A 52 year old, ASA grade I, female patient was posted for open reduction and internal fixation of a left olecranon fracture under GA. She also had a concomitant 2 week old inter-trochanteric fracture of left femur which was being immobilized by a Thomas splint since the time of injury.

After checking all routine investigations and adequate NPO status, patient was shifted to the OT table. Monitors attached and IV line was secured. Patient was induced with injection propofol 100mg and fentanyl 100 mcg and after achieving adequate muscle relaxation with vecuronium 5mg, Proseal LMA #3 was placed. After checking adequate placement and EtCO2, patient turned to right lateral position for surgery. After tourniquet application, surgery was started. 15 minutes into the surgery, patient developed systolic hypertension with a BP of 175/84 mmHg.  Injection propofol 30mg , 1 mg vecuronium was given but the next reading continued to be elevated 185/76 mmHg and after about a minute, the saturation started falling. Immediately 100% oxygen started using a Bain’s circuit and injection hydrocortisone 100mg was given. A few seconds later she developed tachycardia and HR increased from 102 to 145/min, with ST segment depression, BP dropped to 84/52mmHG, EtCO2 fell from 30 to 22 mmHg and saturation continued to fall. In view of these findings, a clinical suspicion of pulmonary thromboembolism was made.

In the lateral position itself, we replaced the Proseal LMA with a size 7 mm cuffed ETT and continued IPPV with 100% oxygen but the saturation continued to remain low 70-77%. EtCO2 fell further to 11 mmHg with persisting hypotension and tachycardia.

Surgeons were informed and surgery was stopped. Patient was made supine and ABG was taken and empirically unfractionated heparin 2500 units IV was given. Norepinephrine infusion started at 5mcg/min. After 3-5 minutes her saturation fell further to 50% followed by central cyanosis, bradycardia and cardiac arrest. Immediately CPR was started and injection adrenaline 1mg IV was given; after 2 cycles of cardiac massage, sinus rhythm returned followed by a marked and dramatic improvement in saturation to 100%.

The BP improved to 98/60 mmHg on Norepinephrine infusion and an increase in EtCO2 to 20 mm HG was also observed. ABG revealed a pH – 6.88, PaO2 – 112 mmHg, PaCO2 – 79.2 mmHg, HCO3 – 14 mmHg.

Bicarbonate correction was given in OT and the patient was shifted to ICU on ventilatory and vasopressor support. In ICU, all relevant investigations including D dimer and cardiac enzymes were sent. Patient was started on LMWH injection Clexane 40 mg subcutaneous BD.

The second ABG revealed a pH – 7.10, PaCO2 – 71 mmHg, PaO2 –88 mmHg and hence subsequent ventilator settings modified.  

Since we do not have a provision for Trans Oesophageal Echocardiography (TEE), hence a bedside ECHO was advised followed by a spiral CT of the chest once the patient was stable.

The D- dimer was 251 ng/ml, cardiac enzymes were raised (CPK-MB- 143 ng/ml) and her TLC was also high 20,000. The bedside 2D Echocardiography revealed LVEF- 60% and dilated right atrium and right ventricle although a poor echo window to comment on anything else. The patient regained consciousness after six hours of the event and had no neurological deficit. Serial blood gases improved and vasopressors were tapered off over the next 2 days and she was extubated. A spiral CT revealed bilateral pleural effusion and basal atelectasis, with normal pulmonary artery calibre (Figure 1). CT pulmonary angiography could not be done as she developed deranged kidney function in the post resuscitation phase with a creatinine of 2.5.

Figure 1: Spiral CT Scan of the patient.

On the 3rd day in ICU, she vomited and coughed out two large ascaris worms one from the mouth and one from the nose respectively (Figure 2). She was started on Tablet albendazole. Blood tests ESR, absolute eosinophil count (AEC) and stool test were sent.  The ESR was high – 40, AEC was raised 750 and the stool test was negative.

Figure 2: Ascaris that was vomited out.

Intraoperative pulmonary thromboembolism (PTE) is a relatively uncommon entity with a reported incidence of approximately 4.1% in gynaecological abdominal surgery for malignancy and 0.4% for non-abdominal surgeries (orthopaedic procedures) [1]. Pulmonary embolism occurs in approximately 0.3% to 1.6% of the surgical population [2]. Most often it goes undiagnosed as symptoms are non-specific and a high index of clinical suspicion is required especially in the presence of risk factors [4]. 

Massive PTE can cause sudden intra-operative cardiovascular collapse [3,4] causing death in 50% patients within 15 minutes and only 33% surviving over the next 2 hours [5]. PTE is a complication of underlying venous thrombosis in the deep venous system of the lower extremities and the pelvis. Micro thrombi are formed and lysed continuously but a larger thrombus may lodge at the bifurcation of the main pulmonary artery or lobar branches leading to hemodynamic compromise.

Hence it is of utmost importance to correlate the signs and symptoms with the associated risk factors and reach a clinical diagnosis as early as possible. Moreover, the intraoperative period itself poses a challenge mainly due to limitations in definitive diagnosis and therapeutic options [8]. The sensitivity of intraoperative TEE in identifying PTE as direct emboli is only 26% while left pulmonary artery emboli are located in just 17% of cases [7].

Since our patient was getting operated for an upper limb surgery in the lateral position it was the movement and positioning of the left fractured leg after the removal of the Thomas splint that possibly led to PTE. Additionally patient was immobilised for two weeks but DVT prophylaxis was omitted by the orthopaedics team in view of her low haemoglobin and platelet counts preoperatively.

In our patient, we made the diagnosis based on a high index of clinical suspicion. Our patient was bedridden since the past 2 weeks due to a long bone fracture. Initially after observing persistent desaturation  along with falling ETCO2 which occurred soon after the patient’s splint was removed and since it did not improve with our interventions (steroid, change of airway device, giving 100% oxygen and bronchodilator), a clinical diagnosis of PTE was made. This prompted us to administer unfractionated heparin empirically. A further decrease in EtCO₂, a widened EtCO2- PaCO2 difference (11 – 79.2 mmHg) and central cyanosis along with persistent tachycardia and hypotension further corroborated our diagnosis [5,6,8,11]. Effective and immediate CPR proved to be life saving for our patient. Since the heparin had been administered which may have softened the thrombus and the

External chest compression helped in its fragmentation [8]. These are usually soft clots which have travelled to the pulmonary circulation and the right ventricle from the deep venous system and in our case there was a dramatic improvement in saturation after the second cycle of cardiac massage.

In literature, cases of acute symptomatic PTE that were managed successfully using unfractionated heparin have been reported [9,10]. Unlike thrombolysis, uncontrolled haemorrhage is uncommon after heparin administration.

Massive pulmonary embolism is defined as PTE with either hemodynamic collapse or an occlusion of the pulmonary artery that exceeds 50% of its cross-sectional area [12]. Even in the modern era, operative deaths of patients with massive PTE who require CPR may approach 75% as compared to 12% for those who do not [13].

 The facility for an intraoperative TEE is not available at our hospital. It is of limited use intra-operatively as only indirect evidence (tricuspid regurgitation, RV dysfunction and leftward inter-atrial bowing) maybe supportive in making a diagnosis of PTE. Even though a bedside 2D echo had a poor window and a D dimer value came back negative, the intraoperative clinical evidence in support of PTE was strongly positive. Gibson et al recommend that a physician should ignore a normal D-dimer test when there is high clinical probability of thromboembolism [15]. As per the clinical predictability indicators scoring g; our patient had a score of 6 which indicates a high clinical probability of PTE [16] (Table 1).

Table 1: Patients with ≤ 4 points have low clinical probability of PTE and >4 points have a high probability of PTE.

The incidental appearance of ascaris in the patient’s GI and respiratory tract proves to be additional and extremely rare risk factor for causing PTE as has been reported in literature by Stermer et al [14].  In our country, where ascaris infection is very common, it is advisable to keep this dreaded complication in mind.

To conclude, we would like to emphasize that the key to a successful outcome in this extremely lethal condition is the importance of recognizing the clinical evidence available to us intra-operatively that is per se the patient itself. Even in the absence of definitive investigative procedures like TEE and CT pulmonary angiography, we were able to make a clinical diagnosis of PTE and in the light of reported evidence empirically administer therapy with unfractionated heparin intra-operatively and provide an effective CPR which revived our patient. Lastly, a high index of clinical suspicion, good team work and role allocation as in our case, proved fruitful in this difficult situation.

1. Martino Ma, Borges E, Williamson E, Siegfried S et al. Pulmonary embolism after major abdominal surgery in gynaecological oncology. Obs Gyn. 2006; 107: 666-671.
2. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet. 1999; 353: 1386-1389.
3. Laxenaire MC, Moneret-Vautrin DA, Vervolet D. The French experience of anaphylactoid reactions. Int Anesthesiol Clin. 1985; 23:145-160.
4. Dohring DJ, Arens JF. Pulmonary thromboembolism: disease recognition and patient management. Anesthesiology. 1990; 73: 146-164.
5. Lewis K, Windokun A, Arciaga P, Arfai K, Soni M. Intraoperative pulmonary embolism presenting as a widened PACO2-ETCO2 gradient. Chest. 2006;130: 295S
6. Pharo GH, Andonakakis A, Chandrasekaren K, Amron G, Levitt JD. Survival from Catastrophic Intraoperative Pulmonary Embolism. Anesth Analg. 1995; 81:188-190.
7. Pruszczyk P, Torbicki A, Pacho R, Chlebus M, Kuch Wocial A. Non-invasive diagnosis of suspected severe pulmonary embolism: TEE versus spiral CT. Chest. 1997; 112: 722-728.
8. Ekaterini NA, Georgia GT, Nektarios AK, Panagiota GM. Unexpected complication of massive intraoperative pulmonary embolism following elective sigmoidectomy in the supine position. J Anesth. 2008; 22: 177-181.
9. Buller HR, Davidson BL, Decousus H, Gallus A. Subcutaneous fondaparinaux versus intravenous unfractionated heparin in the intial treatment of pulmonary embolism. N Eng J Med. 2003; 349: 1695-1702.
10. Quinlan DJ, Mc Quillan A, Eikelboom JW. LMWH compared with intravenous unfractionated heparin for treatment of pulmonary embolism: a meta-analysis of randomized, controlled trials. Ann Intern Med. 2004; 140: 175-183.
11. Desciak CM, Martin DE. Perioperative pulmonary embolism: diagnosis and anesthetic management. J Cli Anes. 2011; 23: 153-165.
12. Dalen JE, Dexter L. Diagnosis and management of massive pulmonary embolism. Dis Mon. 1967; 1-34.
13. Dauphine C, Omari B. Pulmonary embolectomy for acute massive pulmonary embolism. Ann Thorac Surg. 2004; 77: 819-823.
14. Stermer E, Bassan H, Oliven A, Grishkan A, Boss Y . Massive thrombosis as a result of triple infestation of the pulmonary arterial circulation by Ascaris, Candida, and Mucor. Hum Pathol. 1984; 15: 996-998.
15. Konstantinides S. Clinical Practise. Acute Pulmonary embolism. N Eng J Med. 2008; 359: 2804-2813.
16. Gibson NS. The importance of clinical probability assessment in interpreting a normal D-dimer in patients with suspected PTE. Chest. 2008; 134: 789-793.
17. Wells PS, Anderson DR, Rodger M et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism; increasing the models utility with simpliRED D -dimer. Thrombo Haemost. 2000; 83: 418.