Pulmonary embolism

1
Pulmonary embolism

• 93/12/7
• Dr.???

2
Clinical outcomes in the International
Cooperative Pulmonary Embolism Registry (ICOPER).
Lancet 3531386, 1999.

• Overall cumulative mortality due to PE in the
  International Cooperative Pulmonary Embolism
  Registry (ICOPER) of 2454 patients was 11.4
  percent at 2 weeks and 17.4 percent at 3 months.
• After exclusion of patients in whom PE was first
  discovered at autopsy, the mortality rate was
  15.3 percent.

3
Mortality rate
4
Risk factors
5
(No Transcript)
6
FREQUENCY OF CLASSIC COAGULATION PROTEIN
DEFICIENCIES AMONG PATIENTS WITH VENOUS
THROMBOSIS
7
(No Transcript)
8
ACQUIRED CONDITIONS THAT MAY PRECIPITATE VENOUS
THROMBOSIS

• Surgery/immobilization/trauma
• Obesity
• Increasing age
• Cigarette smoking
• Systemic arterial hypertension
• Oral contraceptives/pregnancy/postpartum
• Cancer (sometimes occult adenocarcinoma) and
  cancer chemotherapy
• Stroke/spinal cord injury
• Indwelling central venous catheter

9
Clinical presentation
10
MOST COMMON SYMPTOMS AND SIGNS
11
DDx

• Myocardial infarction
• Pneumonia
• Congestive heart failure (left-sided)
• Cardiomyopathy (global)
• Primary pulmonary hypertension
• Asthma
• Pericarditis
• Intrathoracic cancer
• Rib fracture
• Pneumothorax
• CostochondritisMusculoskeletal pain
• Anxiety

12
Nonimaging Diagnostic Methods

• PLASMA D-DIMER ELISA. for screeninggt90
  sensitivity not specific
• ARTERIAL BLOOD GASES. PaO2, ?-aDO2, ??????
• ELECTROCARDIOGRAM. right heat strain?76 at
  hospital admission.
• VENOUS ULTRASONOGRAPHY for R/O DVT

13
ECG S1Q3T3
14
ECG S1Q3T3
15
CXR (Westermark's sign)
16
CXR(Hampton's hump)
17
Pulmonary infarct
18
CT in pulmonary infarction. (A) Typical CT
appearance of a pulmonary infarct a
pleurally-based truncated cone containing an air
bronchogram. (B) Ten weeks later the pulmonary
infarct is clearing by retraction and resolution
around its edges.
19
Echo

• Direct visualization of thrombus (rare)
• Right ventricular dilatation
• Right ventricular hypokinesis (with sparing of
  the apex?McConnell's sign)
• Abnormal interventricular septal motion
• Tricuspid valve regurgitation
• Pulmonary artery dilatation
• Lack of decreased inspiratory collapse of
  inferior vena cava

20
Echo
21
High-probability radionuclide scan for pulmonary
embolism. The upper pair are anterior views
showing multiple defects in the perfusion scan
(left) not matched on the ventilation scan
(right). The lower pair are posterior
projections.
22
Pulmonary embolism
23
Pathophysiology
24
Severity
25
(No Transcript)
26
SMALL TO MODERATE PULMONARY EMBOLISM.

• This syndrome is characterized by both normal
  systemic arterial pressure and normal right
  ventricular function.
• Patients usually have a good prognosis if
  anticoagulation or an inferior vena caval (IVC)
  filter is used to prevent recurrent PE.

27
MODERATE TO LARGE PULMONARY EMBOLISM.

• Echo right ventricular hypokinesis on
  echocardiography but normal systemic arterial
  pressure.
• Lung scan more than 30 percent of the lung is
  not perfused.
• They may be at risk for recurrent (and possibly
  fatal) PE, even with adequate anticoagulation.
• Therefore, especially if right ventricular
  dysfunction persists, one should consider using
  thrombolytics or embolectomy.

28
MASSIVE PULMONARY EMBOLISM.

• Patients with massive PE are at risk for
  cardiogenic shock.
• They have thrombosis often affecting at least
  half of the pulmonary arterial system. Clot is
  almost always present bilaterally.
• Dyspnea is usually the cardinal symptom, and
  systemic arterial hypotension requiring pressore
  support is the predominant sign.

29
CT
30
(No Transcript)
31
(No Transcript)
32
The ManagementStrategy and Prognosis of
Pulmonary EmbolismRegistry 1001 patients in
Germany
33
Management strategy
34
Proposed strategy for treatment of pulmonary
embolism in which risk stratification, often with
echocardiography.
35
Therapeutic Considerations

• Anticoagulation with heparin has long been the
  standard treatment for normotensive patients with
  PE.
• By preventing clot propagation, heparin allows
  endogenous fibrinolysis to occur, with eventual
  resolution of thromboemboli.

36
hypotension or shock

• However, in the absence of an absolute
  contraindication, patients with PE-induced
  hypotension or shock are usually treated with
  thrombolytic agents.

37
hemodynamically unstable?t-PA

• PE hemodynamically unstable. The definition of
  hemodynamically unstable is controversial and
  varies from systemic arterial hypotension to
  normal systemic arterial pressure with moderate
  or severe right ventricular dysfunction.

38
Thrombolytic therapy(1)

• New S/S to presentation 14 days.
• t-PA 100mg IVF for 2 hours.
• The potential benefits of immediately reversing
  right heart failure and preventing recurrent PE
  must be balanced by the risk of hemorrhage.
• ICH1 to 2 percent

39
Thrombolytic therapy(2)

• (1) prevent the downhill spiral of right-sided
  heart failure by physical dissolution of
  anatomically obstructing pulmonary arterial
  thrombus
• (2) prevent the continued release of serotonin
  and other neurohumoral factors that might
  otherwise lead to worsening pulmonary
  hypertension
• (3) dissolve much of the source of the thrombus
  in the pelvic or deep leg veins, thereby
  decreasing the likelihood of recurrent large PE

40
Thrombolytic therapy(3)

• Quantitative assessment showed that t-PA
  recipients had a significant decrease in right
  ventricular end-diastolic area during the 24
  hours after randomization compared with none
  among those allocated to heparin alone (p lt
  0.01).
• Recipients of t-PA also had an absolute
  improvement in pulmonary perfusion of 14.6
  percent at 24 hours, compared with 1.5 percent
  improvement among heparin-alone recipients (p lt
  0.0001).

41
Thrombolytic therapy(4)

• Most importantly, no clinical episodes of PE
  recurred among patients receiving t-PA,
• but there were five (two fatal and three
  nonfatal) clinically suspected recurrent PEs
  within 14 days in patients randomized to heparin
  alone (p 0.06).
• RV wall motion t-PA group 39 improve, 2.4
  worsened heparin group 17 improve, 17
  worsening

42
(CHEST 2004 12515391545)

• The Impact of Right Ventricular Dysfunction on
  the Prognosis and Therapy of Normotensive
  Patients With Pulmonary Embolism John W. Kreit,
  MD, FCCP

43
Four groups

• (1) normal BP and right ventricular (RV) function
• (2) normal BP with RV dysfunction
• (3) hypotension without hypoperfusion,
• (4) hypotension with hypoperfusion (shock) or
  cardiac arrest.

44
Criteria for RV dysfunction
45
Echo
46
(No Transcript)
47
(No Transcript)
48
(No Transcript)
49
80 of pts with PE have normal SBP at
presentation2755 patients have evidence of RV
dysfunction
50
Vascular obstruction vs RV dysfunction

• Wolfe and associates lung scan with a perfusion
  score 0.3 (reflecting loss of perfusion to 30
  of the lungs) accurately discriminated between
  patients with and without echocardiographic
  evidence of RV dysfunction.
• Most recently, a study by Miller et al found no
  significant correlation between the extent of
  perfusion defects and the presence of RV
  dysfunction.

51
The essential question

• Prognosis and is rapidly improved by
  thrombolysis, the essential question is whether
  normotensive patients with PE-induced RV
  dysfunction actually benefit from thrombolytic
  therapy.

52
Management Strategy and Prognosis ofPulmonary
Embolism Registry. 719 patients
thrombolytic therapy remained an independent
predictor of survival
53
Hamel and colleaguesretrospective analysis of
normotensive PE patients64 thyrombolysis64
heparin alone

• The same PE recurrence 3 patient in each group
• Higher in-hospital mortality in thrombolytic
  group(6.3 vs 0 in heparin alone)

54
Prospective study 256 patientsKonstantinides
and colleagues

• primary end point was in-hospital death or
  clinical deterioration that required an
  escalation of therapy.
• At first glance, patients treated with
  anticoagulation alone were much more likely to
  die or require treatment escalation than those
  who received rt-PA (24.6 vs 11.0 p 0.006),
  and there was no difference in the incidence of
  major bleeding or intracranial hemorrhage
• Further analysis, however, raises concerns about
  the design of the study and its conclusions.

55
Controversial result at present

• Therefore, despite this large, prospective,
  randomized trial, the use of thrombolysis in
  normotensive patients with PE-induced RV
  dysfunction will remain controversial.

56
ICH

• Thrombolytic group 1.5 4.7
• Heparin 00.3

57
ICH or bleeding, that requires BT or surgery

• Thrombolytic therapy 11.9
• Heparin alone 1.8

58
Conclusion(1)

• 1 .the presence of RV dysfunction identifies a
  subgroup of normotensive patients with PE who
  have substantially increased morbidity and
  mortality.
• 2. thrombolytic therapy rapidly improves
  PE-induced RV dysfunction.
• 3. What remains far less clear is whether this
  effect translates into one or more clinically
  important benefits, and whether these benefits
  outweigh the substantial risk of major
  hemorrhage.

59
Conclusion(2)

• all normotensive patients with acute PE should be
  treated with anticoagulation alone
• In the absence of an absolute contraindication,
  patients with hypotension or shock should undergo
  secondary or rescue thrombolysis.
• echocardiography should be used solely to
  stratify these patients into high- and low-risk
  subgroups based on the presence or absence of RV
  dysfunction.