Pulmonary embolism - Diagnosis and management

Pulmonary Embolism
Dr Vivek Baliga
Consultant, Internal Medicine
Director, HeartSense
www.heartsense.in
Background
 Common and potentially lethal disease
 The diagnosis is often missed because
patients with PE present with
nonspecific signs and symptoms
 If left untreated, approximately one third
of patients who survive an initial PE
subsequently die from a future embolic
episode
Risk Factors
 Immobilization
 Venous stasis
 Hypercoagulable states – Factor V
leiden mutation
 Surgery and trauma
 account for 15% of all postoperative deaths
 hip, pelvic, and spinal surgery are
associated with the highest risk.
Risk Factors
 Malignancy
 Malignancy has been identified in 17% of patients
with venous thromboembolism
 neoplasms most commonly associated with PE, in
descending order of frequency, are pancreatic
carcinoma; bronchogenic carcinoma; and
carcinoma of the genitourinary tract, colon,
stomach, and breast.
 Pregnancy
 Oral contraceptives
Clinical features
 Categorized into 4 classes based on
the acuity and severity of pulmonary
arterial occlusion:
 Massive PE
 Acute pulmonary infarction
 Acute embolism without infarction
 Multiple pulmonary emboli
Clinical features
 Massive PE
 Large emboli compromise pulmonary
circulation to produce circulatory collapse
and shock
 The patient has hypotension; appears
weak, pale, sweaty, and oliguric; and
develops impaired mentation
Clinical features
 Acute pulmonary infarction
 10% of patients have peripheral occlusion
of a pulmonary artery causing parenchymal
infarction.
 Acute onset of pleuritic chest pain,
breathlessness, and hemoptysis
 Normal electrocardiogram findings and no
response to GTN rules out cardiac cause.
Clinical features
 Acute embolism without infarction
 nonspecific symptoms of unexplained
dyspnea and/or substernal discomfort.
Clinical features
 Multiple pulmonary emboli
 First subset has repeated documented episodes
of pulmonary emboli over years, eventually
presenting with signs and symptoms of pulmonary
hypertension and cor pulmonale.
 Second subset has no previously documented
pulmonary emboli but have widespread
obstruction of the pulmonary circulation with clot.
They present with gradually progressive
dyspnoea, intermittent exertional chest pain, and,
eventually, features of pulmonary hypertension
and cor pulmonale
Clinical features
 Most patients with PE have no obvious
symptoms at presentation
 In contrast, patients with symptomatic
deep vein thrombosis (DVT) commonly
have PE confirmed on diagnostic
studies in the absence of pulmonary
symptoms.
Clinical features
 Most common symptoms of PE in the
Prospective Investigation of Pulmonary
Embolism Diagnosis (PIOPED) study
were:
 Dyspnoea (73%)
 Pleuritic chest pain (66%)
 Cough (37%)
 Hemoptysis (13%).
Investigations
 Arterial blood gases
 hypoxemia, hypocapnia, and respiratory
alkalosis
 predictive value of hypoxemia is quite low
 D-dimer
 misses 10% of patients with PE
 only 30% of patients with positive D-dimer
findings have a confirmatory diagnosis of
PE
Investigations
 Chest radiograph
 Initially, normal
 later stages :

Westermark sign (dilatation of pulmonary
vessels and a sharp cutoff)

atelectasis

small pleural effusion

elevated diaphragm
Pulmonary embolism - Diagnosis and management
Investigations
 CT Pulmonary angiography
 Gold standard for the diagnosis of PE
 Positive results consist of a filling defect or
sharp cutoff of the affected artery
 Ventilation-perfusion (V/Q) scanning
 Normal V/Q scan findings indicate an
absence of any perfusion defects
 4% of these patients still may have PE
Investigations
 Echocardiography
 sensitivity and specificity for central and
peripheral PE is 59% and 77%
 Electrocardiogram
 Tachycardia and nonspecific ST-T wave
abnormalities
 S1-Q3-T3 pattern is observed in only 20%
of patients with proven PE
Treatment
 Oxygen
 Full anticoagulation is mandatory
 Thrombolytic therapy
 hemodynamically unstable
 patients who have right-heart strain
 high-risk patients with underlying poor
cardiopulmonary reserve
Thrombolytic Therapy
 Alteplase is recommended
 Streptokinase and Reteplase may also
be used
 Although most studies demonstrate
superiority of thrombolytic therapy with
respect to resolution of radiographic and
hemodynamic abnormalities within the first
24 hours, this advantage disappears 7
days after treatment
Thrombolytic Therapy
 The role of thrombolytic therapy in the
management of acute PE remains
controversial
 Currently accepted indications for
thrombolytic therapy include
hemodynamic instability or right
ventricular dysfunction demonstrated on
echocardiography.
Thrombolytic Therapy
 Konstantinides and colleagues
 "submassive" pulmonary embolism,
defined as right ventriculardysfunction
but preserved systemic arterial
pressure
 256 patients with acute PE and right
ventricular dysfunction or pulmonary
hypertension but with no systemic
hypotension.
Thrombolytic Therapy
 The primary endpoint (in-hospital death
or clinical deterioration that required
escalation of treatment) occurred
significantly less often in the alteplase
group than in the placebo group (11%
vs. 25%).
 Thrombolytic therapy for submassive
PE did not reduce mortality
Anticoagulation
 LMW Heparin
 Warfarin for 6 months if no risk factors
identified
 Warfarin for longer if concurrent risk
factors such as malignancy, immobility
etc
IVC Filters
 Greenfield filter
 Indicated in the following settings
 Patients with acute venous thromboembolism who
have an absolute contraindication to anticoagulant
therapy, eg, recent surgery, hemorrhagic stroke,
or significant active or recent bleeding
 Massive PE who survived but in whom recurrent
embolism will be invariably fatal
 Documented recurrent venous thromboembolism,
adequate anticoagulant therapy notwithstanding
IVC Filters
 One large trial has shown that during
the first 12 days after insertion of IVC
filters, significantly fewer patients had
recurrent PE
 Following a 2-year follow-up, no
significant differences in survival rates
existed between the 2 groups
Pulmonary embolism - Diagnosis and management
Complications
 Sudden cardiac death
 Secondary pulmonary arterial hypertension
 Pulseless electrical activity
 Atrial or ventricular arrhythmias
 Cor pulmonale
 Severe hypoxemia
 Lung infarction
 Paradoxical embolism
Prognosis
 Most patients treated with anticoagulants do
not develop long-term sequelae upon follow-
up evaluation
 Mortality rate in patients with undiagnosed PE
is 30%
 At 5 days of anticoagulant therapy, 36% of
lung scan defects are resolved; at 2 weeks,
52% are resolved; at 3 months, 73% are
resolved.
Further studies?
 Organizing trials of thrombolysis for
pulmonary embolism ischallenging
 the illness is difficult todetect
 public awareness of this major
cardiopulmonary illness is unacceptably
low.
Thank you!
1 de 29

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Pulmonary embolism - Diagnosis and management

  • 1. Pulmonary Embolism Dr Vivek Baliga Consultant, Internal Medicine Director, HeartSense www.heartsense.in
  • 2. Background  Common and potentially lethal disease  The diagnosis is often missed because patients with PE present with nonspecific signs and symptoms  If left untreated, approximately one third of patients who survive an initial PE subsequently die from a future embolic episode
  • 3. Risk Factors  Immobilization  Venous stasis  Hypercoagulable states – Factor V leiden mutation  Surgery and trauma  account for 15% of all postoperative deaths  hip, pelvic, and spinal surgery are associated with the highest risk.
  • 4. Risk Factors  Malignancy  Malignancy has been identified in 17% of patients with venous thromboembolism  neoplasms most commonly associated with PE, in descending order of frequency, are pancreatic carcinoma; bronchogenic carcinoma; and carcinoma of the genitourinary tract, colon, stomach, and breast.  Pregnancy  Oral contraceptives
  • 5. Clinical features  Categorized into 4 classes based on the acuity and severity of pulmonary arterial occlusion:  Massive PE  Acute pulmonary infarction  Acute embolism without infarction  Multiple pulmonary emboli
  • 6. Clinical features  Massive PE  Large emboli compromise pulmonary circulation to produce circulatory collapse and shock  The patient has hypotension; appears weak, pale, sweaty, and oliguric; and develops impaired mentation
  • 7. Clinical features  Acute pulmonary infarction  10% of patients have peripheral occlusion of a pulmonary artery causing parenchymal infarction.  Acute onset of pleuritic chest pain, breathlessness, and hemoptysis  Normal electrocardiogram findings and no response to GTN rules out cardiac cause.
  • 8. Clinical features  Acute embolism without infarction  nonspecific symptoms of unexplained dyspnea and/or substernal discomfort.
  • 9. Clinical features  Multiple pulmonary emboli  First subset has repeated documented episodes of pulmonary emboli over years, eventually presenting with signs and symptoms of pulmonary hypertension and cor pulmonale.  Second subset has no previously documented pulmonary emboli but have widespread obstruction of the pulmonary circulation with clot. They present with gradually progressive dyspnoea, intermittent exertional chest pain, and, eventually, features of pulmonary hypertension and cor pulmonale
  • 10. Clinical features  Most patients with PE have no obvious symptoms at presentation  In contrast, patients with symptomatic deep vein thrombosis (DVT) commonly have PE confirmed on diagnostic studies in the absence of pulmonary symptoms.
  • 11. Clinical features  Most common symptoms of PE in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study were:  Dyspnoea (73%)  Pleuritic chest pain (66%)  Cough (37%)  Hemoptysis (13%).
  • 12. Investigations  Arterial blood gases  hypoxemia, hypocapnia, and respiratory alkalosis  predictive value of hypoxemia is quite low  D-dimer  misses 10% of patients with PE  only 30% of patients with positive D-dimer findings have a confirmatory diagnosis of PE
  • 13. Investigations  Chest radiograph  Initially, normal  later stages :  Westermark sign (dilatation of pulmonary vessels and a sharp cutoff)  atelectasis  small pleural effusion  elevated diaphragm
  • 15. Investigations  CT Pulmonary angiography  Gold standard for the diagnosis of PE  Positive results consist of a filling defect or sharp cutoff of the affected artery  Ventilation-perfusion (V/Q) scanning  Normal V/Q scan findings indicate an absence of any perfusion defects  4% of these patients still may have PE
  • 16. Investigations  Echocardiography  sensitivity and specificity for central and peripheral PE is 59% and 77%  Electrocardiogram  Tachycardia and nonspecific ST-T wave abnormalities  S1-Q3-T3 pattern is observed in only 20% of patients with proven PE
  • 17. Treatment  Oxygen  Full anticoagulation is mandatory  Thrombolytic therapy  hemodynamically unstable  patients who have right-heart strain  high-risk patients with underlying poor cardiopulmonary reserve
  • 18. Thrombolytic Therapy  Alteplase is recommended  Streptokinase and Reteplase may also be used  Although most studies demonstrate superiority of thrombolytic therapy with respect to resolution of radiographic and hemodynamic abnormalities within the first 24 hours, this advantage disappears 7 days after treatment
  • 19. Thrombolytic Therapy  The role of thrombolytic therapy in the management of acute PE remains controversial  Currently accepted indications for thrombolytic therapy include hemodynamic instability or right ventricular dysfunction demonstrated on echocardiography.
  • 20. Thrombolytic Therapy  Konstantinides and colleagues  "submassive" pulmonary embolism, defined as right ventriculardysfunction but preserved systemic arterial pressure  256 patients with acute PE and right ventricular dysfunction or pulmonary hypertension but with no systemic hypotension.
  • 21. Thrombolytic Therapy  The primary endpoint (in-hospital death or clinical deterioration that required escalation of treatment) occurred significantly less often in the alteplase group than in the placebo group (11% vs. 25%).  Thrombolytic therapy for submassive PE did not reduce mortality
  • 22. Anticoagulation  LMW Heparin  Warfarin for 6 months if no risk factors identified  Warfarin for longer if concurrent risk factors such as malignancy, immobility etc
  • 23. IVC Filters  Greenfield filter  Indicated in the following settings  Patients with acute venous thromboembolism who have an absolute contraindication to anticoagulant therapy, eg, recent surgery, hemorrhagic stroke, or significant active or recent bleeding  Massive PE who survived but in whom recurrent embolism will be invariably fatal  Documented recurrent venous thromboembolism, adequate anticoagulant therapy notwithstanding
  • 24. IVC Filters  One large trial has shown that during the first 12 days after insertion of IVC filters, significantly fewer patients had recurrent PE  Following a 2-year follow-up, no significant differences in survival rates existed between the 2 groups
  • 26. Complications  Sudden cardiac death  Secondary pulmonary arterial hypertension  Pulseless electrical activity  Atrial or ventricular arrhythmias  Cor pulmonale  Severe hypoxemia  Lung infarction  Paradoxical embolism
  • 27. Prognosis  Most patients treated with anticoagulants do not develop long-term sequelae upon follow- up evaluation  Mortality rate in patients with undiagnosed PE is 30%  At 5 days of anticoagulant therapy, 36% of lung scan defects are resolved; at 2 weeks, 52% are resolved; at 3 months, 73% are resolved.
  • 28. Further studies?  Organizing trials of thrombolysis for pulmonary embolism ischallenging  the illness is difficult todetect  public awareness of this major cardiopulmonary illness is unacceptably low.