1. Pulmonary Embolism IN THE ICU
James Hayward
SHO Anaesthetics Worthing

2. Pulmonary Embolism Critical care patients Virchov’s triad
Premorbid conditions
Significant admitting diagnoses
ICU events
CV catheters
Invasive tests and procedures
Immobility
Virchov’s triad
Venous stasis
Hypercoaguability
Vessel wall inflammation

3. Incidence PE DVT Of 100/103 patients admitted to ICU
1% of all hospitalized patients
15% of patients at post mortem
DVT
10% of patients have ultrasound evidence of DVT when entering the ICU.
Studies suggest that nearly every patient with thrombus in the upper leg or thigh will have a PE if a sensitive enough test is done to look for it. (80% with most sensitive imaging).
Thrombus in the popliteal segment of the femoral vein is the cause of PE in more than 60% of cases.
Of 100/103 patients admitted to ICU
No prophylaxis – 56% / 25% developed DVT
LMWH – 40% / 19% developed DVT
ICS – 33% / 25% developed DVT
Of the trauma/surgical admissions
60% developed DVT

4. Other Emboli
Pieces of tumours, particularly seen with adenocarcinomas that have eroded into the systemic veins.
foreign bodies such as broken intravenous catheters or particulate matter accidentally or deliberately injected into veins;
fat and tissue emboli from orthopaedic injury, operative procedures,
fat emboli may result in a distinct syndrome with systemic manifestations as a result of the breakdown of free fatty acids in the microcirculation and their systemic effects.
bone marrow infarction as seen in acute chest syndrome in patients with sickle cell disease;
air introduced through intravenous lines, lung rupture, or decompression during ascent from underwater diving;
amniotic fluid

5. Symptoms Many patients with PE are initially completely asymptomatic
Classic triad of signs and symptoms of PE - haemoptysis, dyspnea, chest pain
Neither sensitive nor specific. They occur in fewer than 20% of patients in whom the diagnosis of PE is made.
Of patients who go on to die from massive PE, only 60% have dyspnea, 17% have chest pain, and 3% have haemoptysis.
Chest wall tenderness
Back pain
Shoulder pain
Upper abdominal pain
Syncope
Haemoptysis
Shortness of breath
Painful respiration
New onset of wheezing
New cardiac arrhythmia
Pleuritic chest pain is a significant symptom.
PE has been diagnosed in 21% of young, active patients who complain only of pleuritic chest pain.
Symptoms that should provoke a suspicion of PE must include chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain, syncope, haemoptysis, shortness of breath, painful respiration, new onset of wheezing, any new cardiac arrhythmia, or any other unexplained symptom referable to the thorax.
The classic triad of signs and symptoms of PE (haemoptysis, dyspnea, chest pain) are neither sensitive nor specific. They occur in fewer than 20% of patients in whom the diagnosis of PE is made, and most patients with those symptoms are found to have some etiology other than PE to account for them. Of patients who go on to die from massive PE, only 60% have dyspnea, 17% have chest pain, and 3% have haemoptysis. Nonetheless, the presence of any of these classic signs and symptoms is an indication for a complete diagnostic evaluation.
Many patients with PE are initially completely asymptomatic, and most of those who do have symptoms have an atypical presentation.
Patients with PE often present with primary or isolated complaints of seizure, syncope, abdominal pain, high fever, productive cough, new onset of reactive airway disease ("adult-onset asthma"), or hiccoughs. They may present with new-onset atrial fibrillation, disseminated intravascular coagulation, or any of a host of other signs and symptoms.
Pleuritic or respirophasic chest pain is a particularly worrisome symptom. PE has been diagnosed in 21% of young, active patients who come to the ED complaining only of pleuritic chest pain. These patients usually lack any other classical signs, symptoms, or known risk factors for pulmonary thromboembolism. Such patients often are dismissed inappropriately with an inadequate workup and a nonspecific diagnosis, such as musculoskeletal chest pain or pleurisy.

6. Signs Massive PE causes hypotension due to acute cor pulmonale
Physical examination findings early in submassive PE may be completely normal.
New wheeze.
If pleural lung surfaces are affected, a pulmonary rub may be heard.
In patients with recognized massive PE, the incidence of physical signs has been reported as follows:
96% have tachypnoea
58% develop rales
53% have an accentuated second heart sound
44% have tachycardia
43% have fever
36% have diaphoresis
34% have an S3 or S4 gallop
32% have clinical signs and symptoms suggesting thrombophlebitis
24% have lower extremity edema
23% have a cardiac murmur
19% have cyanosis
After hours - loss of pulmonary surfactant occurs
Atelectasis and alveolar infiltrates - indistinguishable from pneumonia on clinical examination and by x-ray.

7. ICU Signs
Patients with worsening hypoxemia or increased physiologic dead space, increased pulmonary artery pressure (in the absence of other causes), unexplained tachycardia or hypotension, or other features of unclear cardiopulmonary insufficiency should be suspected of having pulmonary thromboembolic disease
The use of end-tidal CO2 monitors is a noninvasive means for detecting an acute change in dead space ventilation that may be an early clue for pulmonary embolism.

8. Differential Pneumonia Musculoskeletal pain Herpes zoster Tuberculosis
Pleurisy
Costochondritis
Chronic obstructive pulmonary disease
Rib fractures
Pericarditis
Asthma
Congestive heart failure
Hyperventilation
Pneumothorax
Hepatitis
Pancreatitis
Splenic flexure syndrome
Bronchitis
Salicylate intoxication
Myositis
Tuberculosis
Sepsis
Pericardial tamponade
Angina or myocardial infarction

9. Lab studies (1)
The PO2 on arterial blood gases analysis (ABG) has a zero or even negative predictive value in a typical population of patients in whom PE is suspected clinically.
Other etiologies that masquerade as PE are more likely to lower the PO2 than PE.
In most settings, fewer than half of all patients with symptoms suggestive of PE actually turn out to have PE as their diagnosis.
Conversely, in a patient population with a very high incidence of PE and a lower incidence of other respiratory ailments a low PO2 (or sP02) has a strongly positive predictive value for PE.
In general, pulse oximetry is extremely insensitive and is normal in the majority of patients with PE.
The PO2 on arterial blood gases analysis (ABG) has a zero or even negative predictive value in a typical population of patients in whom PE is suspected clinically.
Other etiologies that masquerade as PE are more likely to lower the PO2 than PE.
Chronic obstructive pulmonary disease [COPD], pneumonia, CHF affect oxygen exchange more than PE, the blood oxygen level often has an inverse predictive value for PE.
In most settings, fewer than half of all patients with symptoms suggestive of PE actually turn out to have PE as their diagnosis.
In such a population, if any reasonable level of PaO2 is chosen as a dividing line, the incidence of PE will be higher in the group with a PaO2 above the dividing line than in the group whose PaO2 is below the divider.
Conversely, in a patient population with a very high incidence of PE and a lower incidence of other respiratory ailments a low PO2 has a strongly positive predictive value for PE.
True also for pulse oximetry
In general, pulse oximetry is extremely insensitive and is normal in the majority of patients with PE

10. Lab studies (2)
The white blood cell (WBC) count may be normal or elevated.
Clotting study results are normal in most patients with pulmonary thromboembolism.
Prolongation of the prothrombin time (PT), activated partial thromboplastin time (aPTT), or clotting time have no prognostic value in the diagnosis of PE.
DVT and PE can and often do recur in patients who are fully anticoagulated.

11. Lab studies (3)
D-dimer is a degradation product produced by plasmin-mediated proteolysis of cross-linked fibrin. D-dimer is measured by an enzyme-linked immunosorbent assay (ELISA) test that is considered positive if the level is greater than 500 ng/mL.
In a population with a PE prevalence of 50%, sensitivity is as low as 79%. Under the best of circumstances, the D-dimer study misses 10% of patients with positive pulmonary angiograms, while only 30% of those with a positive D-dimer will have a positive angiogram.
D-dimer alone is not sensitive or specific enough to diagnose of PE. Its use has increased the number of patients undergoing some evaluation for PE but has not led to any significant change in the frequency with which the diagnosis is confirmed.
In a population with a PE prevalence of 50%, sensitivity is as low as 79%. Under the best of circumstances, the D-dimer study misses 10% of patients with positive pulmonary angiograms, while only 30% of those with a positive D-dimer will have a positive angiogram.

12. CXR
The initial chest x-ray (CXR) findings of a patient with PE are virtually always normal.
On rare occasions they may show the Westermark sign, a dilatation of the pulmonary vessels proximal to an embolism along with collapse of distal vessels, sometimes with a sharp cutoff.
Over time, an initially normal CXR often begins to show atelectasis, which may progress to cause a small pleural effusion and an elevated hemidiaphragm.
After hours, one third of patients with proven PE develop focal infiltrates that are indistinguishable from an infectious pneumonia.
A rare late finding of pulmonary infarction is the Hampton hump, a triangular or rounded pleural-based infiltrate with the apex pointed toward the hilum, frequently located adjacent to the diaphragm.

13. CTPA
High-resolution CT angiography (CTPA) has been shown to have sensitivity and specificity comparable to that of contrast pulmonary angiography
In many patients, multidetector CT scans with intravenous contrast can resolve third-order pulmonary vessels without the need for invasive pulmonary artery catheters.
CTPA is more likely to miss lesions in a patient with pleuritic chest pain due to multiple small emboli that have lodged in distal vessels, but these lesions also may be difficult to detect using conventional angiography.
The overall sensitivity value of CTPA for pulmonary embolism is greater than 99%.

14. V/Q
V/Q scanning is indicated whenever the diagnosis of PE is suspected and no alternative diagnosis can be proved.
A Diagnostic V/Q patterns classified as high probability or as normal perfusion may be relied upon to guide the clinical management of patients when the prior clinical assessment is concordant with the scan result.

15. Pulmonary Angiogram
CPTA has overridden the need for pulmonary angiography but it remains a useful diagnostic modality when CTPA cannot be performed.
A positive pulmonary angiogram provides virtually 100% certainty that an obstruction to pulmonary arterial blood flow does exist.
A negative pulmonary angiogram provides greater than 90% certainty in the exclusion of PE.
Small emboli cannot be seen angiographically. These small emboli can produce pleuritic chest pain and a small sterile effusion even though the patient has a normal V/Q scan and a normal pulmonary angiogram.
In most patients, both large and small emboli already present by the time the diagnosis is first suspected. Under these circumstances, both the V/Q scan and the angiogram are likely to detect at least some of the emboli.

16. Doppler + ECG Duplex ultrasound ECG
In two thirds of patients with PE, the site of DVT cannot be visualized by ultrasound, so a negative duplex ultrasound does not markedly reduce the likelihood of PE
ECG
Normal
Sinus tachycardia
Right heart strain
S1Q3T3
20% of all patients

17. Echocardiography
Haemodynamically significant PE is unlikely in the presence of a normal echocardiogram.
Dilated, hypokinetic RV
Increased RV/LV ratio
Interventricular septum bulging LV into RV.
Dilated pulmonary arteries
Increased velocity of the jet of tricuspid regurgitation (usually in the range of 3–3·5 m/s),
93% sensitive only 81% specific for diagnosis of PE
Disturbed flow velocity pattern in the RV outflow tract.
Inferior vena cava dilated and does not collapse on inspiration.
Recently, RV regional systolic wall motion abnormalities were suggested as a more specific diagnostic sign of acute PE.
According to another report, a severely disturbed RV ejection pattern (acceleration time <60 ms) in the setting of only moderate elevation of pulmonary arterial systolic pressure, as assessed by trans-tricuspid systolic gradient <60 mmHg,
98% specific although only 48% sensitive for acute PE.

18. Effect of PE (1)
Obstruction of the pulmonary circulation resulting in haemodynamic compromise.
Patients with a previously normal pulmonary circulation and right ventricular function can generally tolerate occlusion of even a large pulmonary artery with maintenance of sufficient cardiac output to avoid shock.
However, acute pulmonary thromboembolism in a patient with preexisting pulmonary hypertension or heart failure may cause acute right heart failure and subsequent circulatory collapse.
The same may happen to a previously normal patient in whom a large pulmonary embolus lodges in the main pulmonary artery or who has multiple moderately sized emboli in several major branches.
The clinical manifestations of pulmonary thromboembolism reflect two pathologic processes: obstruction of the pulmonary circulation resulting in hemodynamic compromise and gas exchange abnormalities. The degree of circulatory compromise depends on the size and number of thromboemboli and the preembolic state of the right heart and pulmonary circulation. The terms massive and submassive pulmonary emboli have been applied to the angiographic occlusion of two or more lobar pulmonary arteries or greater than 50% of the pulmonary circulation as seen by noninvasive radionuclide perfusion scanning. These large or multiple emboli may or may not be associated with circulatory collapse and shock. Patients with a previously normal pulmonary circulation and right ventricular function can generally tolerate occlusion of even a large pulmonary artery with maintenance of sufficient cardiac output to avoid shock. However, acute pulmonary thromboembolism in a patient with preexisting pulmonary hypertension or heart failure may cause acute right heart failure and subsequent circulatory collapse. The same may happen to a previously normal patient in whom a large pulmonary embolus lodges in the main pulmonary artery or who has multiple moderately sized emboli in several major branches.
Occlusion of pulmonary arteries results in decreased regional perfusion of the lungs. If ventilation to these areas is maintained, then high areas contribute to increased dead space ventilation. Minute ventilation requirements increase if PaCO2 is maintained. Arterial hypoxemia is much more common. Although the mechanism of hypoxemia is not completely understood, it probably results from a combination of ventilation-perfusion mismatching from atelectasis, redistribution of pulmonary blood flow, and increased blood transit time. Occasionally, acute pulmonary hypertension leads to opening of a patent foramen ovale with intra-atrial right-to-left shunt and severe refractory hypoxemia.
The manifestations of pulmonary thromboembolism often appear to be greater than can be explained by the degree of vascular occlusion by thrombi. Although this is often due to lack of cardiopulmonary reserve in patients with chronic illness, it is probable that vasoactive and bronchoactive substances play a role as well as normal compensatory processes in the lung circulation and parenchyma. Among candidates for participation in the response to pulmonary embolism are products released by platelets and endothelial cells. In addition, occlusion of a pulmonary artery is associated with a decreased amount or decreased effectiveness of surfactant in the region of lung supplied by that vessel, contributing to atelectasis.
Pulmonary infarction is another potential manifestation of pulmonary thromboembolism. However, this diagnosis does not seem to alter outcome or management other than by causing different abnormalities on chest x-ray or somewhat different clinical manifestations. Pulmonary infarction is uncommon in pulmonary embolism, probably because of the dual systemic and pulmonary artery blood supplies to the lung. Patients who present with pulmonary infarction are more frequently those with congestive heart failure in whom both pulmonary venous congestion and systemic perfusion may be compromised.
Because the lungs receive the total cardiac output, a variety of other emboli can make their way into the pulmonary arterial circulation. These include pieces of tumors, particularly seen with adenocarcinomas that have eroded into the systemic veins; foreign bodies such as broken intravenous catheters or particulate matter accidentally or deliberately injected into veins; fat and tissue emboli from orthopedic injury, operative procedures, or bone marrow infarction as seen in acute chest syndrome in patients with sickle cell disease; air introduced through intravenous lines, lung rupture, or decompression during ascent from underwater diving; and amniotic fluid introduced into the systemic circulation during a tumultuous obstetric delivery. The pathophysiologic consequences of these emboli depend somewhat on the clinical situation, the size and number of emboli, and concomitant medical problems. In particular, fat emboli may result in a distinct syndrome with systemic manifestations as a result of the breakdown of free fatty acids in the microcirculation and their systemic effects.

19. Effect of PE (2)
Gas exchange abnormalities. Occlusion of pulmonary arteries results in decreased regional perfusion of the lungs.
If ventilation to these areas is maintained, then high areas contribute to increased dead space ventilation.
Minute ventilation requirements increase if PaCO2 is maintained.
Arterial hypoxemia is much more common.
Ventilation-perfusion mismatching from atelectasis,
Redistribution of pulmonary blood flow,
Increased blood transit time.
Acute pulmonary hypertension can lead to opening of a patent foramen ovale with intra-atrial right-to-left shunt and severe refractory hypoxemia.

20. Effect of PE (3)
The manifestations of pulmonary thromboembolism often appear to be greater than can be explained by the degree of vascular occlusion by thrombi.
Often due to lack of cardiopulmonary reserve in patients with chronic illness.
Likely that vasoactive and bronchoactive substances contribute.
Occlusion of a pulmonary artery is associated with a decreased amount or decreased effectiveness of surfactant in the region of lung supplied by that vessel, contributing to atelectasis.
Pulmonary infarction is uncommon probably because of the dual systemic and pulmonary artery blood supplies to the lung.
Patients who present with pulmonary infarction are more frequently those with congestive heart failure in whom both pulmonary venous congestion and systemic perfusion may be compromised.

21. Management Supportive Anticoagulation Thrombolysis
Inferior Vena Cava Filter
Emergency Pulmonary Thrombectomy

22. Prevention All ICU patients are at risk: Optimise fluids
Hip fracture, total hip replacement, or total knee replacement have a 40-70% chance of developing DVT
Other surgical and medical patients have approximately a 15-50% risk.
Myocardial infarction have about a 24% overall incidence of deep venous thrombosis
Stroke may have up to a 55% risk
Optimise fluids
LMWH (up to 6 weeks post-op)
TEDS/ICS

23. Remaining Issues
The incidence of pulmonary embolism complicating critical illness is unknown, but 5-10% of deaths may be associated with unsuspected pulmonary emboli.
Abnormal pulmonary gas exchange and hemodynamic compromise resulting from new pulmonary emboli may not be identified in patients who already have underlying lung or heart disease.

24. Summary Common disorder Mimics and is mimicked by many other diseases
All ICU patients are at risk
Prophylaxis should be instigated unless specifically contraindicated
Supportive and anticoagulate if possible
CTPA and V/Q most useful diagnostic tools but very difficult practically for ICU