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Successful management of massive intra-operative pulmonary embolism
 

Successful management of massive intra-operative pulmonary embolism

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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 ...

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.

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    Successful management of massive intra-operative pulmonary embolism Successful management of massive intra-operative pulmonary embolism Document Transcript

    • Successful management of massive intra-operative pulmonary embolism
    • 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
    • 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
    • 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
    • 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
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