Ward 14 (puolmonary embolism)

Question 1

What is a pulmonary embolism?

Answer 1

A blood clot obstructs the pulmonary artery or its branches.

Question 2

What is a deep vein thrombosis?

Answer 2

A thrombus develops within the deep veins

Question 3

Where do DVTs most commonly occur?

Answer 3

Lower extremities

Question 4

How do PE usually occur?

Answer 4

PE usually occurs when a part of a DVT’s thrombus breaks off and passes through the veins and the right side of the heart before lodging in the pulmonary circulation

Question 5

What is a VTE?

Answer 5

It refers to the interrelated diagnoses of deep vein thrombosis (DVT) and pulmonary embolism (PE)

Question 6

Risk factors for VTE

Answer 6

• PE risk factors are the same as DVT.
• Virchow’s triad of hypercoagulability, venous stasis, and endothelial injury provides an understanding of these risk factors.
• Risk factors can be classified as genetic and acquired

Question 7

Genetic risk factors for VTEs

Answer 7

Thrombophilia, such as factor V Leiden mutation, prothrombin gene mutation, protein C deficiency, protein S deficiency, and hyperhomocysteinemia

Question 8

Acquired risk factors for VTEs

Answer 8

Acquired risk factors include immobilization for prolonged periods (bed rest of greater than 3 days, anyone traveling greater than 4 hours, whether by air, car, bus, or train, reduced mobility), recent orthopedic surgery, malignancy, indwelling venous catheter, obesity, pregnancy, cigarette smoking, and oral contraceptive pill use, fracture of lower limb, major trauma, history of previous VTE, CHF or respiratory failure, postpartum period, Infection, MI (right ventricle thrombus), thrombophilia, recent hospitalization, HRT, central venous lines, hip or knee replacement, Hospitalization for heart failure or atrial fibrillation/flutter within the previous 3 months

Question 9

Types of PE

Answer 9

Categorize PE based on the presence or absence of hemodynamic stability into , hemodynamically unstable PE (previously called massive (describing the hemodynamic effect and not size) or high risk PE), and hemodynamically stable PE

Question 10

What is hemodynamically unstable PE?

Answer 10

PE that results in hypotension (as defined by systolic blood pressure (SBP) less than 90 mm Hg or a drop in SBP of 40 mm Hg or more from baseline or hypotension that requires vasopressors or inotropes)

Question 11

What is hemodynamically stable PE?

Answer 11

A spectrum ranging from small, mildly symptomatic, or asymptomatic PE (low-risk PE or small PE) to PEs, which cause mild hypotension that stabilizes in response to fluid therapy, or those who present with RV dysfunction (submassive or intermediate-risk PE), but is hemodynamically stable

Question 12

Mortality rate of PE

Answer 12

30% of untreated patients with PEs die, while only 8% die after timely therapy

Question 13

Symptoms of PE

Answer 13

• Small emboli may be asymptomatic, whereas large emboli are
  often fatal.
  -Often none except breathlessness
• The most common symptoms of PE include the following: acute dyspnea, pleuritic chest pain, cough, hemoptysis, dizziness, presyncope, or syncope
• In patients with preexisting heart failure or pulmonary disease, worsening dyspnea may be the only symptom
  -In older people, the first symptom of pulmonary embolism may be confusion or deterioration of mental function

Question 14

Signs of PE

Answer 14

• Increased JVP, increased RR, increased HR, decreased BP, RV heave, hypotension, pleural rub, pleural effusion, cyanosis, ±pyrexia.
• Less common presentations include arrhythmias (eg, atrial fibrillation), syncope, and hemodynamic collapse (shock)
• Other examination findings include calf swelling, tenderness, erythema, palpable cords, pedal edema, and rales
• Tachycardia and tachypnoea may be the only clinical signs

Question 15

Testing in patients with suspected PE

Answer 15

• FBC, U&E, baseline clotting, D-dimers
• ABG
• Imaging: CXR or CTPA
• ECG.
  In patients with no known provoking risk factors, consider investigation
  for possible underlying malignany. Undertake full history, examination
  (including breast), CXR, FBC, calcium, LFTS, urinalysis. Patients >40yrs consider abdopelvic CT and mammography in women. Consider antiphospholipid and thrombophilia
  testing if family history positive

Question 16

X ray in PE

Answer 16

CXR usually normal or might show nonspecific abnormalities such as atelectasis or effusion
Can show oligaemia of affected segment, decreased vascular markings, dilated pulmonary artery, linear atelectasis, small pleural effusion, wedge-shaped opacities of infarction or cavitation (rare)

Question 17

ECG findings in PE

Answer 17

Non specific. Commonly normal or sinus tachycardia, right bundle branch block, right ventricular strain (inverted T in V1 to V4), right axis deviation

Question 18

Downfalls of CTPA in PE

Answer 18

The CT- PA offers excellent diagnostic accuracy but exposes your patient
to 3.6yr of background radiation, along with nephrotoxic IV contrast medium,
while taking up significant resources

Question 19

When is D dimer elevated?

Answer 19

Will be raised in many situations (infection, malignancy, MI, CVA to name a few)

Question 20

D dimer reliability in PE

Answer 20

The value of D- dimer testing lies in the excellent negative predictive value when the risk of a PE is low. In those at high risk, negative D- dimer levels do not provide sufficient reassurance.
The Wells score for PE is a clinically reliable method of identifying the risk of PE, and hence deciding on further testing.

Question 21

Testing in PE based on D dimer

Answer 21

• T hose scoring ≤4 are low risk: test for D- dimers.10 If elevated, proceed to
  CT- PA ; if negative, then consider alternative diagnoses
• T hose scoring >4 are high risk: proceed to CT- PA testing and start treatment dose of LMWH.

Question 22

Management pathway of PE

Answer 22

Acute treatment: Sit up (unless low BP) and give 15L/ min O2.
- If life- threatening (hypotension +shock) seek immediate senior support, arrange an urgent CTPA
+ echo and consider thrombolysis. Otherwise parenteral anticoagulation
, eg enoxaparin 1.5mg/ kg/ 24h SC and pain relief; IV fluids if dBP.

Question 23

What will ABG show in PE

Answer 23

• hyperventilation + poor gas exchange: decreased PaO2, decreased PaCO2, increased pH.
• It is important to note that hypercapnia, respiratory, or lactic acidosis is uncommon but can be present in patients with massive PE associated with obstructive shock and respiratory arrest

Question 24

Gold standard diagnostic test for PE

Answer 24

CTPA, V/Q scan if unavailable

Question 25

How fast can PE cause death

Answer 25

Most deaths occur within 1 hour

Question 26

Specificity of D dimer test

Answer 26

The specificity of D-dimer decreases steadily with age to approximately 10% in patients greater than 80 years of age. Using age-adjusted cut-offs for patients older than 50 may improve the performance of D-dimer testing in the elderly. In one study, using the age-adjusted cut-off instead of the standard D-dimer cut-off of 500 ng/mL or more increased the number of patients in whom the possibility of PE could be ruled out from 6.4% to 30%, without additional false-negative findings.[28] The formula is age (years) x 10 mcg/L for patients more than 50 years of age. Example: Patient age 75 = age-adjusted d-dimer of 750 mcg/L.

Question 27

Length of treatment for PE

Answer 27

Question 28

Score used to predict mortality in PE

Answer 28

PESI score

Question 29

Complications of PE

Answer 29

The major complications associated with PE include the following:

Recurrent thromboembolism
Chronic thromboembolic pulmonary hypertension
Right heart failure
Cardiogenic shock