal bleeding
•Known bleeding diathesis
•Intracranial or intraspinal surgery within 3 months
•A cerebrovascular accident within 2 months.

74. Relative contraindications :
•Recent internal bleeding
•Recent surgery or organ
biopsy
•Uncontrolled hypertension
•Pregnancy
•Age 75 years

77. Pulmonary Embolectomy
Surgical embolectomy rarely done. It should
be reserved for pts with hemodynamic
instability despite heparin and
cardiopulmonary support, who either fail
thrombolytic therapy or have a
contraindication to it.

78. Catheter-Based Thrombus Removal
for the Initial Treatment of Patients
With PE
In patients with acute PE associated with hypotension and
who have
(i) contraindications to thrombolysis,
(ii) failed thrombolysis,
(iii) shock that is likely to cause death before systemic
thrombolysis can take effect (eg, within hours).
if appropriate expertise and resources are available, we
suggest catheter-assisted thrombus removal over no such
intervention

79. Vena Cava Filters
indicated in the following settings:
•Patients with acute venous thromboembolism who have
an absolute contraindication to anticoagulant therapy
•Patients with massive PE who survived but in whom
recurrent embolism invariably will be fatal

80. IVC filter

81. Pulmonary embolism In Pregnancy
• Pregnancy increases the risk of VTE 4-fold to 5-
fold over the nonpregnant state.
• Overall, the prevalence of VTE in pregnancy is
0.5-2.0 per 1,000 pregnancies .
• PE is one of the commenest cause of maternal
death in pregnancy
• accounts for 1.1 deaths per 100,000
pregnancies.

82. Pulmonary embolism In Pregnancy

83. AETIOLOGY
• Increase in the levels of coagulation factors
VII, VIII, IX, and X.
• Increased fibrinogen levels.
• Increased platelet activation.
• increases resistance to the anti-thrombotic
factors such as protein C and protein S.
• Venous stasis in the lower limbs due to
pressure by the gravid uterus

84. Risk factors for DVT / PE during
pregnancy
• Maternal age > 35 years.
• Pre-pregnancy weight > 80 kg.
• Pre-existing Thrombophilia.
• Previous DVT.
• Severe varicose veins (V.Vs).
• Prolonged bed rest.
• Multi foetal pregnancies.
• Severe pre-eclampsia.
• Caesarean section delivery.

85. Laboratory Evaluation
D-dimer
• Pregnancy limits the usefulness of this test.
• Studies indicate that d-dimer values increase
with gestational age, making the d-dimer test
less specific.
• Nonetheless, it remains a test with good
negative predictive value in pregnancy.

86. Imaging for PE
• If at initial presentation a patient has
concomitant symptoms or signs consistent with
DVT and PE, compression ultrasonography
may be considered first.
• A negative compression ultrasonography of
lower extremity veins however does not exclude
PE.
• If clinical suspicion still exists, further chest
imaging is necessary.

87. A chest radiograph
•Recommended prior to the evaluation for
PE to define other etiologies that may
explain the symptoms (eg, pneumonia,
atelectasis) and define the appropriate next
imaging test.

88. •Two alternative radiologic modalities exist for
diagnosis of PE are spiral CT pulmonary
angiography (CT-PA) and ventilation-perfusion
(V/Q) scan.
•In the pregnant patient with no known pulmonary
disease and a normal chest
radiograph,ventilation-perfusion scan is the
recommended study to evaluate for PE.
• If the patient has an abnormal chest radiograph
or known pulmonary disease, spiral CT
pulmonary angiography is recommended.

89. CTPA versus V/Q scan
• Spiral CT scanning and V/Q lung/can be safely performed in all
trimesters.
• Fetal radiation exposure for CTPA varies from 0.03
mGy to 1.3 mGy; increased with gestation and
enlarged gravid uterus
• - Fetal radiation dose for V/Q scanning is estimated as 1–
3.7 mGy
• The risk of abnormality is considered to be negligible at ≤ 5
rads (50 mGy) and the risk of malformations is increased at
doses > 15 rads (150 mGy).
British Journal of Radiology,2006 (79):441-444 •
• - ESC (2008): Guidelines on the diagnosis and management of acute pulmonary embolism

90. CTPA versus V/Q scan
CTPA
•More sensitive and specific
•Short acquisition time, easy access and interpretation
• Lower radiation dose to the fetus (<10% of that with V/Q
scanning)
• Identify other pathology: aortic dissection.
• Iodinated contrast medium can potentially alter fetal or neonatal
thyroid function.
V/Q scan
- Not suitable if there is X-ray abnormalities or other chest disease
as asthma or COPD
- High incidence of indeterminate scans
- Advantage over CTPA: Less radiation to maternal breast

92. Treatment
•Heparin, both low molecular weight and unfractionated does not
cross the placenta or the breast. It is therefore safe for the fetus
and for the breast-fed infant.
• warfarin, cross the placenta In the first trimester warfarin
•UFH, LMWHs, and warfarin are not secreted in breast milk in
clinically significant amounts, and so are safe for use in breast-feeding
patients. So after labour oral anticoagulant can be
introduced

93. Duration of therapy
•A pregnant patient with a DVT or PE should be
anticoagulated for the duration of the pregnancy and
at least six weeks postpartum, or for six months,
whichever is longer
•Subcutaneous LMWH is preferred over IV UFH or SC
UFH in most patients .
•UFH (either IV or SC) is preferred over SC LMWH in
patients who have severe renal failure.

94. Labor and delivery
•Treatment with SC LMWH should be discontinued at least 24 hour
Prior to delivery if the delivery time is predictable .
•A period of 24 to 36 hours without anticoagulant therapy may be
undesirable in pregnant women who are at high risk for recurrent VTE
(eg, those with an acute PE or proximal DVT that developed within the
past month).
•Such patients may benefit from having their SC LMWH or SC UFH
switched to IV UFH, which can be discontinued 4 to 6 hours prior to
delivery .

95. Postpartum
•Anticoagulation may be restarted with UFH or LMWH 4-
6 hours following vaginal delivery or 6-12 hours following
cesarean delivery.
• If neuraxial blockade was used, prophylactic anti-coagulation
should not be restarted any sooner than 2
hours following epidural removal.
• Although the ideal time to restart therapeutic
anticoagulation following epidural removal is unclear,
waiting 12 hours after removal of the epidural may be a
reasonable approach

96. Thrombolytic agents in pregnancy
. Streptokinase (and probably other thrombolytic drugs) does not
cross the placenta because of its high molecular weight.
•However in the mother, bleeding is the major side effect, usually
from the genital tract and often severe.incidence of bleeding is
about 8%.
• Because of the risk of bleeding, thrombolysis should not be used
routinely in pregnancy,
•Should not be used at the time of delivery unless it appears that
the patient is likely to die

97. Malignancy
• Four- to sevenfold higher risk of thrombosis compared with
patients without cancer,
•caused by prothrombotic effects of the tumor and also because
of treatment, particularly with surgery, use of a central venous
catheter, and chemotherapy.
•~20% of patients presenting with VTE have active cancer,
associated with reduced survival.
•Value (specificity) of D-dimer testing is reduced, leading to an
increased need for imaging.

98. Malignancy
• initial treatment with heparin and warfarin is given in the standard
manner.
• The relative risk of recurrence is 3 and of bleeding is 6 compared
with other
•Duration of treatment is arbitrary.
• For those with recurrence in spite of adequate anticoagulation,
options include:
(a) aiming for a higher INR of 3.0–3.5 (which further increases the
risks of bleeding)
(b) switching to longterm LMWH while continuing anticoagulation,
(c) insertingan IVC filter, the value of which is questionable.307

99. Patients with liver cirrhosis
• Characterized by decreased synthesis of both pro-and
anticoagulant factors.
• Although bleeding is the most common clinical
manifestation as a result of decreased platelet function
and number, diminished clotting factors and excessive
fibrinolysis,
• Hypercoagulability may play an under recognized but
important role in many aspects of chronic liver
disease.

100. • Particular patients with cirrhosis appear to have a higher
incidence of DVT and pulmonary embolism(PE) compared with
the general population.
• The incidence of DVT/PE ranges from 0.5% to 1.9%, similar to
patients without comorbidities, but lower than patients with other
chronic diseases (i.e, renal or heart disease).
• Serum albumin level was independently associated with the
occurrence of thrombosis
•Cirrhotic patient should not be considered as an auto-anticoagulated
patient.

101. Liver disease as a risk DVT/PE
•Patients w autoimmune liver disease have a higher incidence of
portal vein thrombosis
•Cholestatic liver disease are characterized by a hypercoagulable
state .
• patients with non-cirrhotic liver disease are at greater risk of
DVT/PE.
• Non-alcoholic fatty liver disease have been associated with a
great risk of atherosclerosis and endothelial dysfunction
•

102. Liver disease as a risk DVT/PE
•Patients with hepatocellular carcinoma are known to be
at greater risk of thrombo embolic complications (i.e.
portal vein thrombosis and PE), and increased levels of
thrombin–antithrombin complexes have been
demonstrated.

103. Risk factors for DVT/PE
• Same risk factors as other non-cirrhotic patients such
as venous stasis, infection, congestive heart failure,
acute respiratory disease and immobilization.Surgery .
• liver resection such as for hepatocellular carcinoma
has been shown to correlate with a higher incidence of
thrombotic complications.

104. Thrombotic prophylaxis
•Current American College of Chest Physicians (ACCP) guidelines
for thrombo prophylaxis in patients with important risk factors for
bleedings state: ‘for medical patients with risk factors for VTE, and
for whom there is a contraindication to anticoagulant
thromboprophylaxis, we recommend the optimal use of
mechanical thromboprophylaxis with graduated compression
stockings or intermittent pneumatic compression.
•The statement has the maximum grade of evidence and strength
of recommendation,

105. •Current guidelines on antithrombotic prophylaxis do
not specifically comment on the cirrhotic population as
a result of the perceived risk of bleeding complications
•Thromboprophylaxis should be recommended in
patients with liver cirrhosis at least when exposed to
high-risk conditions for thrombotic complications.
•Low molecular weight heparins (LWMHs) seem to be
relatively safe in this group of patients.
•when important risk factors for bleeding are present,
graduated compression stockings or intermittent
pneumatic compression should be considered.

106. •Disadvantage of the use of LMWH and fondaparinux
inpatients with cirrhosis, is the unpredictable efficacy, as
these drugs require antithrombin to exert its
anticoagulant function, and antithrombin levels are
frequently decreased in these patients.
•The use of antithrombotic agents, directly inhibiting
factor (F)Xa or thrombin, will need very careful
evaluation in this subset of patients due to the risk of
haemorrhagic complications.

107. •The FXa inhibitors rivaroxaban and apixaban are
metabolized in the liver and they are contraindicated
in severe hepatic disease
•Idraparinux, an antithrombin dependent FXa inhibitor,
has no hepatic clearance,but its long half-life
(approximately 80 h) and the lack of antidote do
represent major problems if bleeding occurs.
•Finally, all these drugs must be used with caution or
are contraindicated in the presence of renal failure.