Acute Pulmonary Embolism has a high rate of mortality (26%) due to blockade of the pulmonary artery leading to acute increase in right ventricular pressure causing sudden cardiac decompensation. Lack of specific tests for early diagnosis is one of the causes for high rate of mortality but timely diagnosis and active intervention can save the life of the patient.
2. Case Report
Successful management of massive intra-operative
pulmonary embolism
Arindam Ghosh a,
*, Uzma Khan b
, Naresh Anand c,
**
a
Senior Consultant and Head, Department of Gastrosurgery, SPS Apollo Hospital, Ludhiana, India
b
Professor, Department of Physiology, Christian Medical College and Hospital, Ludhiana, India
c
Consultant Anaesthesiologist, Department of Anaesthesia, SPS Apollo Hospital, Ludhiana, India
a r t i c l e i n f o
Article history:
Received 3 October 2013
Accepted 12 November 2013
Available online 7 December 2013
Keywords:
Massive Acute Embolism
Pulmonary artery
Cardiac decompensation
a b s t r a c t
Acute Pulmonary Embolism has a high rate of mortality (26%) due to blockade of the
pulmonary artery leading to acute increase in right ventricular pressure causing sudden
cardiac decompensation. Lack of specific tests for early diagnosis is one of the causes for
high rate of mortality but timely diagnosis and active intervention can save the life of the
patient.
Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
1. Introduction
Acute Pulmonary Embolism is a common and fatal condition.
It occurs due to blockage of the pulmonary artery leading to
decrease in the systemic perfusion and death in less than one
hour. The commonest cause is deep vein thrombosis or the
iliac vein thrombosis.
2. Case report
43 year old female patient admitted in our hospital with the
diagnosis of Ulcerative Colitis since 17 years. She was on
treatment with Tab prednisolone 30 mg and Tab Azathio-
prine 12.5 mg daily. She was not responding to medical line
of treatment satisfactorily and hence advised total procto-
colectomy with Ileal Pouch Anal Anastomosis (IPAA) with
diverting ileostomy. Pre-operative assessment revealed
nothing except long standing history of steroid intake. Her
vital signs and systemic examination was within normal
limits. Investigations revealed Hb ¼ 8.1 gm%, Hct ¼ 24.3%,
TLC ¼ 10,700 /cmm, platelets count ¼ 3.73 L/cmm, PT
(INR) ¼ 1.4, BU ¼ 37 mg/dl, S.creat. ¼ 0.63 mg/dl, Na/K ¼ 139/
4.7 meq/l, RBS ¼ 90 mg/dl, BT ¼ 2 min 40 s, CT ¼ 5 min 50 s,
Bil ¼ 0.1, SGOT/SGPT ¼ 28/22, Prot. ¼ 6.1, Alb. ¼ 2.9. ECG and
Chest X-ray ¼ Normal. Three units of Packed Red Blood Cells
(pRBCs) and 4 units of Fresh Frozen Plasma (FFP) arranged for
* Corresponding author. Tel.: þ91 (0)9814117997.
** Corresponding author. Tel.: þ91 (0)9814802683.
E-mail addresses: arindam.absolute@yahoo.com (A. Ghosh), nareshanand21@gmail.com, drnareshalu@yahoo.co.in (N. Anand).
Available online at www.sciencedirect.com
ScienceDirect
journal homepage: www.elsevier.com/locate/apme
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 3 0 6 e3 0 9
0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.apme.2013.11.004
3. surgery. The vital parameters on Operation Theater table
recorded. Pulse rate ¼ 100/mins, Blood Pressure ¼ 130/
90 mmhg, Respiratory Rate ¼ 14/mins, Temperature ¼ 98.6*F,
SpO2 ¼ 99%. Apart from this patient monitored with
Electrocardiogram (ECG), End tidal carbon-dioxide (EtCo2).
Lumber Epidural catheter inserted at L2-L3 level for post-
operative analgesia. After General Anesthesia Urine output,
Central Venous Pressure, Arterial Pressure, Core tempera-
ture, Airway pressure, respiratory gases and minute venti-
lation too recorded during surgery. After few minutes of
starting surgery a gradual fall in SpO2 noticed while rest of
the parameters were normal. EtCo2 decreased from 26 to
22 mmhg. There was no improvement in oxygen saturation
with all the possible corrective measures like changing the
position of probe, change of monitor etc. ABG showed
pH ¼ 7.2, pCO2 ¼ 57.9, PaO2 ¼ 44.1, HCO3 ¼ 21, O2% ¼ 63.3%,
Hb ¼ 6.9. Possibility of pulmonary embolism suspected and
surgery stopped immediately. Abdomen closed en-masse
and patient shifted to CT scan. CT chest with contrast
showed bilateral massive pulmonary embolism with multi-
ple thrombi in Inferior Vena Cava (IVC) and iliac vessels.
Embolectomy decided and patient shifted to cardiac cath lab.
After embolectomy an IVC filter put to prevent the further
emboli. 10000 IU of heparin given during embolectomy. Pa-
tient shifted to operation theater for completion of surgery.
Oxygen saturation improved to 100%. Total colectomy with
ileostomy and Hartmann closure of rectal stump done and
abdomen closed in layers. Patient shifted to intensive care
unit for the post-operative care. Anticoagulation started in
post-operative period with heparin 1000 units/h with APTT
monitoring every six hourly. Patient extubated once fully
recovered from anesthesia and discharged on 7th post-
operative day.
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 3 0 6 e3 0 9 307
4. 3. Discussion
Pulmonary embolism is one of the unnoticed causes of
morbidity and mortality. It has been seen that 15% of all
sudden deaths are due to PE. Only 6e9 cases of DVT and Pul-
monary embolism reported from India in 2010e2011.1
In a
conscious patient it presents with sudden-onset of breath-
lessness, tachycardia, chest pain, cough and hemoptysis.
More severe cases can present with cyanosis, collapse and
hemodynamic instability. Systemic examination can present
with pleuritic rub, loud P2 or raised JVP but most of the time it
is normal. Under Anaesthesia, it presents with sudden
decrease in oxygen saturation and EtCo2 followed by ar-
rhythmias, hypotension or cardiac arrest.2
Contrast to this our
patient had a gradual fall in oxygen saturation which was
refractory to treatment and non-significant decrease in EtCo2
(26e22 mmhg). Rest of the parameters remained normal.
Mismatch in the ventilation and perfusion is the reason for
hypoxemia and as reported by Itti E and Nguyen S shunting of
the venous blood from lungs, heart or both is the cause of
hypoxemia or refractory hypoxemia. They also mentioned
that a complete obstruction of the pulmonary arteries can
cause sudden hypoxemia and fall in EtCo2 but an incomplete
obstruction causes early hypoxemia followed by decrease in
EtCo2 or raised pCO2.3
This supports our finding that our pa-
tient had only hypoxemia as the first sign and he may have
developed hypercarbia, arrhythmias, hypotension, shock or
cardiac arrest if the diagnosis of suspicion would have been
delayed. Vandenbroucke and his colleagues suggested multi-
ple risk factors for developing PE like major surgery, steroids
intake, trauma, smoking, cancer, pregnancy or hormone
replacement therapy and Wells score also included the clin-
ical suspicion and tachycardia (HR ¼ 100/min) as the probable
predictors for DVT and PE.4
Based on these reports a strong possibility of pulmonary
embolism suspected.
Wells score is the most accepted predictor for developing
DVT and pulmonary embolism and it includes
clinically suspected DVT e 3.0 points
alternative diagnosis is less likely than PE e 3.0 points
tachycardia (heart rate > 100) e 1.5 points
immobilization (3 d)/surgery in previous four weeks e 1.5
points
history of DVT or PE e 1.5 points
hemoptysis e 1.0 points
malignancy (with treatment within 6 months) or palliative
e 1.0 points.
Interpretation
Score 6.0 e High (probability 59% based on pooled data)
Score 2.0e6.0 e Moderate (probability 29% based on pooled
data)
Score 2.0 e Low (probability 15% based on pooled data).
Our patient had h/o of steroids intake and she was un-
dergoing major surgery but she was mobile and did not have
any history suggestive of DVT. This made us to overlook for
giving DVT prophylaxis pre-operatively. Schaefer-Prokop C
and Prokop M reported that Chest X-ray, Echocardiogram or
estimation of D-Dimer can be done to establish the diagnosis
but CT- pulmonary angiogram is the gold standard for the
earliest detection and confirmation of PE.5
To confirm the
diagnosis we did Pulmonary angiogram that showed of bilat-
eral pulmonary emboli with multiple thrombi in IVC and iliac
vessels. Augustinos P and Ouriel K published a paper in 2004
where they concluded that an early invasive approach to treat
venous thromboembolism has better outcome than the non-
invasive approach and this supports our decision to go for
Embolectomy for immediate relief of the symptoms and pre-
ventions of hemodynamic instability.6
Post-embolectomy
oxygen saturation improved to 100%. IVC filters are placed to
prevent the further showers of emboli from distal veins into
the pulmonary circulation7
as suggested by Decousus H and
Leizorovicz A and we placed an IVC filter for the same purpose
and more so the pulmonary angiogram showed multiple
thrombi in IVC and iliac vessels. Jirong Y, Liu G et al reported
that thrombolytic drugs and anticoagulants are used to treat
and prevent the thromboembolism and we also started our
patient on heparin infusion for few days. Once patient stabi-
lized treatment shifted to LMWH and then to oral anticoagu-
lants before discharging patient.8
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 3 0 6 e3 0 9308
5. 4. Conclusion
To conclude an early diagnosis and aggressive management
can save the life of such patients and all patients scheduled for
major surgery should receive DVT prophylaxis even in the
absence of any signs and symptoms of DVT.
Conflicts of interest
All authors have none to declare.
r e f e r e n c e s
1. Goldhaber SZ, Visan L. Acute pulmonary embolism: clinical
outcome in International Cooperative Pulmonary Embolism
Registry (ICOPER). Lancet. 1999;353:1386e1389.
2. Wells PS, Anderson DR, Rodger M. Excluding pulmonary
embolism at the bedside without diagnostic imaging:
management of patients with suspected pulmonary embolism
presenting to the emergency department by using a simple
clinical model and d-dimer. Ann Intern Med. 2001;135(2):98e107.
3. Itti E, Nguyen S, Robin F, et al. Distribution of ventilation/
perfusion in pulmonary embolism: an adjunct to the
interpretation of ventilation/perfusion lung scan. J Nucl Med.
2002;43:1596e1602.
4. Schaefer-Prokop C, Prokop M. MDCT for the diagnosis of acute
pulmonary embolism. Eur Radiol. 2005;15(Suppl 4):D37eD41.
5. Vandenbroucke JP, Rosing J, et al. Oral contraceptives and risks
of venous thrombosis. N Engl J Med. 2001;344:1527e1535.
6. Augustinos P, Ouriel K. Invasive approaches to treatment of
venous thromboembolism. Circulation. 2004;110(9 Suppl 1):I27eI34.
7. Decousus H, Leizorovicz A, Parent F. A clinical trial of vena
caval filters in the prevention of pulmonary embolism in
patients with proximal deep-vein thrombosis. N Engl J Med.
1998;338(7):409e415.
8. Jirong Y, Liu G, Wang Q, et al. Thrombolytic therapy for
pulmonary embolism. Cochrane Database Syst Rev. In: Dong Bi
Rong, ed. 2006; 2.
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 3 0 6 e3 0 9 309