© Acta Anæsthesiologica Belgica, 2009, 60, n° 4
Abstract : We report the case of a 41 year-old man
admitted for lower limb and liver trauma following a car
accident. Surgical repair of a tibial fracture was per-
formed under general anesthesia 5 days after admission
while the liver injury was managed conservatively. At the
time of tourniquet inflation, the patient presented a pul-
monary embolism. Low-molecular-weight heparin
administration had been delayed for 72 hours after
admission due to the liver injury. Risk factors for bleed-
ing and thromboembolism in trauma patients with liver
injury are discussed.
Key words : Pulmonary embolism ; thromboprophylax-
is ; lower limb fracture ; liver trauma and low-molecular-
A 41 year-old man was admitted to the emer-
gency department following a car accident. He had
no significant previous medical history. Upon
admission, the patient was conscious and had no
neurological deficit. He complained of pain at the
left leg. The blood pressure was 145/80 mmHg and
the pulse 107 beats per minute. The skin was cold
but well colored. The rest of the physical examina-
tion revealed a painful deformation of the left leg.
Initial evaluation included blood tests, total
body computed tomography (CT) and left lower
limb X-ray. Blood tests showed a hemoglobin level
at 15.5 gr. per dl, a platelet count at 304,000 per
mm-3, liver cytolysis and coagulation in the normal
range. The total body CT-scan revealed fractures of
the posterior arches of 4th, 5thand 6thleft ribs asso -
ciated with a small pleural effusion. At the abdomi-
nal level, a liver contusion encompassing segments
II, III and IV and a subcapsular hematoma were
observed. A small capsular breach on the lateral
edge of the liver resulted in a small peritoneal
effusion (Fig. 1). This is a grade III liver injury
according to the American Association for Surgery
of Trauma. Indeed, although the subcapsular
hematoma is smaller than 50 percent of the liver
surface the laceration of the parenchyma is deeper
than 3 centimetres (1). Radiographs of the left
lower limb showed a complex fracture of the exter-
nal tibial plateau as well as a non-displaced fracture
of the head of the fibula.
The liver contusion was managed conserva-
tively. The tibial fracture was immobilized and the
patient was admitted to the ICU for close monitor-
ing. After discussion with the surgeon, it was
decided to postpone the administration of low-
molecular-weight heparin. The patient remained
stable clinically and was transferred to the orthope-
dic surgery ward the day after admission. A control
abdominal CT-scan performed 72 hours after
admission disclosed stability of the liver contusion.
Subcutaneous enoxaparin (Clexane®, 40 mg/day)
was initiated for venous thromboprophylaxis.
Five days after the accident, the patient under-
went reduction and osteosynthesis of the articular
tibial fracture. The induction of general anesthesia
was uneventful. At the time of tourniquet inflation,
a sudden decrease in end-tidal CO2 (from 32 to
25 mmHg) was observed. Simultaneously the spO2
(Acta Anaesth. Belg., 2009, 60, 259-262)
Pulmonary embolism in a trauma patient with liver and orthopedic
C. LEGRAIN (*), G. A. HANS (*), A. DEFRESNE (*), C. HONORE (**), M. LEWIN (***), W. KURTH (****)
and J.-F. BRICHANT (*****)
C. LEGRAIN, M.D. ; G. A. HANS, M.D., Ph.D. ; A. DEFRESNE,
M.D. ; C. HONORE, M.D. ; M. LEWIN, M.D. ; W. KURTH ;
M.D., J.-F. BRICHANT, M.D., Ph.D.
(*) Resident, Department of Anesthesia and Intensive Care
Medicine, CHU of Liège, University of Liège, Liège,
(**) Resident, Department of Abdominal Surgery and
Transplantation, CHU of Liège, University of Liège, Liège,
Belgium (***) Staff radiologist, Department of Medical
Imagery, CHU of Liège, University of Liège, Liège,
(****) Staff surgeon, Department of Orthopedic Surgery and
Traumatology, CHU of Liège, University of Liège, Liège,
(*****) Professor and chair, Department of Anesthesia and
Intensive Care Medicine, CHU of Liège, University of
Liège, Liège, Belgium.
Correspondence address : Dr. Grégory Hans, Department of
Anesthesia and Intensive Care Medicine, CHU of Liège,
University of Liège, Avenue de l’hôpital Bat. B35,
4000 Liège, Belgium. Tel. :
+3243667636. E-mail : G.Hans@chu.ulg.ac.be
+3243667179. Fax :
© Acta Anæsthesiologica Belgica, 2009, 60, n° 4
C. LEGRAIN et al.
dropped from 99% to 92%. The hemodynamic
parameters remained stable. Airway pressure and
electrocardiogram did not change. A pulmonary
embolism (PE) was suspected. The inspired oxygen
fraction was increased to 0.8. This resulted in an
improvement of the spO2. It was decided to pro-
ceed with the osteosynthesis. No problem occurred
during the surgery and the patient was extubated in
the operating room at the end of the surgical proce-
dure. He was transferred to the postanesthesia care
unit (PACU). He was well but remained dependent
on supplemental oxygen to maintain an spO2above
90%. A computed tomography pulmonary
angiogram performed soon after the end of surgery
confirmed the diagnosis of PE (Fig. 2).
An intravenous infusion of heparin was initiat-
ed at the PACU. Clinical evolution was favorable.
After 48 hours, intravenous heparin was replaced
by a subcutaneous injection of 1 mg•kg-1of
enoxaparin (Clexane®) twice daily and the patient
was transferred to the orthopedic ward. He was
discharged from the hospital one week later without
Conservative management is currently recom-
mended for hemodynamically stable patients with
blunt liver trauma (2, 3). The more frequent compli-
cations after conservative treatment of liver injuries
are bleeding, abdominal compartment syndrome,
biliary problems and infections (4). Bleeding and
abdominal compartment syndrome tend to occur
within the first 72 hours while infectious and biliary
complications usually arise later (4). Therefore we
decided to delay the administration of low-molecu-
lar-weight heparin for venous thromboprophylaxis
until a control abdominal CT-scan was performed
72 hours later. There is however no recommenda-
tion in the literature to guide the administration of
thromboprophylaxis in similar situations. A study
from GEERTS et al. concluded that heparin thrombo-
prophylaxis is safe in trauma patients with an
injury severity score above 9 and no intra cranial
hemorrhage or coagulopathy (5). However, more
than 80 percent of the patients included in their
study were initially managed surgically and heparin
was introduced after surgical control of the
bleeding . The results of this study can therefore not
be extrapolated to our patient.
Because of the tibial fracture, our patient was
at high risk for venous thromboembolic complica-
tions (6). Moreover, fixation of the tibial plateau
was postponed due to the important soft-tissue
swelling and the need for specific osteosynthesis
material. This delay was an additional risk factor
for venous thrombosis (7). The patient and his
family were informed of the necessity to balance
the risk of venous thrombosis and the risk of
bleeding regarding low-molecular-weight heparin
Mechanical methods for venous thrombopro-
phylaxis are highly recommended (Grade 1A) for
Fig. 1. — Abdominal CT-scan performed at admission. Arrows
indicate a liver laceration encompassing segments II, III and IV
and appearing as a hypodense area at the portal phase after
intravenous contrast injection.
Fig. 2. — Thoracic CT-scan performed postoperatively. Arrow
indicates a voluminous thrombus in the right pulmonary artery.
© Acta Anæsthesiologica Belgica, 2009, 60, n° 4
patients at high risk for bleeding (8). In our patient,
a graduated compression stocking was used on the
non-injured leg only. Pain and edema precluded its
use on the fractured side.
The tibial fixation was performed five days
after the trauma. Before his transfer to the operating
room, the patient had no complaint or clinical sign
suggesting venous thrombosis. However, in the
setting of lower limb fracture, up to 80 percent of
venous thrombosis detectable by venography or
ultrasound are asymptomatic (9).
Intraoperative signs of pulmonary embolism
have been reviewed previously (10). They include
sudden hypoxemia, systemic hypotension and
decreased end-tidal CO2. Associated increased
central venous pressure and pulmonary arterial
pressure with normal pulmonary capillary wedge
pressure can also be observed when appropriate
monitoring is available. Risk factors for intraopera-
tive pulmonary embolism include older age, obesi-
ty, leg manipulation and previous immobilization.
Application of Esmarch bandages as well as tourni-
quet inflation have been reported to be potential
triggering events (11-13). In our case, no Esmarch
bandage was used for lower limb exsanguination
but clinical signs of pulmonary embolism strictly
coincided with the inflation of the tourniquet. A
pulmonary embolism was readily suspected. An
intraoperative transesophageal echocardiography
could have been performed to confirm the diagno-
sis. It has a poor sensitivity for direct visualization
of thromboemboli but discloses signs of right ven-
tricle dysfunction in 96% of cases (14).
The diagnosis of pulmonary embolism was
confirmed in the immediate postoperative period.
Patients with pulmonary embolism who are hemo-
dynamically stable require no other treatment than
anticoagulation. Although low-molecular-weight
heparin is currently the first line therapy, we used
intravenous unfractionated heparin due to the risk
of bleeding associated with recent surgery (15).
Clinical evolution was favourable. Intravenous
heparin was replaced by low molecular heparin
after 48 hours and by acenocoumarol three weeks
This report illustrates the difficulty to balance
hemorrhagic and thromboembolic risks in trauma
patients with multiples injuries. Patients whose
bleeding lesions are controlled surgically are
probably at lower risk of hemorrhage. Therefore
low-molecular-weight heparin could be recom-
mended to prevent venous thrombosis in such
cases (5). No evidence-based data currently exist
for the increasing number of patients who are man-
aged conservatively. Moreover, it is unlikely that
such data will be available shortly due to the great
heterogeneity of this population. Therefore the
prescription of thromboprophylaxis should be dis-
cussed on an individual basis by a multidisciplinary
team, taking into account risk factors for bleeding
and thrombosis, respectively (table I and II). Each
time it is possible, informing the patient or his
family is suitable.
1. Yoon W., Jeong Y., Kim J., Seo J., Lim H., Shin S., Kim J.,
Jeong S., Park J., Kang H., CT in blunt liver trauma,
RADIOGRAPHICS, 25, 87-104, 2005.
2. Schroeppel T., Croce M., Diagnosis and management of
blunt abdominal solid organ injury, CURR. OPIN. CRIT.
CARE, 13, 399-404, 2007.
3. Croce M., Fabian T., Menke P., Waddle-Smith L.,
Minard G., Kudsk K., Patton J. J., Schurr M., Pritchard F.,
Nonoperative management of blunt hepatic trauma is the
treatment of choice for hemodynamically stable patients.
Results of a prospective trial, ANN. SURG., 221, 744-53 ;
discussion 753-5, 1995.
4. Kozar R., Moore F., Cothren C., Moore E., Sena M.,
Bulger E., Miller C., Eastridge B., Acheson E.,
Brundage S., Tataria M., McCarthy M., Holcomb J., Risk
PULMONARY EMBOLISM IN A TRAUMA PATIENT
Risk factors for thromboembolism after trauma
Risk factorOdds ratio
Age ? 40 years
Lower limb fracture
Spinal cord injury with paralysis
Mechanical ventilation > 3 days
Shock on admission
Major surgical procedure
P<0.0001 for all factors, univariate analysis (knudson).
Risk factors for hepatic related morbidity in patient with con-
servative treatment of blunt hepatic injuries
Risk factorOdds ratio
Injury grade 4 (AAST*)
Injury grade 5 (AAST)
Red blood cell transfusion required
Fresh frozen plasma required
Platelets transfusion required
P < 0.05 for all fractors, univariate analysis (kozar).
* American Association for the Surgery of Trauma.
© Acta Anæsthesiologica Belgica, 2009, 60, n° 4 Download full-text
C. LEGRAIN et al.
factors for hepatic morbidity following nonoperative
management : multicenter study, ARCH. SURG., 141, 451-8 ;
discussion 458-9, 2006.
5. Geerts W., Jay R., Code K., Chen E., Szalai J., Saibil E.,
Hamilton P., A comparison of low-dose heparin with low-
molecular-weight heparin as prophylaxis against venous
thromboembolism after major trauma, N. ENGL. J. MED.,
335, 701-7, 1996.
6. Knudson M., Ikossi D., Khaw L., Morabito D.,
Speetzen L., Thromboembolism after trauma : an analysis
of 1602 episodes from the American College of Surgeons
National Trauma Data Bank, ANN. SURG., 240, 490-6 ;
discussion 496-8, 2004.
7. Abelseth G., Buckley R., Pineo G., Hull R., Rose M.,
Incidence of deep-vein thrombosis in patients with frac-
tures of the lower extremity distal to the hip, J. ORTHOP.
TRAUMA, 10, 230-5, 1996.
8. Geerts W., Bergqvist D., Pineo G., Heit J., Samama C.,
Lassen M., Colwell C., Prevention of venous thrombo -
embolism : American College of Chest Physicians
Evidence-Based Clinical Practice Guidelines (8th Ed.),
CHEST, 133, 381S-453S, 2008.
9. Samama C. M., Albaladejo P., Benhamou D., Bertin-
Maghit M., Bruder N., Doublet J. D., Laversin S.,
Leclerc S., Marret E., Mismetti P., Samain E., Steib A.,
Venous thromboembolism prevention in surgery and obstet-
rics : clinical practice guidelines, EUR. J. ANAESTHESIOL.,
23, 95-116, 2006.
10. Dehring D., Arens J., Pulmonary thromboembolism :
disease recognition and patient management, ANESTHE -
SIOLOGY, 73, 146-64, 1990.
11. Araki S., Uchiyama M., Fatal pulmonary embolism follow-
ing tourniquet inflation. A case report, ACTA ORTHOP.
SCAND., 62, 488, 1991.
12. Lu C., Chen Y., Wang M., Massive pulmonary embolism
after application of an Esmarch bandage, ANESTH. ANALG.,
98, 1187-9, table of contents, 2004.
13. Darmanis S., Papanikolaou A., Pavlakis D., Fatal intra-
operative pulmonary embolism following application of an
Esmarch bandage, INJURY, 33, 761-4, 2002.
14. Rosenberger P., Shernan S., Body S., Eltzschig H., Utility
of intraoperative transesophageal echocardiography for
diagnosis of pulmonary embolism, ANESTH. ANALG., 99, 12-
15. Houman Fekrazad M., Lopes R., Stashenko G.,
Alexander J., Garcia D., Treatment of venous thrombo -
embolism : guidelines translated for the clinician, J.
THROMB. THROMBOLYSIS, 2009.