2. Outline
• Introduction
• History
• Epidemiology
• Relevant anatomy
• Pathogenesis
• Risk factors
• Clinical features
• Investigations
• Management
• DVT prophylaxis in specific situations
• Conclusion
3. Introduction
• Definition- Thrombosis refers to the
formation of solid or semisolid mass in the
circulation from the constituents of the
flowing blood.
• Hence DVT---
• PE- embolisation of part of the thrombus to
the lung.
• DVT-PE occur together; nearly all pat wt
DVT have PE
• Great “masqueraders” of med practice
4. Historical Perspective
• Rudolf Virchow 1856 : Triad & described the emboli concept of PE.
• Lannec: Described PE as a “Pulmonary apoplexy”
• Trendelenburg 1908: Ist Pulmonary embolectomy
• Kirschner 1924: Ist successful Pulmonary embolectomy.
• Sharp 1962: Ist Pulm embolectomy with CPB
• McLean 1916: Discovered heparin as a Medical Student.
• Murray et al 1937: confirmed heparin
5. Epidemiology
• True prevalenc is underreported; most calf DVT’s
are silent . >80% of PE also occur without signs
• Annual incidence - 0.1% in white populations,
• 2.5 million cases of DVT in the US each yr.
• Abt 600,000 affected by PE, abt 150000 die & it
contribute to the death of another 150000
• Ilio-femoral vein most commonly involved. Lt >>
Rt
• Uncommon in the UL
• 90% of PE arise from the deep veins of the leg
• 50% of leg thrombi embolise
6. Epidemiology contd
• Routine autopsy finds PE to be
responsible/contrib to 10-25 % of hospital deaths
• Wtout prophylaxis, fPE occurs in 4-7% hip surg
pats & in 0.1-0.8% gen surg pats
11. Pathogenesis-VIRCHOW’S TRIAD
• Millions of vascular wall injuries occur daily…
Vascular wall injury
Injury, inflammation, Previous DVT
stasis/Flow dynamics alterations
During and after operation, debilitating conditions, eg CVA, Ml,
immobilization.
Hypercoagulability/viscosity:
a) increase in procoagulants eg clotting factors,
b) Decrease in anticoagulants eg proteins C & S, Antithrombin III
c) Increased Viscosity : Malignancy, D/M, pregnancy,
carcinomatosis, PV, lupus anticoagulant
• Disorders of hemostasis, coagulation, anticoagulation, or
fibrinolysis in the face of the triad leads to recurrent thrombosis
13. Sequelae of DVT
1. Embolization- most feared sequelae
2. Incomplete recanalisation
3. Complete recanalisation/Resolution- best
outcome.
- 80 % of calf dvts lyse spontaneously
4. 20% propagate = venous obstruction.
5. Organisation
6. CVI/postphlebitic syndrome.
14. Major Risk Factors for the Development
of DVT
Venous stasis Hypercoagulability Vessel wall injury
•Heart disease
Congestive heart failure
Myocardial infarct
•Surgery > 30 minutes
•Immobility(bed rest > 48
hours)
•Paralysis or neurologic
disease
•Age > 40 years
•? Obesity
•Trauma or surgery
•Malignancy
•Chemotherapy
•Oral contraceptive or
hormonal therapy
•Pregnancy
• Inherited thrombophilia
Protein C, S deficiency
AT III deficiency
factor V Leiden
AntiPL antibody syndrome
Dysfibrinogeneamia
Dysfibrinolysis
•Systemic infection or
inflammation
•Blood dyscrasias
•DM
•Hyperlipideamia
•? Dehydration
•Trauma
•Infection
•Previous DVT
•Varicose vein (four times
increase in< 45 years)
• Superficial vein thrombosis
•Central venous catheter or
pacemaker
15. Classification of risk of VTE
• High risk- DVT-40-79% : fPE—1-5%
• gen. & urological surgery in pts >40yrs, recent hx of VTE
• Extensive pelvic or abdominal surgery for malignant ds.
• Major orthopaedic surgery of the lower limb
• Major trauma or Burn + HX of VTE
• Moderate risk: DVT-0-40%, fPE- 0.1-0.7%
• Gen surgery in pts >40yr lasting >30mins pts >40 on oral contraceptives.
• Major trauma or burn
• Low risk- DVT<10%, fPE-<0.1%
• Uncomplicated surgery in pts < 40yrs without additional risk factor
• Minor surgery ie <30mins in age > 40 without additional risk factors.
16. Clinical features
Upper limb(axillosubclavian)
• Primary(spontaneous)
–Post exercise in young healthy indiv/
Saturday night palsy
–Swollen painful arm
–Distended upper chest, shoulder, neck, arm
veins
• Secondary
–Usually following central canulation
21. Wells clin prediction rule (A Simplified
Clinical Model for Assessment of DVT)
Clinical variable Score(Points)
Active cancer (treatment ongoing or within previous 6 months or palliative) 1
Paralysis, paresis, or recent plaster immobilization of the lower extremities 1
Recently bedridden for 3 days or more, or major surgery within the previous 12
weeks requiring general or regional anaesthesia
1
Localized tenderness along the distribution of the deep venous system 1
Entire leg swelling 1
Calf swelling at least 3 cm larger than that on the asymptomatic leg (measured
10 cm below the tibial tuberosity)
1
Pitting oedema confined to the symptomatic leg 1
Collateral superficial veins (nonvaricose) 1
Previously documented DVT 1
Alternative diagnosis at least as likely as DVT -2
score ≥3 high probability53%; score 1 or 2-moderate prob17%; & score ≤ 0 -low
prob5% Nxt do D-dimer for low & mod prob OPD pat
22. The Wells score:for PE diagnosis
Criteria Score
Clinically suspected DVT - 3.0 points
Alternative diagnosis is less likely than PE 3.0 points
Tachycardia 1.5 points
Immobilization/surgery in previous 4 weeks 1.5 points
History of DVT or PE 1.5 points
Haemoptysis 1.0 points
Malignancy (treatment for within 6 months,
palliative)
1.0 points
Interpretation
Score >6.0 – High probability 59%
Score 2.0 to 6.0 - Moderate probability 29%
Score <2.0 - Low probability 15%
Do D dimer for OPD
patients
23. Pulmonary Embolism Rule-out Criteria
(PERC rule)
• Designed to rule-out risk of PE in patients
stratified into a low-risk category.
• Patients without any of these may undergo
no further diagnostic testing for PE: Hypoxia
- Sa02 <95%, unilateral leg swelling,
hemoptysis, prior DVT or PE, recent surgery
or trauma, age >50, hormone use,
tachycardia.
• Rationale….
24. Investigations
Gen inv-baseline FBC, INR, aPTT, RFT, LFT,
electrolytes
DVT
• Biochemical
– D dimer- an FDP. >500ng/L
• Radiologic
– Duplex doppler USS- non obliterable vein on probe
compression. Repeat in 1wk if
– Venography- filling defects
– MRV
– Impedance plethysmography- req 50% obstruction
– Radioisotope scan. A125 I Fibrinogen scan
25. Investigations contd
PE
• CXR- Westermark sign, Hampton's hump,
atelectasis, a small pleural effusion, and an elevated
diaphragm.
• ECG-acute cor pulmonale in mod PEs -("S1Q3T3").
Sinus tarchycardia, RAD & RBBB are seen
• Nuclear scintigraphic V/Q scan
• Pulm angiography- gold std
• Multidetector Spiral CT chest/ CT angiography-non
invasive
• MRPV- exptal
30. Management
DVT Prophylaxis/Prevention
• This entails the totality of measures
adopted to ensure that a surgical patient
or persons at risk do not develop morbidity
or fatality due to venous thrombosis or its
embolism.
• It is a very crucial aspect of surgical
prophylaxis.
• Prevention is the mainstay
• Prevention is costeffective
31. Management contd- Prevention
1)General measures
–Optimise pat eg CCF
–Decrease Op time
–Adequate hydration
periop
–Adequate analgesia &
early mobilisation/
physiotherapy
–Regional instead of
GA.
2)Mechanical measures
a)ES/GCS
b)IPC, venous foot
pumps
c)Electrical stimulation
a)Non-pharmacological measures
32. Management contd- Prevention
b)Pharmacological
– LDUH-SC 5000u bid, 1st dose
2hrs b4 surgery
– LMWH-SC 1mg/kg/day bid.
Start 12 hrs post surg in Ortho
– Warfarin-1mg/day. If periop,
start 4 days b4 procedure wt
aPTT kept <3. Prob-bleeding.
• Prophylaxis is continued for about
7 days after surgery, or until
patient becomes mobile
• C)Surgical
– Venacaval filters
– Indications-anticoagulant
therapy is contraindicated
and/or ineffective, in a pat
for surgery
– Decreases PE & not DVT
33. Management contd-
Treatment of DVT- ACCP guidelines
• Anticoagulation
– Initial anticoagulation with heparin, followed by long-
term anticoagulation with warfarin.
Heparin-
– Mechanism of action- potentiates antithrombin
– Dose: IV loading dose 5000u or 80u/kg infusion then
18 U/kg/h adjusted based on 6hrly INR targeting 1.5-
2.5
– High dose heparin- phlegmasia cerulea dolens &
lifethreatening PE. 20000u bolus ffd by 5000u/ hr IV.
Maintain for 24 hr, then reduce by 500-1000u hrly
until conventional levels if improving
34. Anticoagulation contd
–Side effects of Heparin-
• bleeding,
• Heparin- Induced thrombotic
Thrombocytopaenia(HIT),
• osteoporosis,
• retoperitoneal haemorrhage esp in the
elderly on high doses,
• adrenal haemorrhage
35. Anticoagulation contd
LMWH- 1mg/kg bid.
• Drawback- no good monitor. 1st do AT level
Warfarin- vitamin K antagonist
• Dose-
– Initial doses- 5-10mg for 1st 2 days
– Av maintenance dose -5mg dly(1-10mg dly) modified based
on INR.
• Target INR -2-3. Heparin is stopped after 2 consec days
of target INR
• Side effects- bleeding, teratogenic, warfarin induced
skin necrosis, purple toe syndrome
37. Contraindications to Anticoagulant Therapy
Absolute contraindications
• Active bleeding
• Severe bleeding diathesis or platelet count ≤20,000/mm3
• Neurosurgery, ocular surgery, or intracranial bleeding within
the past 10 days
Relative contraindications
• Mild-to-moderate bleeding diathesis or thrombocytopenia
• Brain metastases
• Recent major trauma
• Major abdominal surgery within the past 2 days
• Gastrointestinal or genitourinary bleeding within the past 14
days
• Endocarditis
• Severe hypertension (i.e., systolic BP>200 mm Hg, diastolic
BP>120 mm Hg, or both) at presentation
38. Management contd-
Treatment of DVT
• Thrombolysis-
–Urokinase, streptokinase, tPA(Altepase)
–Mech- plasminogen>>plasmin>>clot lysis
–Catheter admin directed locally at
thrombus
–Indications-
• Symptomatic obstr of major upper extremity vein,
• to preserve valve fxn in the lower limb
39. Management contd-
Treatment of DVT
Thrombolysis contd
–Contraind- surgery in last 10 days,serious GI
bleeding in previous 3mths, known HTNsive,
previous CVA, active intracranial process &
bleeding disorder
–Adv- restores a widely patent outflow channel,
preserve and restore normal venous valve
structure and function if performed early
enough(within 1wk)
–Side effect- Intracranial bleeds
40. Management contd-
Treatment of DVT
• Surgical-
Thromboembolectomy
• Indications–
• Extensive clots,
• phlegmasia cerulea dolens and impending venous
gangrene
• poor candidates for fibrinolysis (recent surgery or
trauma involving the CNS or other noncompressible
areas.)
• Preop- clot localisation- doppler/venography
41. Management contd-Treatment of DVT
• Intra-op-
Pre heparinised
Traditional venous thrombectomy using a Fogarty catheter
• Esmarch bandaging if catheter fails to pass due to valves
• A proximal balloon or a temporary caval filter may be used
to reduce the likelihood of embolization
Newer percutaneous mechanical techniques for removal of
an acute obstructing thrombus, including angioscopic
thromboembolectomy, mechanical disruption
thrombectomy, and aspiration thromboembolectomy
• Adjunctive fibrinolysis
• Construction of a small AV fistula may assist in maintaining
patency by increasing the flow velocity through a
thrombogenic iliofemoral venous segment.
42. Management contd-Treatment of DVT
• Post op- to prev rethrombosis
– Heparinisation for 6-12 months afterward.
– Leg compression devices are useful to maintain venous
flow
• Complications of thrombectomy
– failure to clear the deep venous system,
– rethrombosis, &
– PE.
• Follow up- If thrombosis is associated with an
underlying anatomic defect, the defect must be
identified and corrected
43. Management contd-Treatment of DVT
Venacaval filters
• Indications-
– anticoagulant therapy is contraindicated and/or
ineffective,
– Pat who requires urgent surgery that precludes
anticoagulation
– Chronic pulmonary embolism ->pulmonary HTN
– Propagating iliofemoral venous thrombus in
anticoagulation
• Prev PE
45. Management contd-
Treatment of PE
Surportive- O2, adequate circ, cardiotonic
agents
Anticoagulation
– Wt LMWH as for DVT above is started in patients with
a high or intermediate clinical probability score before
imaging. Massive heparin doses in severe PE
– Oral warfarin is started as soon as PE is confirmed.
INR- 2-3
– Treat for 3-6 mths for a first idiopathic PE & Lifelong
for indiv wt persistent risks
46. Management contd-
Treatment of PE
Thrombolysis
BTS Guidelines recommend thrombolysis for:
• Acute massive PE (causing cardiovascular
collapse.). IV alteplase (tPA) 50 mg bolus having
survived acute episode of PE
• Submassive PE, thrombolyse if haemodynamically
stable & assoc with pulm HTN or right ventricular
dysfxn. IV Alteplase 100 mg is given intravenously
over 90 minutes.
47. Management contd-
Treatment of PE
Pulmonary embolectomy
• Rarely indicated today. Mortality rates range
between 20 and 40%
• Indications- failed thrombolysis or
contraindications to thrombolytics in Pat with
preterminal massive PE
• Performed thru posterolateral thoracotomy with
direct visualization of the pulmonary arteries.
Newer percutaneous mechanical
techniques- as described under DVT above
48. Management contd-
Treatment of PE
Venacaval filters
• Indications
–Contraind to anticoagulation
–To prev recurrence in survivors of
massive acute PE
49. DVT Prophylaxis in specific
situations
• TOTAL HIP REPLACEMENT
• Most common serious complication of THR
• Most common cause of death within 3/12
• Resp for >50% post-op mortality after THR .
• Without prophylaxis incidence:40% to 70%, with fPE
in =4-7%
• Mortality for PE in THR with prophylaxis is
2.5times>abdominal & thoracic surg. Pt.
• Risk factors: GA vs RA, large blood loss etc
• Risk of developing DVT present x3wks post op with
peak incidence about 4th day post op and minimal
after 7th day.
• Incidence of PE from untreated DVT lasts 3-8wks post
op.
50. DVT Prophylaxis in specific
situations contd
• TOTAL KNEE REPLACEMENT
• Risk of DVT with no prophylaxis 40-84%
• Risk of asymptomatic PE 10-20%
• Symptomatic… PE 0.5-3%
• Fatal PE up to 2%
• Should all get prophylaxis
51. DVT Prophylaxis in specific
situations contd
• SPINE INJURIES
• Highest risk of DVT/VTE among hospitalised pts
• Risk of DVT is high in acute & rehabilitation phase
• DVT occurs 10 times more in paraetic than non-
paraetic limb
• In the absence of prophylaxis objective evidence of
DVT has been reported to be 67-100%
• Optimal duration of thromboprophylaxis not clearly
defined but incidence of VTE after SCI decreases
significantly after 6/12
• Combination of Mech. & Pharm measures most
effective
52. DVT Prophylaxis in specific
situations contd
• TRAUMA PATIENTS
• 3 components of Virchow’s Triad
• Recent trauma 13 fold rise in risk of DVT
• Major trauma plus immobilization –67% of DVT .
fPE –Rare in Trauma Pts.
• No risk-free preventive measure in trauma
patients.
• BURNS: VTE surprisingly rare in extensive burns
• When it occurs anticoagulation is necessary and
requires high dose of heparin
53. DVT Prophylaxis in specific
situations contd
• Tumour Surgery:
• Urologic surgery:
• General surgery
• Vascular surgery
• Transplant surgery
• Travellers dvt.
54. Current recommendations for DVT
prophylaxis
• All hospital inpatients should be assessed for clinical
risk factors and overall risk of thrombo-embolism
• Should receive prophylaxis according to degree of
risk
– Low risk patients should be mobilised early
– Moderate & high risk patients should receive specific
prophylaxis.
• Prophylaxis should continue until discharge
• Surveilance and high index of suspicion needed for
timely diagnosis and 2ndry prevention.
The Cockett perforator veins drain the medial lower leg and are relatively constant. They connect the posterior arch vein (a tributary of the GSV) and the posterior tibial vein. They may become varicose or incompetent in venous insufficiency states. Boyd's perforator veins connect the greater saphenous vein to the deep veins approximately 10 cm below the knee and 1 to 2 cm medial to the tibia.
Trousseau synd(migratory thrombophlebitis)- an adenoca secretes substances recognised by the body as tissue factor leading to recurent thrombosis. Treat wt heparin indefinitely or until cancer is brought into remission
Paget-Schroetter disease (Paget-von Schrötter disease) is a medical condition in which blood clots form in the deep veins of the arms. These deep venous thromboses typically occur in the axillary vein or subclavian vein.
Axillary-subclavian vein thromboses (ASVTs) are classified into two forms. Primary ASVT comprises only a small minority of all patients with ASVT. In the primary form, no clear cause for the thrombosis is readily identifiable at initial evaluation. Patients with primary ASVT include patients who perform a prolonged, repetitive motion with their upper extremities in the raised position, resulting in damage to the subclavian vein, usually where it passes between the head of the clavicle and the first rib. This condition is known as venous thoracic outlet syndrome. Secondary ASVT is more common and is associated with an easily identified cause such as an indwelling catheter or a hypercoagulable state
May-Thurner syndrome DVT of the iliofemoral vein caused by compression of the left common iliac vein by the overlying right common iliac artery
Homan sign- dorsiflexion causes tenderness. Pratts test- tenderness on palpation
prevalence of deep vein thrombosis based on probability estimates from clinical prediction rules was 5%, 17%, and 53% respectively, in the low, moderate, and high clinical probability groups. Wells et al
Negative D dimer test in low prob pat rules out DVT. Negative High sensitivity D dimer result can also be used to role out DVT in moderate prob pats hence prev further diagnostic investig. All high probability patients require diagnostic imaging to safely rule out DVT. The specificity of D-dimer assays decreases as the clinical probability estimate increases; this leads to more false positive test results, thereby limiting its utility. This emphasizes that D-dimer should not be used as a screening test and indeed some advocate that D dimer assays should not be used for patients at high risk for a false-positive result, ie, elderly patients, patients with cancer, and hospitalized patients.
Negative D dimer result negates further inv for low & moderate probability grps
Doppler US- Lower extremity DVT can be diagnosed by any of the following DUS findings: lack of spontaneous flow (Fig. 23-6), inability to compress the vein (Fig. 23-7), absence of color filling of the lumen by color flow DUS, loss of respiratory flow variation, and venous distention. Again, lack of venous compression on B-mode imaging is the primary diagnostic variable
Venography side effect
Venography is also associated with pain in the foot while dye is being injected or 1 to 2 days after injection. The procedure may be complicated by superficial phlebitis and even DVT in 1 to 2% of patients with normal results on venography. Other less common complications include dye hypersensitivity or aggravation of renal insufficiency.
Iodine-125 Fibrinogen Uptake (FUT).
FUT is a seldom used technique which involves intravenous administration of radioactive fibrinogen and monitoring for increased uptake in fibrin clots. An increase of 20% or more in one area of a limb indicates an area of thrombus
CXR in PE
Most times uninformative
Westermark sign (dilatation of pulmonary vessels and a sharp cutoff),
Hampton’s hump- triangular or rounded pleural based infilterate with the apex towards the hilum , usually located adjacent to the diaphragm
atelectasis, a small pleural effusion, and an elevated diaphragm.
A) After inhalation of 20.1 mCi of Xenon-133 gas, scintigraphic images were obtained in the posterior projection, showing uniform ventilation to lungs.(B) After intravenous injection of 4.1 mCi of Technetium-99m-labeled macroaggregated albumin, scintigraphic images were obtained, shown here in the posterior projection. This and other views showed decreased activity in multiple regions.
CT pulmonary angiography (CTPA) showing a saddle embolus and substantial thrombus burden in the lobar branches of both main pulmonary arteries
Heparin- 80 U/kg bolus, then 18 U/kg/h adjusted based on INR targeting 1.5-2.5
Severe HIT. Withdraw heparin & give lepirudin; a direct thrombin inhibitor
Heparin is a glycosaminoglycan and its anticoagulant
effect is mediated largely through its interaction
with antithrombin III (ATIII). This produces a
conformational change in ATIII and therefore markedly
accelerates its ability to inactivate the coagulation enzymes
thrombin (factor IIa), factor Xa, and factor IXa.63
Of these, thrombin is the most sensitive to inhibition by
heparin-ATIII interaction
Major bleeding is any overt bleeding associated with a marked fall in hemoglobin, any intracranial or retroperitoneal bleeding, or any situation requiring transfusion or re-operation, whereas minor bleeding could be considered as hematoma at wound sites or other forms of bleeding not associated with a significant fall in hemoglobin
LMWH-Drawback- no good monitor. 1st do AT(antithrombin) level. If low, not suitable, use UFH instead
LMWHs have five main changes in their properties compared to standard heparin resulting
from the reduced binding of LMWHs to proteins or cells:
reduced binding to thrombin because of the smaller fragments, but the ability to inactivate factor Xa is retained;
improved predictability and greater bioavailability because of reduced nonspecific binding to plasma proteins;
increased plasma half-life because of reduced binding to macrophages and endothelial cells;
reduced binding to platelets, which may explain the lower incidence of HIT, and possibly reduced bleeding complications;
possibly reduced binding to osteoblasts that results in less activation of osteoclasts and hence a lower incidence of osteopenia.
Warfarin excess: IV vit K 5-10mg for bleeding. If not responding, give prothrombin complex concentrate or 10-20ml/kg FFP
Skin necrosis is due to its initial reduction of natural anticoagulants eg protein C & S b4 the onset of its effect
Unlike heparin, which has equivalent activity against thrombin and factor IIa, LMWHs have greater activity against factor Xa.
The anticoagulant effect of LMWHs is more predictable because of better bioavailability, and thus laboratory monitoring is unnecessary in the vast majority of patients. For patients with renal insufficiency, laboratory monitoring would be preferable because the drug is excreted through the kidney, and hence dosage may need to be adjusted in these patients. The plasma anti-factor Xa assay, which measures the inhibition of Xa activity, would be the appropriate test but currently is not widely available.
WARFARIN
Warfarin-acts by inhibiting vitamin K epoxide reductase, an enzyme that recycles oxidized vitamin K to its reduced form after it has participated in the carboxylation of several blood coagulation proteins, mainly prothrombin and factor VII. The vitamin K coagulation factors II, VII, IX, and X require γ-carboxylation for their procoagulant activity, and treatment with coumarins results in the hepatic production of partially carboxylated and decarboxylated proteins with reduced coagulant activity
Another rare complication that may occur early during warfarin treatment (usually within 3 to 8 weeks) is purple toe syndrome. This condition is thought to result from small deposits of cholesterol breaking loose and flowing into the blood vessels in the skin of the feet, which causes a blueish purple color and may be painful.
Loading regimens
Because of warfarin's poorly-predictable pharmacokinetics, several researchers have proposed algorithms for commencing warfarin treatment:
The Kovacs 10 mg algorithm was better than a 5 mg algorithm.[36]
The Fennerty 10 mg regimen is for urgent anticoagulation[37]
The Tait 5 mg regimen is for "routine" (low-risk) anticoagulation[38]
Some clinicians prefer to use a larger starting dose (eg, 7.5 to 10 mg), while a starting dose of < 5 mg might be appropriate in the elderly, in patients with impaired nutrition liver disease, or congestive heart failure, and in patients who are at high risk of bleeding. When the INR has been in the therapeutic range on two measurements approximately 24 h apart, heparin therapy is discontinued.
Frequency of monitoring (warfarin)
In hospitalized patients, PT monitoring is usually performed daily starting after the second or third dose until the therapeutic range has been achieved and maintained for at least 2 consecutive days, then two or three times weekly for 1 to 2 weeks, then less often, depending on the stability of INR results. In outpatients who have started receiving warfarin therapy, initial monitoring may be reduced to every few days until a stable dose response has been achieved. When the INR response is stable, the frequency of testing can be reduced to intervals as long as every 4 weeks, although there is evidence152153 to suggest that testing more frequently than every 4 weeks will lead to greater TTR. If adjustments to the dose are required, then the cycle of more frequent monitoring should be repeated until a stable dose response can again be achieved.
The heparin/AT complex inactivates thrombin factor IIa and factors Xa, IXa, XIa, and XIIa.4 Thrombin and factor Xa are most sensitive to inhibition by heparin/AT, and thrombin is about 10-fold more sensitive to inhibition than factor Xa.
One milligram of protamine will neutralize approximately 100 U UFH. Admin over 5-10min
Monitor D dimer, plasminogen & fibrinogen levels
Indications for a Vena Cava Filter include:
Recurrent thromboembolism despite adequate anticoagulation
Deep venous thrombosis in a patient with contraindications to anticoagulation
Chronic pulmonary embolism and resultant pulmonary hypertension
Complications of anticoagulation
Propagating iliofemoral venous thrombus in anticoagulation
complications are wound hematoma, migration of the device into the pulmonary artery, and caval occlusion due to trapping of a large embolus.
Emergency pulmonary embolectomy for acute PE is rarely indicated. Patients with preterminal massive PE (Fig. 23-11) who have failed thrombolysis or have contraindications to thrombolytics may be candidates for this procedure. Open pulmonary artery embolectomy is performed through a posterolateral thoracotomy with direct visualization of the pulmonary arteries. Mortality rates range between 20 and 40%. 77–79