Download Slide 1

Pulmonary Embolism IN THE ICU
James Hayward
SHO Anaesthetics Worthing
Pulmonary Embolism

Critical care patients
– Premorbid conditions
– Significant admitting diagnoses
– ICU events
» CV catheters
» Invasive tests and procedures
» Immobility

Virchov’s triad
– Venous stasis
– Hypercoaguability
– Vessel wall inflammation
Incidence

PE
– 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
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
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.
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 24-72 hours - loss of pulmonary surfactant occurs
–
Atelectasis and alveolar infiltrates - indistinguishable from pneumonia on clinical examination and by x-ray.
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.
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
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.
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.
Lab studies (3)

D-dimer is a degradation product produced by plasminmediated 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.
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 24-72 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.
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%.
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.
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.
Doppler + ECG

Duplex ultrasound
– 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
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.
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.
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.
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.
Management
Supportive
 Anticoagulation
 Thrombolysis
 Inferior Vena Cava Filter
 Emergency Pulmonary Thrombectomy

Prevention

All ICU patients are at risk:
– 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
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.
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
