Alexandria University

Faculty of Nursing

Doctorate Program

Seminar in Critical Care and Emergency Nursing

2015-2016

Venous Thromboembolism
(VTE)

 Supervised by/ Prof. Dr. Azza El-Soussi.

 Prepared by/ Mohamed Ezzelregal Mohamed.

Learning Objectives
At the end of this seminar the doctorate students will be able to:

1-Knowledge and Understanding:

 Discuss risk factors of VTE.

 Describe the diagnosis and assessment of VTE.

 Review management stratigies for VTE.

2-Intellectual capabilities

 Differentiate between different types of embolus pathway.

 Describe the pathophysiology of VTE.

 Formulate nursing care plan for patient who have VTE.

 Summarize the role critical care nurse in the prevention of VTE.

3-Professional and practical skills

 Collaporate with multidiscplinary team in the prevention of VTE.

 Provide nursing care for patients who have VTE.

4-General and transferable skills

 Practice within ethical principles & professional practice standards while caring for

critically ill patient who have VTE.

 Value the benefits of VTE preventive stratigies.

 Communicate effectively with patients, family, and health care providers.

 Document data reflecting critically ill patient's conditions.

Outline

 Introduction
 Definitions of VTE and embolism
2
  The pathway of the embolus
 Pathophysiology of VTE
 Risk factors for VTE
 Risk stratification of DVT
 Diagnosis of DVT
 Deep Vein Thrombosis Prevention Techniques
 Risk stratification according to expected VTE -related early mortality rate
 Diagnosis of VTE
 Clinical prediction rules for VTE
 Prevention of VTE in the ICU
 Management of VTE

Venous Thromboembolism (VTE)

Introduction:
The threat of pulmonary shower is a daily concern in ICU patients, who typically have
one or more risk factors for venous thrombosis (the precursor of pulmonary shower). Thrombus
formation occurs most frequently in proximal leg veins, and becomes apparent only when a
portion of the thrombus breaks loose and travels to the lungs to become a pulmonary embolus.
This progression from silent leg thrombosis to symptomatic pulmonary shower is a significant,
and preventable, problem in ICU patients. Other sites of clot formation include the heart (as in
untreated atrial fibrillation) and other deep vessels of the pelvic region. In fact, pulmonary
shower is considered the most common preventable cause of death in ICU patients, and the

3
prevention of venous thrombosis is considered the single most important measure for ensuring
patient safety during ICU stay.

Definitions

A venous thrombosis: a blood clot that originates in a vein and does not move. The
formation, development, or existence of a blood clot or thrombus within the vascular system is a
life-saving process when it occurs during hemorrhage. It is a life-threatening event when it occurs
at any other time because the clot can occlude a vessel and stop the blood supply to an organ or a
part. The thrombus, if detached, becomes an embolus and occludes a vessel at a distance from
the original site; for example a clot in the leg may break off and cause a pulmonary shower. An
embolus results when the blood clot breaks away from where it originates and travels through the
bloodstream.

The Pathway of Embolus

The pathway of the embolus can be one of three types:

 Anterograde  Retrograde  Paradoxical

In anterograde embolism, the movement of emboli is in the direction of blood flow. In

retrograde embolism, however, the emboli move in opposition to the blood flow direction; this is
usually significant only in blood vessels with low pressure (veins) or with emboli of high weight.
In paradoxical embolism, also known as crossed embolism, an embolus from the veins crosses to
the arterial blood system. This is generally found only with heart problems such as septal defects
between the atria or ventricles.

Pathophysiology

Development of pulmonary shower appears to be the result of multiple simultaneously

operating factors. The combination with one or more factors highly increases the risk for a
thromboembolic episode. The pathogenesis of pulmonary shower is associated with the triad of
interdependent factors described by Virchow more than 100 years ago. Virchow's triad was first
formulated by the German physician Rudolf Virchow (1821-1902) in 1856. It consists of
hemodynamic imbalance (blood stasis), endothelial vessel wall damage, and a local or systemic
state of hypercoagulability. Accordingly, venous thrombosis develops when stasis in the deep
veins of the legs occurs at times of increased blood coagulability and when vessel wall injury is
present simultaneously.

4
 1- Blood Stasis

Venous stasis represents an important pathogenic factor in the development of PE. It has
been suggested that blood pooling leads to activation of the coagulation system, thus resulting in
a state of local hypercoagulability. In addition, possible endothelial damage from distension of the
vessel walls by the pooling blood leads to further activation of the homeostasis system. The
activation products of clotting and fibrinolysis can also induce endothelial damage which, in turn,
promotes a local state of hypercoagulability.

2- Hypercoagulability
The risk of venous thrombosis is increased when the homeostatic balance between pro-
and anticoagulant forces is shifted in favor of coagulation. When this imbalance is due to an
inherited defect, the resulting hypercoagulable state remains a life-long risk factor for thrombosis.
Hypercoagulability can be a consequence of numerous possible risk factors such as hyper
viscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or
burn, disseminated cancer, late pregnancy and delivery, race, age, smoking, and obesity.
3- Vessel Wall Injury

Vessel wall damage is believed to be another essential component of venous

thrombogenesis. After injury, certain changes develop in the clotting system, particularly an
increase in platelet aggregability which could further contribute to the state of hypercoagulability.

Risk factors for pulmonary shower

o Strong predisposing factors o Moderate predisposing factors

 Fracture (hip or leg)  Arthroscopic knee surgery
 Hip or knee replacement  Central venous lines
 Major general surgery  Chemotherapy
 Major trauma  Chronic heart or respiratory
 Spinal cord injury failure
o Weak predisposing factors  Hormone replacement therapy
 Bed rest > 3 days  Malignancy
 Immobility  Oral contraceptive therapy
 Increasing age  Paralytic stroke
 Laparoscopic surgery  Pregnancy/postpartum
 Obesity  Previous VTE
5
  Pregnancy/antepartum  Thrombophilia
 Varicose veins

DEEP VENOUS THROMBOSIS

Deep vein thrombosis, the formation of a thrombus in one of the deep veins of the body, is
the single most preventable thrombo-embolic disorder, and is asymptomatic in many cases.
Predisposing factors to DVT
 Trauma: During surgical procedures, IV injection or therapeutic interventions might
cause serious endothelial damage to veins and vein dilation.
 Blood coagulation factors: Hypercoagulation – due to dehydration, malignancy or oral
contraceptives – has the potential to alter normal blood hemostasis mechanisms
 Stasis of venous circulation: Caused by immobility that deprive the deep veins of the
lower limbs from the pumping action of the calf muscles, leading to stasis of venous
blood, particularly behind the valve cusps of deep veins, which can predispose to thrombus
formation.

The clinical risk factors for pulmonary shower can be remembered by "mnemonic"
THROMBOSIS
 T: Trauma, Travel
 H: Hypercoagulable, Hormonal replacement
 R: Recreational drugs "IV drugs"
 O: Old > 60 years old
 M: Malignancy
 B: Birth control bills
 O: Obesity, Obstetrics
 S: Surgery, Smoking
 I: Immobilization
 S: Sickness "CHF/ MI, nephritic syndrome, vasculitis"
Risk stratification of DVT

DVT predictors Points

Active cancer +1
Bed ridden > 3 days or major surgery within 4 weeks +1
6
 Localized tenderness along the distribution of deep venous system +1
Entire leg swollen +1
Calf swelling 3 cm > asymptomatic side (10 c below tibial tuberosity) +1
Pitting edema confined to the symptomatic leg +1
Collateral superficial veins (non-varicose) +1
Paralysis, paresis, or recent plaster immobilization of the lower extremity +1
Previously documented DVT +1
Alternative diagnosis to DVT as likely or more likely? -2
Probability: > 2 (high), 1-2 (moderate), 0 or less (low)

Diagnosis of DVT

1. Signs and symptoms:

 Abnormal swelling of the affected limb
This can be due to localized edema resulting from:
1- Thrombosis occlusion of the affected deep vein, which impedes venous blood return and
can also affect the efficiency of collateral venous drainage.
2- Capillary damage causes leakage of intravascular fluid into the surrounding tissues
(extravasation), distal to the thrombosis site.
Bilateral baseline limb-girth measurements should be performed daily, and form an important part
of ongoing patient monitoring.
 Warmth of affected limb
This is due to localized venous congestion and accumulation of metabolites in the affected limb.
 Localized pain
Lower limb pain might be experienced in the calf muscle region during dorsiflexion movements
of the foot (positive Homan's sign). Localized symptoms are commonly due to edema in the
tissues surrounding the site of thrombophlebitis where clot is present.
 Dilatation of veins
Due to the venous thrombus occlusion of the respective vein, a distal dilatation of veins might
occur as a result of systemic and peripheral venous circulatory-stasis obstruction.
 Color changes of the leg

7
Initially, as a result of the venous thrombosis, pallor of the leg might be the only indicator. In
other cases, a peripheral skin erythema (redness) of the affected limb occurs immediately over the
DVT site, which might be due to the superficial thrombophlebitis.
 Fever
A systemic increase in body temperature to 39-40°C can be caused by the accumulation of tissue
metabolites at the site of the thrombosis formation, and intravascular thrombophlebitis occurs.
 Asymptomatic
In 50 % of cases the DVT has no initial observable symptoms & of patients with a PE, up to 75 %
might have no sign of a preceding DVT. All patients who are identified to be at risk should be
carefully assessed, examined and monitored.

2. Diagnostic studies
 Plasma D-dimer assay.

 Impedence plethysmography:

It is less expensive, and is portable technique detects increased venous outflow resistance
in the deep veins of the proximal lower extremities. It is a sensitive method for evaluating the rate
of venous return from the lower extremity.
 Doppler ultrasound

 Contrast venography

 Computed tomography venography

 Radioactive fibrinogen scanning

This test can be performed to define the location of a clot and any subsequent secondary
emboli. Radioactive fibrinogen is administered intravenously and in patients who develop a DVT,
it will be transformed into fibrin. Daily leg scanning is performed to monitor the DVT episode.
 Magnetic resonance imaging:

MRI was at least 90% sensitive and specific for acute symptomatic proximal DVT. Magnetic
resonance imaging appears useful in evaluating upper extremity venous thrombosis.

Deep Vein Thrombosis Prevention Techniques

1. Mechanical Prophylactic Measures

8
  Exercises  Graduated stockings

 Range of motion  Pneumatic compression devices

Each improves venous return and reduces venous stasis in leg veins. These measures are
simple to use and do not increase the risk of bleeding, making them ideal for most hospital
patients. Mechanical measures are best suited for those individuals at low risk for developing
DVT, or those that have contraindications to the use of pharmacologic measures.

Foot and ankle exercises encourage plantar and dorsiflexion to improve venous return,
using a very basic, natural technique. They do not require anything other than patient
comprehension and willingness to perform exercises on a regular basis. For those patients who
are unable to perform foot and ankle exercises, passive range of motion is an appropriate
substitute to reduce venous pooling by passively exercising muscles. The use of these exercises is
safe for all patients except those with bone injuries. Friction concerns may require heel protection
in those patients at risk for skin breakdown, and may be as simple as elevating heels off bed
linens to reduce friction. Early ambulation is another useful technique for decreasing venous
thromboembolism that is encouraged in patients with low risk of developing DVT. These low-risk
patients include those under age 40 with no other risk factors, who have undergone minor surgery
including laparoscopic surgeries. Monitoring and therapeutic intervention equipment should be
evaluated for necessity as soon as patients are able to get out of bed. Those items that are not
necessary should be removed so that patients may quickly return to their prior level of activity.

Graduated compression stockings are another option in the prevention of DVT that are
easily tolerated by most patients and can be continued on an outpatient basis. They are best used
in hospital patients with low risk for DVT, especially when paired with foot and ankle exercises
in those individuals who are able to perform them. Individuals with arterial insufficiency of the
lower extremities should use stockings with caution as arterial circulation is already
compromised. Proper fit is required to obtain maximum benefit and avoid stockings that are too
tight causing a tourniquet effect. They should be applied as soon as ordered and removed once a
shift for 30 minutes to assess underlying skin.

Intermittent pneumatic compression devices work by creating pressure on the leg

muscles, using air-filled sleeves. This pressure assists in improving venous blood return while
decreasing blood pooling and can be applied either in sequential compression devices or
longitudinally in rapid inflation, asymmetrical compression devices.
9
 The ACCP guidelines currently recommend using mechanical prophylaxis measures in all
hospitalized patients with anticoagulant contraindications. Use in combination with
anticoagulants is also recommended for those patients at high risk for developing DVT without
anticoagulant contraindications. Mechanical measures should be used initially in surgical patients
with a high risk for bleeding until anticoagulants can be reconsidered. Compression modalities
were all found to be safe and effective. However, to be effective, these measures must be used for
the duration of bed rest, not just a few hours a day. Nurses must encourage patient use and
compliance.

2. Pharmacologic Prophylactic Measures

Pharmacologic measures involve various types of anticoagulation in order to reduce blood

coagulability. These anticoagulants include:-

 Aspirin  Unfractionated heparin  Low-molecular-weight heparin

 Warfarin  Pentasaccharides

The medications are best used in patients with moderate to high risk factors in order to
provide greater protection than mechanical devices alone can provide.

Aspirin decreases platelet aggregation and is considered effective prophylaxis treatment

for arterial thrombosis, which consists mostly of platelet aggregates. Venous thrombi contain
fibrin and red blood cells, which is why aspirin is ineffective in preventing venous
thromboembolism in patients. Current ACCP guidelines recommend not using aspirin as a sole
means for the prevention of venous thromboembolism in any patient. Those patients who are
taking aspirin for other reasons should be considered for additional methods of DVT prevention,
such as mechanical measures, unfractionated heparin, or low-molecular-weight heparins.

Unfractionated heparin is one option for DVT prophylaxis. It has been used for a number
of years and side effects are well known. Heparin can be administered intravenously or
subcutaneously. Intravenous dosing provides immediate anticoagulant effect, whereas
subcutaneous dosing leads to delayed response of approximately 1 hour. If given subcutaneously,
low- to moderate-risk patients need twice-daily dosing, whereas high-risk patients may require
dosing 3 times a day. However it is administered, heparin requires activated partial
thromboplastin time monitoring and dose adjustments based on results.

10
 Low-molecular-weight heparins, including enoxaparin, dalteparin, and tinzaparin, can be
administered subcutaneously without coagulation monitoring. They offer easy and convenient
administration in hospital patients with fixed dosing available in prefilled syringes with common
doses for thromboprophylaxis. They have been shown to be safe for use in the elderly, although
dose adjustments may be necessary in obese patients and individuals with renal impairment.
Patients at higher risk of bleeding should be started on low-molecular-weight heparin rather than
unfractionated heparin. The Prime study, a randomized, double-blind, placebo-controlled trial
involving 959 high-risk medical patients at multiple facilities, concluded that enoxaparin was
only slightly more effective than unfractionated heparin, but had significantly lower bleeding risk.

Current ACCP guidelines recommend unfractionated heparin or low-molecular-weight

heparin prophylaxis in all acutely ill medical patients without anticoagulant contraindications
who have more than 1 risk factor for DVT. Critical care patients with moderate risk of DVT
should receive prophylaxis with either unfractionated heparin or low-molecular-weight heparin,
whereas high-risk critical care patients should receive low-molecular-weight heparin. Patients
over the age of 40 having moderate to high-risk general surgery with a limited number of other
risk factors should receive prophylaxis with either unfractionated heparin or low-molecular-
weight heparin.

Pentasaccharides are another class of medication used in the prevention of DVT.

Fondaparinux, a synthetic Pentasaccharides anticoagulant that can be given subcutaneously once
daily, is currently approved for thromboprophylaxis in patients undergoing orthopedic surgery. In
a randomized controlled trial of 849 elderly, medical patients, Fondaparinux was found to reduce
the incidence of DVT from 10.5% in the placebo control group to 5.6% in the treatment group.
Dose adjustments may be required in those individuals with renal impairment, and Fondaparinux
should not be used in patients with renal failure. Despite a low occurrence of major bleeding, one
concern is the lack of response to protamine sulfate as an antidote.

Warfarin offers the convenience of a pill that can be taken orally in the hospital and
continued at home for those patients at risk after discharge. However, it does have a narrow
therapeutic window and requires frequent monitoring of prothrombin time or international
normalized ratio. A large number of foods, drugs, and disease processes alter warfarin's
effectiveness, making it difficult to regulate. Many hospitalized patients are receiving antibiotic
therapy, which commonly interferes with warfarin dosing. Elderly patients should be started on

11
lower doses and monitored more frequently. Major side effects include bleeding that can be life
threatening and may preclude use in a large number of hospital patients.

Current ACCP guidelines recommend low-molecular-weight heparin, Fondaparinux, or

warfarin for initial and continued thromboprophylaxis in orthopedic patients having hip or knee
surgery. Continued prophylaxis is strongly recommended in orthopedic patients for
approximately 1 month after surgery. In patients that have undergone elective hip replacement,
continued prophylaxis with low-molecular-weight-heparin or warfarin is preferred over
Fondaparinux. However, Fondaparinux is preferred over low-molecular-weight heparin for
continued prophylaxis use after fractured hip repair.

3. Combination Therapy

Combination therapy using mechanical and pharmacologic methods needs to be

considered in patients with high-risk for DVT and those who need lower doses of anticoagulants.
Patients undergoing high-risk general surgery with multiple risk factors are candidates for
combination therapy. Elderly medical patients should also be considered for combination therapy
because of multiple risk factors and increased risk of bleeding. Mechanical measures have few
contraindications and are good adjuncts for those individuals that require reduced dosing of
pharmacologic measures.

PULMONARY SHOWER

Pulmonary shower continues to be responsible for substantial morbidity and mortality and
remains a challenging diagnostic problem. In fact, the diagnosis is frequently not established
until massive, life-threatening pulmonary shower occurs or until autopsy. In addition, there is
evidence that pulmonary shower is the most common undiagnosed cause of death in hospitalized
patients, responsible for the death of thousands of patients each year. Even more worrying is the
fact that, if diagnosed and treated, many of the deaths attributable to pulmonary shower are
potentially preventable.

Virchow’s triad of venous stasis, hypercoagulability, and vessel wall damage triggers a
venous thrombus (clot) to develop in susceptible patients. Pulmonary embolism results when
fragments detach from a thrombus, travel through the venous system, pass through the right side
of the heart, and lodge in the main branches of the pulmonary artery.

12
 A pulmonary shower can also occur as a result of other fluids or material entering the
vasculature. Deep vein thrombosis, amniotic fluid, air, and iatrogenic causes are all sources of
pulmonary embolism. A venous thrombus most commonly originates in the lower extremities, the
pelvis, or the kidneys. The main symptom of pulmonary embolism is often a vague complaint of
dyspnea or chest pain, and death commonly occurs within 1 hour of the onset of signs and
symptoms if the correct diagnosis is not established.

Pulmonary shower may be classified as massive, sub massive, or minor, depending on the
amount of pulmonary vasculature affected. Massive pulmonary shower is defined as thrombus
occluding more than 50% of the pulmonary vasculature. Thrombus that occludes the bifurcation
of the pulmonary artery is termed a saddle embolus. When the embolus lodges in the pulmonary
vasculature, blood flow to the alveoli beyond the blockage is eliminated. The obstruction causes a
section of lung to be ventilated but not perfused, thus creating intrapulmonary "dead space." The
blockage acts like a dam, causing blood pressure to increase in the vessels upstream. The right
ventricle must then generate tremendous pressure to overcome this obstacle and maintain forward
blood flow and perfusion to distal organs.

If the right ventricle is unable to maintain adequate forward blood flow, right-sided heart
failure develops and leads to hypoxemia, dyspnea, hypotension, and syncope. In a massive
pulmonary embolism, cardiac arrest occurs because the left ventricle is unable to maintain
adequate cardiac output. Pulseless electrical activity is the most common rhythm seen in cardiac
arrest. Only 25% of patients with cardiac arrest survive the ordeal, and a preoperative cardiac
arrest is the strongest predictor of postoperative mortality.

Massive pulmonary shower with cardiovascular collapse indicates a significant

accumulation of thrombus within the pulmonary arteries and carries a grim prognosis if not
diagnosed and treated quickly. Although most patients with massive pulmonary embolism do not
present in shock, mortality reaches 30% for those who do.

13
Risk stratification according to expected pulmonary embolism-related early mortality rate
Pulmonary embolism Risk markers Potential treatment
Clinical (shock Right Myocardial
related early mortality implications
or hypotension) ventricular injury
risk
dysfunction
Thrombolysis or
High > 15 % + + +
embolectomy
Intermediate + + Hospital admission
3- 15 % - + -
Non- high - +
Low < 1 % Early discharge or
- - -
home treatment
In the presence of shock or hypotension it is not necessary to confirm RV dysfunction/injury to
classify as high risk of PE-related early mortality.
Diagnosis of pulmonary shower
Symptoms
 Chest pain (pleuritic): The pain is usually caused by pleural irritation due to distal emboli
causing a so-called pulmonary infarction, an alveolar hemorrhage, sometimes
accompanied by haemoptysis
 Chest pain (sub sternal)  Syncope  Dyspnea / Cough
Signs
 Tachypnea ( > 20/min)  Tachycardia ( > 100/min)  Signs of DVT
 Fever ( > 38.58C)  Cyanosis
ECG
While ECG abnormalities may develop in the setting of acute pulmonary shower, they are
generally nonspecific mostly only shows sinus tachycardia; however, there are some recognized
patterns which include non specific ST-T wave inversion (deep S wave, inverted T wave) in leads
V1-V3. Right axis deviation and Right Bundle Branch Block can also be noted.
Arterial blood gases
Hypoxemia is common in acute pulmonary shower, but is not universally present. The
diagnosis of acute PE cannot be excluded on the basis of a normal PaO2 and although the
alveolar–arterial difference is usually elevated, it may be normal in patients without preexisting

14
cardiopulmonary disease. Pulmonary shower is generally associated with hypoxemia, but up to
20% of patients with pulmonary shower have a normal arterial oxygen pressure (PaO 2) and a
normal alveolar-arterial oxygen gradient [D (A-a) O2].
Chest X-ray
Common radiographic findings include plate-like atelectasis, pleural effusion, pulmonary
infiltrates, and elevation of a hemi diaphragm. A normal chest radiograph in the setting of
severe dyspnea and hypoxemia without evidence of bronchospasm or anatomic cardiac shunt is
strongly suggestive of pulmonary shower. The chest radiograph cannot be used to prove or
exclude pulmonary shower conclusively. However, the chest X-ray is very useful in excluding
other causes of dyspnoea and chest pain.
D-dimer
D-dimer is a specific degradation product released into the circulation when cross-linked
fibrin undergoes endogenous fibrinolysis. D-dimer levels are elevated in plasma in the presence
of an acute clot because of simultaneous activation of coagulation and fibrinolysis. On the other
hand, although D-dimer is very specific for fibrin, the specificity of fibrin for pulmonary shower
is poor because fibrin is produced in a wide variety of conditions, such as cancer, inflammation,
infection, necrosis, dissection of the aorta, and the positive predictive value (PPV) of D-dimer is
low.
Ventilation–Perfusion (V/Q) scan:
The ventilation–perfusion scan has long been considered the pivotal diagnostic test in
acute pulmonary shower. Unfortunately, the scan is diagnostic in a minority of cases; that is, it is
rarely interpreted as normal or high probability. Most lung diseases affect pulmonary blood flow
to some extent as well as ventilation, decreasing the specificity of the scan. Pulmonary embolism
frequently occurs in the setting of concomitant lung disease such as chronic obstructive
pulmonary disease (COPD) or pneumonia, further complicating the diagnostic evaluation. This
shows areas of ventilated lung with perfusion mismatch i.e. inadequate oxygen transfer.
Pulmonary angiography
Pulmonary angiography has been considered the gold standard diagnostic technique for
pulmonary shower. The most common diagnostic algorithm for pulmonary shower has consisted
of scanning followed by pulmonary angiography when the scan is non-diagnostic and the clinical
suspicion high. Pulmonary angiography for the purpose of diagnosing acute pulmonary shower is
unnecessary when the perfusion scan is normal.
Relative contraindications to the procedure include significant bleeding risk and renal
insufficiency. The procedure can generally safely be performed when the platelet count is at least
15
75,000/mm3 and if coagulation studies are normal or minimally abnormal. In patients with renal
insufficiency, adequate hydration must be maintained before, during, and after the angiogram.
Diseases such as diabetes or multiple myeloma may increase the frequency of acute renal
insufficiency after angiography. The presence of a left bundle branch block is an indication for a
temporary pacemaker during the procedure to protect against complete heart block. The
electrocardiogram should be reviewed for any potential arrhythmias. The most frequent site of
access is the femoral vein, preferably on the right. The Basalic vein or the right internal jugular
may also be used.
Spiral CT Chest:
If the V/Q scan is not conclusive and /or symptoms persist despite having normal blood
results, a CT scan can be arranged (this has 63- 98% reported sensitivity for diagnosis of
pulmonary shower). This technique involves continuous movement of the patient through the CT
scanner and allows concurrent scanning by a constantly rotating gantry and detector system. This
technique enables rapid scanning with continuous volume acquisitions obtained during a single
breath. Spiral CT has the greatest sensitivity for emboli in the main, lobar, or segmental
pulmonary arteries.
An advantage of spiral CT includes the ability to define nonvascular structures such as
lymphadenopathy, lung tumors, emphysema, and other parenchymal abnormalities as well as
pleural and pericardial disease. Smaller lymph nodes may result in false-positive studies.
Magnetic resonance imaging:
Magnetic resonance imaging (MRI) is also being utilized to evaluate clinically suspected
pulmonary shower. The authors emphasize that the technique is rapid, accurate, avoids
nephrotoxic iodinated contrast, and is better accepted by patients than pulmonary angiography. It
has excellent sensitivity and specificity for the diagnosis of DVT together with the potential for
performing perfusion imaging. This technique may ultimately allow the simultaneous and
accurate detection of both pulmonary shower and DVT.

Echocardiography:
Right ventricular failure is the ultimate cause of death in patients who sub-acute to acute
pulmonary shower. Dysfunction of the right ventricle frequently accompanies massive pulmonary
shower, and this finding has been shown to correlate not only with larger emboli but also with
recurrence of pulmonary shower.

16
Unfortunately, the finding of right ventricular dysfunction is nonspecific and certain clinical
conditions commonly confused with pulmonary shower (such as acute COPD exacerbations) are
also associated with abnormal right ventricular function. Visualization of large emboli within the
main pulmonary artery has been reported with surface echocardiography, but this appears to be
unusual.
Trans esophageal echocardiography has been utilized to document emboli in the main or
right pulmonary artery and in some cases the left pulmonary artery. The use of contrast may
enhance the visualization of the left pulmonary artery.
1- Clinical prediction rules for pulmonary shower: the revised Geneva score
Revised Geneva score
Variable Points
Predisposing factors
 Age > 65 years +1
 Previous DVT or pulmonary shower +3
 Surgery or fracture within 1 month +2
 Active malignancy +2
Symptoms
 Unilateral lower limb pain +3
 Haemoptysis +2
Clinical signs
 Heart rate
 > 100 beats/min +3
 ≥ 95 beats/min +5
 Pain on lower limb deep vein at palpation and unilateral edema +4
Clinical probability Total
 Low 0-3
 Intermediate 4-10
 High ≥ 11
2- Clinical prediction rules for pulmonary shower: the Wells score
Wells score
Variable Points
Predisposing factors
 Previous DVT or PE +1.5
 Recent surgery or immobilization +1.5
 Cancer +1
Symptoms
 Haemoptysis +1
Clinical signs
 Heart rate
 > 100 beats/min +1.5
 Clinical signs of DVT +3
Clinical judgment
 Alternative diagnosis less likely than pulmonary shower +3
Clinical probability (3 levels) Total
17
  Low 0-31
 Intermediate 2-6
 High ≥7
Clinical probability (2 levels)
 PE unlikely 0-4
 PE likely >4

Figure 1 Proposed diagnostic algorithm for patients with suspected high-risk PE, i.e.
presenting with shock or hypotension. *CT is considered not immediately available also if
the critical condition of a patient allows only bedside diagnostic tests. (1)

18
Figure 2 Proposed diagnostic algorithm for patients with suspected non-high-risk PE (i.e. without shock and hypotension).

Prevention of pulmonary shower in the ICU

While the risks of pulmonary shower in critically ill patients vary considerably depending
primarily on their reason for intensive care, most ICU patients have multiple risk factors for
pulmonary shower. Some of these risk factors predate admission to the ICU, and include recent
surgery, trauma, sepsis, malignancy, stroke, advanced age, heart or respiratory failure, previous
pulmonary shower, and pregnancy. Other thrombotic risk factors may be acquired during the ICU
stay, and include immobilization, pharmacologic paralysis, central venous lines, surgical
procedures, sepsis, mechanical ventilation, vasopressor use, and renal dialysis. However, neither
d-dimer levels nor tests of molecular hypercoagulability had any predictive value for DVT in
critically ill patients. At the same time, critical care patients also frequently have risk factors for
bleeding, including recent surgery, trauma or GI bleeding, thrombocytopenia, and renal
insufficiency.
Recommendations for critical care
1. For patients admitted to a critical care unit, routine assessment for pulmonary shower risk
and routine thromboprophylaxis in most (Grade 1A).
2. For critical care patients who are at moderate risk for pulmonary shower (eg, medically ill
or postoperative general surgery patients), low-molecular-weight heparin (LMWH) or low-
dose unfractionated heparin (LDUH) thromboprophylaxis should be used (Grade 1A).
3. For critical care patients who are at higher risk (eg, following major trauma or orthopedic
surgery), LMWH thromboprophylaxis should be used (Grade 1A).
19
 4. For critical care patients who are at high risk for bleeding, the optimal use of mechanical
thromboprophylaxis with graduated compression stockings (GCS) and/or intermittent
pneumatic compression (IPC) at least until the bleeding risk decreases (Grade 1A). When
the high bleeding risk decreases, that pharmacologic thromboprophylaxis should be
substituted for or added to the mechanical thromboprophylaxis (Grade 1C).
Recommendations: Acute Spinal Cord Injury
1. For all patients with acute SCI, routine thromboprophylaxis should be provided (Grade
1A).
2. For patients with acute SCI, thromboprophylaxis with LMWH should be commenced once
primary hemostasis is evident (Grade 1B). Alternatives include the combined use of IPC
and either LDUH (Grade 1B) or LWMH (Grade 1C).
3. For patients with acute SCI, the optimal use of IPC and/or GCS should be done if
anticoagulant thromboprophylaxis is contraindicated because of high bleeding risk early
after injury (Grade 1A). When the high bleeding risk decreases, pharmacologic
thromboprophylaxis should be substituted for or added to the mechanical
thromboprophylaxis (Grade 1C).
4. For patients with an incomplete SCI associated with evidence of a spinal hematoma on CT
or MRI, the use of mechanical thromboprophylaxis should be used instead of
anticoagulant thromboprophylaxis at least for the first few days after injury (Grade 1C).
5. Following acute SCI, the use of LDUH alone should not be administered (Grade 1A).
6. For patients with SCI, the use of an IVC filter should not be used as thromboprophylaxis
(Grade 1C).
7. For patients undergoing rehabilitation following acute SCI, the continuation of LMWH
thromboprophylaxis or conversion to an oral vitamin K antagonists (VKA) should be used
(INR target, 2.5; range, 2.0 to 3.0) (Grade 1C)
Recommendations: Trauma
1. For all major trauma patients, routine thromboprophylaxis is recommended if possible
(Grade 1A).
2. For major trauma patients in the absence of major contraindication, clinicians should use
LMWH thromboprophylaxis starting as soon as it is considered safe to do so (Grade 1A).
An acceptable alternative is the combination of LMWH and the optimal use of a
mechanical method of thromboprophylaxis (Grade 1B).
3. For major trauma patients, if LMWH thromboprophylaxis is contraindicated due to active
bleeding or high risk for clinically important bleeding, mechanical thromboprophylaxis
20
 with IPC, or possibly with GCS alone, be used (Grade 1B). When the high bleeding risk
decreases, pharmacologic thromboprophylaxis should be substituted for or added to the
mechanical thromboprophylaxis (Grade 1C).
4. In trauma patients, routine Doppler US (DUS) screening should not be done for
asymptomatic DVT (Grade 1B). DUS screening should be done only in patients who are at
high risk for pulmonary shower (eg, in the presence of a SCI, lower-extremity or pelvic
fracture, or major head injury), and who have received suboptimal thromboprophylaxis or
no thromboprophylaxis (Grade 1C).
5. For trauma patients, the use of an IVC filter as thromboprophylaxis should not be used
(Grade 1C).
6. For major trauma patients, the continuation of thromboprophylaxis should be used until
hospital discharge (Grade 1C).
7. For trauma patients with impaired mobility who undergo inpatient rehabilitation,
continuing thromboprophylaxis with LMWH or a VKA should be instituted (target INR,
2.5; range, 2.0 to 3.0) (Grade 2C).
MANAGEMENT OF PULMONARY SHOWER
The goals of medical and/or surgical interventions
o To relieve pulmonary obstruction
o Stop clot propagation
o Regain or maintain hemodynamic stability
o Prevent clot recurrence
o Prevent pulmonary hypertension

CIRCULATORY SUPPORT
Medical interventions for treating massive pulmonary shower are aimed at preserving circulatory
support by:
o Managing the airway
o Maintaining blood pressure
o Preventing new thrombus formation
Airway management and oxygen administration are paramount in the treatment of
pulmonary embolism. Oxygen consumption should be minimized with measures to reduce fever
and agitation, and by instituting mechanical ventilation if the work of breathing is excessive.
When mechanical ventilation is required, care should be taken to limit its adverse haemodynamic
effects. In particular, positive intrathoracic pressure induced by mechanical ventilation may
21
reduce venous return and worsen RV failure in patients with massive pulmonary shower.
Therefore, positive end-expiratory pressure should be applied with caution. Cautious use of
sedatives during induction is warranted as these drugs can blunt the catecholamine response that
the patient depends on to maintain blood pressure through peripheral vasoconstriction.
Hypotension is initially treated with judicious volume resuscitation of 1 to 2 L of crystalloid
infused over 1 hour. If hypotension persists, the addition of a vasopressor such as norepinephrine,
epinephrine, dopamine, or phenylephrine is warranted.
THROMBOLYSIS

Patients in stable condition are treated with anticoagulation alone, but thrombolytics are
the treatment of choice in hemodynamically unstable patients. Thrombolytics convert
plasminogen to plasmin and directly lyse the clot. Plasminogen activation interferes with
coagulation by inactivating fibrinogen and factors II, V, and VII. Clot lysis results in faster
improvement in pulmonary perfusion, hemodynamic alterations, and gas exchange, which rapidly
reduces right ventricular afterload and dysfunction. The thrombolysis process is nonselective and
can cause a major bleeding event. Bleeding complications occur in 20% of patients, and
intracranial hemorrhage occurs in 3% of patients.
Streptokinase, a bacterial protein derivative, is produced from streptococcal bacteria and
often causes febrile reactions. Streptokinase is administered as an intravenous infusion of 250000
IU over 30 minutes, followed by 100000 IU/h intravenously for 24 to 72 hours. This product is
highly antigenic and may be administered only once during a 6-month period. Febrile reactions
respond to treatment with acetaminophen (Tylenol). Accelerated regimen: 1.5 million IU over 2 h.
Urokinase is produced from cultures of human source materials and thus has a small
potential to transmit infectious agents. Urokinase is administered as an intravenous bolus of 4400
U/kg over 10 minutes, followed by 4400 U/kg per hour intravenously for 12-24 hours. Accelerated
regimen: 3 million IU over 2 h.

The third choice, alteplase (rtPA) uses recombinant DNA technology and is synthesized by
a human melanoma cell line. This enzyme binds to fibrin in a thrombus, causing conversion of
plasminogen to plasmin. Alteplase is administered as a 100-mg intravenous infusion over 2 hours
or 0.6 mg/kg over 15 min (maximum dose 50 mg). Heparin should not be infused concurrently
with streptokinase or urokinase, but it can be given during alteplase administration. Thrombolytic
therapy carries a significant risk of bleeding, especially when predisposing conditions or
comorbidities exist.

22
Contraindications to fibrinolytic therapy
Absolute contraindications
 Hemorrhagic stroke or stroke of unknown origin at any time
 Ischemic stroke in preceding 6 months
 Central nervous system damage or neoplasms
 Recent major trauma/surgery/head injury (within preceding 3 weeks)
 Gastrointestinal bleeding within the last month
 Known bleeding
Relative contraindications
 Transient ischemic attack in preceding 6 months
 Oral anticoagulant therapy
 Pregnancy or within 1 week post partum
 Non-compressible punctures
 Traumatic resuscitation
 Refractory hypertension (systolic blood pressure .180 mmHg)
 Advanced liver disease
 Infective endocarditis
 Active peptic ulcer

INITIAL ANTICOAGULATION
Anticoagulation with unfractionated heparin LMWH, warfarin or Fondaparinux is the
standard treatment for pulmonary shower in stable patients while awaiting definitive diagnostic
confirmation. Because of the risk of heparin-induced thrombocytopenia (HIT), monitoring of the
platelet count is necessary during treatment with unfractionated or low-molecular-weight heparin.

 Heparin

Heparin acts as a catalyst to activate prothrombin, which inhibit factor Xa and thrombin.
Heparin is unable to dissolve existing thrombus because of the inability to inhibit thrombin bound
to fibrin. The activated partial thromboplastin time (aPTT) is maintained at 60 to 100 seconds or
according to institutional policy..

 Low-Molecular-Weight Heparin
23
 Low-molecular-weight heparin is a heparin-based product used in patients with sub
massive pulmonary embolism and deep venous thrombosis, but it remains an unproven treatment
option for patients with massive pulmonary embolism. Low-molecular- weight heparin is also
contraindicated in patients with heparin-induced thrombocytopenia (HIT).

 Warfarin
Warfarin (Coumadin) therapy should overlap with heparin therapy for 4 days to avoid
transient hypercoagulability that may occur with isolated administration of warfarin. The
warfarin-induced decline in levels of coagulation factors is a function of the half-life of each
factor, which varies from 5 hours for factor VII to 72 hours for factor II. The half-life of warfarin
is 36 to 42 hours; therefore, an increase in the international normalized ratio (INR) is not seen
until 2 days after the first dose is administered. The goal for the INR is 2 to 2.5 for 3 to 6 months.
Warfarin may be initiated after 48 hours of direct thrombin inhibitor therapy as long as the
platelet count is greater than 100 x 109/L.25 Warfarin is contraindicated in pregnancy because it
crosses the placenta. Warfarin is safely used in lactating patients because it is not excreted in
breast milk.

SURGICAL MANAGEMENT
1- Percutaneous catheter embolectomy and fragmentation

Surgical interventions are usually reserved for patients in unstable condition with
contraindications to thrombolytic therapy. Percutaneous catheter embolectomy is performed
during pulmonary angiography in an effort to remove the obstructive embolus.

This procedure may be performed by one of 2 techniques. The first method is aspiration
embolectomy, in which suction is applied to remove the embolic material. The second technique is
mechanical embolectomy, which involves maceration or fragmentation of the embolus.
Mechanical embolectomy has a success rate of 80%, but there is danger of distal migration of the
pulmonary embolism.

Complications of percutaneous procedures include local damage to the puncture site, usually
the femoral vein, perforation of cardiac structures, tamponade and contrast reactions.
2- Vena Caval Filters

Percutaneous filters are placed in the inferior vena cava to prevent recurrent pulmonary
embolism by preventing clot migration. These filters are often used for patients with
24
contraindications to anticoagulation, those with recurrent pulmonary embolism, or those who have
underlying cardiac or pulmonary disease in whom a pulmonary embolism would be fatal.

Complications of filter placement include thrombosis at the insertion site, filter migration,
erosion through the wall of the inferior vena cava, or obstruction of the inferior vena cava during
deployment of the filter.

3- Surgical Embolectomy

Surgical embolectomy involves manual removal of the thrombus from the pulmonary artery.
This procedure is usually reserved for patients in unstable condition who have contraindications to
thrombolytic therapy. Extracorporeal membrane oxygenation is a temporary cardiopulmonary
support system used sparingly in the treatment of patients with circulatory collapse due to
pulmonary embolism. Extracorporeal membrane oxygenation is used to maintain oxygenation and
tissue perfusion until the thrombus can be dissolved or removed.

NURSING CARE

Preventive measures for deep venous thrombosis must be used routinely for any hospitalized
patient.

 Compression stockings should be placed on the lower extremities before the patient gets out
of bed.
 External pneumatic compression boots, which intermittently compress the calf and accelerate
deep venous flow, may be used in bed-bound patients.

 Adequate hydration and early ambulation are encouraged to prevent deep venous thrombosis.

 Daily assessment of extremities for pain, erythema, and size discrepancy is vitally important.
The Homan sign (pain on dorsiflexion) is apparent in only 30% of the cases.

 The nurse must recognize risk factors for pulmonary embolism and vigilantly monitor
patients who are immobilized or have had their activity restricted for unexplained tachypnea,
tachycardia, and restlessness. These signs must not be attributed to anxiety unless a physical
cause has been sought first.

25
 Critically ill or postoperative patients are at high risk for venous thromboembolism and should
be assessed for use of prophylactic heparin or low-molecular-weight heparin subcutaneously
or intravenously.

If pulmonary embolism is discovered and the patient is hemodynamically unstable,

 The nurse will institute appropriate fluid administration and inotropic support to maintain a
systolic blood pressure of 90 mm Hg.

If pulmonary hypertension and right-sided heart failure are present,

 The nurse may consider cautious use of a vasodilator such as nitric oxide.
 The nurse can provide short explanations of the diagnostic tests and invasive procedures to
reassure the patient that this life-threatening condition is treatable.

 Neurological and vascular assessments should be performed hourly to evaluate organ

perfusion. Confusion or agitation may indicate respiratory acidosis (increased PaCO 2 and
decreased pH). Weakened pulses and cool, mottled extremities are late physical findings that
indicate impending circulatory collapse.

 The nurse should suspect pulmonary embolism as an underlying cause of syncope and cardiac
arrest with pulseless electrical activity.

 Vigilance during anticoagulation or administration of thrombolytic agents is warranted to

prevent significant bleeding complications. A decrease in hemoglobin level and hematocrit
may alert the nurse to occult bleeding in the retroperitoneum or gastrointestinal tract. If the
nurse encounters a change in mental status or new focal neurological deficits in a patient
receiving thrombolytics, intracranial hemorrhage must be eliminated as a possible cause.

 An emergent neurosurgical consultation and an unenhanced computed tomography scan of

the brain is warranted in this situation.

 Avoidance of unnecessary phlebotomy, arterial puncture, and other invasive procedures may
reduce the risk of hemorrhage during thrombolytic administration.

 Significant hemorrhage requires discontinuation of the thrombolytic agent and administration

of cryoprecipitate or fresh frozen plasma to reverse the coagulopathy. Decreasing platelet
counts during heparin administration may suggest a diagnosis of HIT.

26
Patient education

During recovery, the nurses were instrumental in preparing the patient for discharge. The nurses
should instruct the patient and the family on:-

 The importance of continued warfarin administration for 3 to 6 months to prevent further

thrombus development.
 Foods high in vitamin K, such as dark green vegetables and apricots, must be limited during
this time period to prevent decreased warfarin action.

 The nurses should inform the patient that a therapeutic INR value is between 2 and 3 and that
adjustments in the dosage of warfarin may be needed to maintain her INR in this range.

 The patient should be advised not to use warfarin with acetaminophen, non-steroidal anti-
inflammatory drugs, amiodarone, or fluoroquinolones antibiotics because such combinations
can quickly elevate the INR.

 The nurses should remind the patient to stretch every hour during confined travel and to
remain well hydrated because patients with history of deep venous thrombosis or pulmonary
embolism are at a greater risk for subsequent development of venous thrombosis.

 The nurses should encourage the patient to recount her history of deep venous thrombosis and
pulmonary embolism to future healthcare providers and to wear a Medic-Alert bracelet
indicating her history of pulmonary embolism.

References
1. National Institute for Health and Care Excellence (2012a) Venous Thromboembolic
Diseases: The Management of Venous Thromboembolic Diseases and the Role of
Thrombophilia Testing. guidance.nice.org.uk/CG144.
2. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein
Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific
Statement from the American Heart Association. Circulation.2011; 123:1788-1830.
3. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galie N, Pruszczyk P, Bengel F, Brady
A, Ferreira D, Janssens U, Klepetko W, Mayer E, Remy-Jardin M, Bassand J. Guidelines
on the diagnosis and management of acute pulmonary embolism. European heart journal,
2008; 29, 2276–2315.

27
4. Bonner L, Johnson J (2014) Deep vein thrombosis: diagnosis and treatment. Nursing
Standard. 28, 21, 51-58.
5. Kroegel C, Reissig A. Principle Mechanisms Underlying Venous Thromboembolism:
Epidemiology, Risk Factors, Pathophysiology and Pathogenesis, 2003;70:7–30
6. Haines S. Venous thromboembolism: pathophysiology and clinical presentation. American
Society of Health-System Pharmacists, 2003; 60(7), S3-S5.
7. Helman A, penciner R. The ABC of Emergency medicine. 11th ed. Toronto, 2008
8. http://en.wikipedia.org/wiki/Embolism accessed at December 2008
9. Makin A, silverman S. Peripheral vascular disease and Virchow triad for thrombogenesis.
QJ Med 2002; 95: 199-210.
10. The diagnosis of deep vein thrombosis in symptomatic outpatients and the potential for
clinical assessment and D-dimer assays to reduce the need for diagnostic imaging, British
Journal of Haematology, 2004; 124, 15–25
11. Wallis M, Autar R. Deep vein thrombosis: clinical nursing management clinical nursing
management. Nursing Standard. 2001 15, 18, 47-54.
12. Geerts W, Bergqvist D, Pineo G, Heit J, Prevention of Venous Thromboembolism. Chest
journal 2008; 133(6): 361- 453.
13. American College of Chest Physicians. Antithrombotic therapy and prevention of
thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice
guidelines. Chest. 2012;41(2 Suppl):e1S-194S.

28