Successful management of massive intra-operative pulmonary embolism

Successful management of massive intra-operative pulmonary embolism

Case Report

Successful management of massive intra-operativepulmonary embolism

Arindam Ghosh a,*, Uzma Khan b, Naresh Anand c,**aSenior Consultant and Head, Department of Gastrosurgery, SPS Apollo Hospital, Ludhiana, Indiab Professor, Department of Physiology, Christian Medical College and Hospital, Ludhiana, IndiacConsultant 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: [email protected] (A. Ghosh), [email protected], [email protected] (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 6e3 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

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 6e3 0 9 307

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 eModerate (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 andwe 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 6e3 0 9308

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: clinicaloutcome in International Cooperative Pulmonary EmbolismRegistry (ICOPER). Lancet. 1999;353:1386e1389.

2. Wells PS, Anderson DR, Rodger M. Excluding pulmonaryembolism at the bedside without diagnostic imaging:management of patients with suspected pulmonary embolismpresenting to the emergency department by using a simpleclinical 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 theinterpretation of ventilation/perfusion lung scan. J Nucl Med.2002;43:1596e1602.

4. Schaefer-Prokop C, Prokop M. MDCT for the diagnosis of acutepulmonary embolism. Eur Radiol. 2005;15(Suppl 4):D37eD41.

5. Vandenbroucke JP, Rosing J, et al. Oral contraceptives and risksof venous thrombosis. N Engl J Med. 2001;344:1527e1535.

6. Augustinos P, Ouriel K. Invasive approaches to treatment ofvenous thromboembolism.Circulation. 2004;110(9Suppl1):I27eI34.

7. Decousus H, Leizorovicz A, Parent F. A clinical trial of venacaval filters in the prevention of pulmonary embolism inpatients with proximal deep-vein thrombosis. N Engl J Med.1998;338(7):409e415.

8. Jirong Y, Liu G, Wang Q, et al. Thrombolytic therapy forpulmonary embolism. Cochrane Database Syst Rev. In: Dong BiRong, 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 6e3 0 9 309

Apollo hospitals: http://www.apollohospitals.com/Twitter: https://twitter.com/HospitalsApolloYoutube: http://www.youtube.com/apollohospitalsindiaFacebook: http://www.facebook.com/TheApolloHospitalsSlideshare: http://www.slideshare.net/Apollo_HospitalsLinkedin: http://www.linkedin.com/company/apollo-hospitalsBlog:Blog: http://www.letstalkhealth.in/