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Successful treatment of peripartum massive pulmonary embolism with extracorporeal membrane oxygenation and catheter-directed pulmonary thrombolytic therapy.

Pregnancy is associated with an increase in cardiac output and oxygen consumption, and concurrent reduction in functional residual capacity. Premorbid or intercurrent cardiac or respiratory disease associated with pregnancy can lead to cardiorespiratory decompensation, with subsequent maternal and neonatal morbidity or mortality (1). Chronic thromboembolic pulmonary hypertension during pregnancy is uncommon but is associated with maternal mortality in excess of 35% (2-4). We describe a case of decompensated thromboembolic pulmonary hypertension requiring emergency caesarean section and postpartum treatment with extracorporeal membrane oxygenation (ECMO) and pulmonary thrombolytic therapy. The use of ECMO, catheter-directed pulmonary thrombolytic therapy and other pulmonary vasodilators for management of this life-threatening disease is discussed.

CASE HISTORY

A 27-year-old, gravida 4 para 3 woman developed acute decompensated right heart failure at 31 weeks gestation, secondary to an acute pulmonary embolus. Her previous pregnancy had been complicated by extensive bibasal pulmonary emboli, confirmed by computed tomography pulmonary angiography (CTPA) four weeks after delivery. The patient had a negative thrombophilia screen and received six months of warfarin therapy. On this occasion she presented to a peripheral hospital with a four-day history of severe pleuritic chest pain, dyspnoea and palpitations. She was then transferred to our tertiary centre, which has access to specialist intensive care, obstetric, anaesthetic, interventional radiology and cardiothoracic services. Her medications included enoxaparin 40 mg subcutaneously daily, which had been commenced in the second trimester of the current pregnancy, for prophylaxis against pulmonary embolus.

On arrival, her arterial oxygen saturation (Sp[O.sub.2]) was 94% on oxygen 10 l/minute delivered via a Hudson mask. Her heart rate was 150 /minute (sinus rhythm), systemic blood pressure 102/60 mmHg, respiratory rate 30 /minute and the jugular venous pulse was visible at 6 cm. An arterial blood gas showed oxygen tension ([P.sub.a][O.sub.2]) of 74 mmHg, carbon dioxide tension ([P.sub.a]C[O.sub.2]) 29 mmHg and serum lactate 5.0 mmol/l. Cardiac troponin was normal. Precordial examination revealed a loud pulmonary component of the second heart sound and a pansystolic murmur over the tricuspid valve. There was reduced air entry to auscultation bibasally, but no added breath sounds. An electrocardiograph showed sinus tachycardia, right axis deviation, P-pulmonale and a [S.sub.I][Q.sub.III][T.sub.III] pattern. The clinical presentation alone virtually established a diagnosis of acute severe pulmonary embolus, but because of her history of thromboembolic disease, we wanted to clarify the extent and anatomical location of both new clot and old clot, assess for right ventricular dysfunction, the presence of chronic cor pulmonale and global cardiac performance. A ventilation/perfusion scan demonstrated bilateral lower lobe pulmonary emboli and a CTPA showed an acute massive pulmonary embolus at the first order branches of the left pulmonary artery (Figure 1), with smaller embolus at the first order branch of the right pulmonary artery. Transthoracic echocardiography demonstrated severe right heart failure with a markedly dilated right ventricle, moderate tricuspid regurgitation and right ventricular systolic pressure of 66 mmHg. The inferior vena cava was dilated without collapse on inspiration and the central venous pressure was 18 mmHg. The estimated pulmonary artery systolic pressure was 84 mmHg. Doppler ultrasonography of the lower limbs demonstrated partial occlusion of the left femoral and right popliteal veins, with only slow flow around the obstruction on each side. For the safety of both mother and baby, a joint team consisting of obstetricians, critical care specialists, anaesthetists and cardiothoracic surgeons reached the decision to proceed to urgent caesarean section, with support by ECMO if required.

[FIGURE 1 OMITTED]

Prior to induction of anaesthesia two 14 gauge peripheral cannulae were inserted. After careful consideration, invasive haemodynamic monitoring was confined to arterial and central venous pressure lines. A pulmonary arterial catheter was not inserted due to concerns of dislodging thrombus at the first order branches of the right and left pulmonary arteries. For general anaesthesia, a rapid sequence induction was achieved using propofol (1 mg/kg) fentanyl (3 [micro]g/kg) and suxamethonium (1.5 mg/kg), and the trachea was intubated with a size 7.0 tracheal tube. Anaesthesia was maintained with 1 to 1.2 minimum alveolar concentration levels of sevoflurane in an oxygen (80%) and air (20%) mixture. Intraoperative transoesophageal echocardiography showed a massively dilated right ventricle with poor right ventricular free wall function. There was significant septal interventricular shift to the left, decreasing left ventricular enddiastolic volume (Figure 2). Aims of supportive therapy were to optimise pulmonary circulation by reducing pulmonary vascular resistance with >80% oxygen, moderate hyperventilation (to a [P.sub.a]C[O.sub.2] of 30 to 35 mmHg), avoidance of lung overinflation, correction of metabolic acidosis, recruitment manoeuvres to minimise ventilation/ perfusion mismatch, and avoidance of endogenous catecholamine release by adequate analgesia and depth of anaesthesia. Hypothermia was prevented with a forced-air heating device. The initial central venous pressure after induction of anaesthesia was 13 cm[H.sub.2]O and right ventricular preload was optimised with cautious volume loading using 200 ml boluses of balanced crystalloid solution guided by continuous central venous pressure measurements, targeted at 12 to 14 mmHg. Specific therapy to augment right and left ventricular contractility and reduce right ventricular afterload by means of pulmonary vasodilatation included a loading dose (50 [micro]g/kg) followed by continuous infusion of milrinone (0.5 [micro]g/kg/minute). To counteract the systemic vasodilatory effects of milrinone, a noradrenaline infusion (1 to 5 [micro]g/minute) was instituted. The baby was expediently delivered but required tracheal intubation and external cardiac massage by the attending neonatologist for low Apgar scores. After delivery of the baby a Syntocinon infusion was commenced, at a low dose of 5 IU/hour, to augment maternal uterine contraction. Boluses of Syntocinon were avoided to minimise sudden increases in pulmonary vascular resistance or reductions in systemic vascular resistance. A tubal ligation was performed. The caesarean section was complicated by postpartum haemorrhage estimated to be 1000 ml.

Immediately post surgery, the patient deteriorated into acute renal failure, with worsening right heart failure refractory to escalating inotropic support. An adrenaline infusion (2 to 6 [micro]g/minute) was commenced to augment right ventricular function. Transoesophageal echocardiography now revealed an akinetic dilated right ventricle and septal bulge into a hyperdynamic and underfilled left ventricle. The pulmonary artery bifurcation was clear of thrombus. A pulmonary artery catheter was inserted under videofluoroscopic guidance and cardiac output was measured by continuous thermodilution (Vigilance, Continuous cardiac output monitor, Edwards Lifesciences, Irvine, CA, USA).

Urgent veno-arterial ECMO was instituted using a centrifugation pump, a pump controller (Capiox-SP -101, Terumo Inc., Tokyo, Japan) and heparinbonded circuit, to minimise heparin dosage and post-delivery bleeding. Under transoesophageal echocardiographic guidance, a 17-French multihole Biomedicus cannula was inserted into the right atrium via the femoral vein and a 20-Femflex perfusion cannula (Edwards Lifesciences, Irvine CA, USA) was inserted into the aorta through the femoral artery. Extracorporeal membrane oxygenation support was achieved with pump flows between 2.5 to 4 l/minute. Activated clotting time was maintained at 200 to 250 seconds. There was immediate stabilisation of the patient's haemodynamics, with mean pulmonary artery pressures reducing from 51 to 35 mmHg and cardiac index increasing from 1.2 to 2.0 l/minute/[m.sup.2]. Continuous veno-venous haemofiltration was instituted for acute renal failure.

[FIGURE 2 OMITTED]

Once haemodynamic stability had been achieved with ECMO, a repeat CTPA was performed, showing bilateral large pulmonary emboli involving the left and right pulmonary arteries and a pulmonary infarct of the left lower lobe (Figure 3). The patient was given radiologically-guided catheter-directed thrombolytic therapy using urokinase, combined with localised catheter suction embolectomy, at the first-order branches of the right and left pulmonary arteries. A 9-French guide catheter was inserted through an 11-French femoral sheath into the left and right pulmonary artery. An 8-French Hincke catheter was then inserted through the guide catheter and wedged into the large pulmonary clots on each side. Urokinase (300,000 IU) was administered directly into the clot, avoiding dissipation into the systemic circulation. Suction thrombectomy was performed by aspirating clot through the Hincke catheter. A continuous systemic urokinase infusion at 100,000 IU/hour was continued through the distal lumen of the pulmonary artery catheter for a further 24 hours, improving filling of the lower lobe pulmonary arteries on CTPA. A Cook Celect removable inferior vena cava filter was inserted into the infrarenal cava to prevent further embolism. The patient was successfully weaned off ECMO after four days and the pulmonary hypertension was treated with a combination of pulmonary vasodilators, including inhaled nitric oxide (20 to 40 ppm), intravenous epoprostenol (2 to 4 ng/kg/minute), and per oral (via nasogastric tube) bosentan (62.5 mg bd) and sildenafil (20 mg tds). The patient underwent a surgical tracheostomy on day 9 and was discharged from the intensive care unit on day 23. The inferior vena cava filter was successfully removed once the patient was adequately anticoagulated on warfarin. Follow-up CTPA confirmed that the emboli had decreased in size. Serial transthoracic echocardiography performed every three months showed gradual normalisation of right ventricular systolic function and pulmonary artery pressures. At eight months post discharge the right ventricular size and function had normalised and the estimated pulmonary artery systolic pressure was 25 mmHg. The patient remains on lifelong warfarin therapy and has a thriving, healthy child.

[FIGURE 3 OMITTED]

DISCUSSION

We have described a case of pulmonary embolism during pregnancy, associated with cardiogenic shock requiring ECMO and targeted thrombolysis. We consider that directed thrombolysis was life-saving and improved the patient's long-term cardiac function.

Thromboembolic pulmonary disease remains one of the most common causes of direct maternal mortality during pregnancy, accounting for up to 20% of all deaths4. Weiss and colleagues reviewed the outcome of pulmonary vascular disease in pregnancy and reported a maternal mortality rate of 30% in pulmonary arterial hypertension and 56% in patients with pulmonary hypertension from other causes (5). The highest mortality rate was in the first month after delivery and the five-year survival rate was particularly poor in those women of New York Heart Association functional class III or IV (6). In view of the high mortality of pulmonary hypertension during pregnancy, a multidisciplinary team should always be engaged to manage these patients (7).

Therapies for severe life-threatening pulmonary emboli can be divided into those directed at resolving the embolism, and those directed to relieving the compromised pulmonary circulation as a result of pulmonary hypertension. The management of pulmonary embolism is initially conservative, using either intravenous unfractionated heparin or low-molecular-weight heparin. If this proves unsuccessful then more invasive therapies are considered. These include systemic thrombolytic therapy, surgical thromboembolectomy and catheter-directed therapy. The latter includes different techniques, with or without pharmacological thrombolysis and mechanical embolectomy, including catheter-directed mechanical embolectomy and catheter-directed thrombolytic therapy, with or without mechanical fragmentation of the clot (8). The surgical selection of pregnant patients with decompensated pulmonary hypertension secondary to massive pulmonary embolus is complex and depends upon carefully defined factors such as the accessibility and presumed age of the thrombi defined by angiography, the degree of haemodynamic or ventilatory impairment as a consequence of the thromboembolic vascular obstruction, and risk-benefit of the intervention to both mother and foetus.

After considered multidisciplinary consultation with cardiac surgery, radiology, intensive care and anaesthesia, given the severity of the pulmonary hypertension, the haemodynamic compromise of this patient and the unknown age of the thrombi, we concluded that the risks associated with open thoracotomy and surgical thromboembolectomy were prohibitive. It was decided that localised catheter-directed thrombolytic therapy with mechanical catheter-directed embolectomy might be potentially life-saving.

There are very few reports in the literature of catheter-directed local thrombolytic therapy for the treatment of pulmonary embolism during pregnancy (8-11). The primary goal of a catheter-based approach to thrombolytic therapy is to improve the rate and efficiency of clot dissolution, with minimal risk of systemic fibrinolysis. This approach has the advantage of immediate removal or fragmentation of the obstructing clot, while avoiding the potential bleeding complications of systemic therapy (12), but no clear advantage of catheter-directed thrombolysis compared with intravenous thrombolysis has been shown (13). In non-pregnant patients with acute pulmonary embolus, no clinical trial or metaanalysis has been large enough to conclusively demonstrate that thrombolytic therapy followed by anticoagulation confers a mortality benefit compared with anticoagulation alone (14-16). Absolute contraindications to thrombolytic therapy include active internal bleeding, recent intracranial or intraspinal surgery, intracranial neoplasm, severe uncontrolled hypertension and known bleeding diathesis. Studies assessing changes in haemodynamics with thrombolysis are inconclusive but demonstrate improvements in right ventricular function, pulmonary arterial blood pressure and pulmonary perfusion when compared to patients receiving anticoagulation alone (16,17). In contrast, other studies have demonstrated more complete resolution of emboli in patients who received thrombolytic therapy, with haemodynamic benefits including lower pulmonary artery pressures and lower pulmonary vascular resistance (18-20). te Raa et al reviewed 13 cases of pregnant women who received treatment with thrombolytic therapy during pregnancy because of pulmonary embolism (21). Six received rt-PA, five streptokinase and two urokinase. There were no maternal deaths, four non-fatal major bleeding complications, two foetal deaths and five preterm deliveries, all just after initiation of thrombolytic therapy. Most authors agree that complication rates of thrombolytic therapy are acceptable and that systemic thrombolysis is beneficial for pregnant women with life-threatening thromboembolism with severe haemodynamic compromise.

While ECMO has been used to support patients with pulmonary hypertension in the non-obstetric population (22-24), there are few reports of its use to treat decompensated acute pulmonary hypertension during pregnancy. Satoh et al presented a case in which a pregnant patient with primary pulmonary hypertension needed ECMO support for successful termination of pregnancy (25). Sugioka et al reported a 27-year-old female with severe pulmonary hypertension and poor cardiopulmonary tolerance who required ECMO to tolerate the haemodynamic changes during surgery under general anaesthesia (26). Finally, Arlte et al reported a case of ECMO in a patient with cardiopulmonary failure and massive bleeding after thrombolysis for massive postpartum pulmonary embolism (27). We think that ECMO support should be considered in any pregnant patient who presents with pulmonary embolus, where there is extensive embolic burden associated with hypoxaemia and cardiogenic shock from right ventricular dysfunction.

Following thrombolytic therapy we used the endothelin-receptor antagonist bosentan, the phosphodiesterase type-5 inhibitor sildenafil, intravenous epoprostenol and inhaled nitric oxide to induce pulmonary vasodilatation and reduce right ventricular afterload. The non-selective endothelinreceptor antagonists, such as bosentan, are generally contraindicated during pregnancy, but may play an important role post-delivery (7). A meta-analysis of five randomised trials evaluated the use of endothelinreceptor antagonists on ambulant patients with pulmonary hypertension and showed beneficial effects on exercise capacity, dyspnoea and haemodynamic parameters such as cardiac index and pulmonary vascular resistance (28). Intravenous epoprostenol has also been widely evaluated in patients with pulmonary hypertension (29-35). It improves pulmonary haemodynamic parameters such as arterial blood pressure and pulmonary vascular resistance and has been advocated as an early intervention in patients with severe pulmonary hypertension. Inhaled nitric oxide stimulates guanylate cyclase to increase cGMP, causing pulmonary vasodilatation without systemic adverse effects (36,37). Given its ease of administration, tolerability and beneficial effects of reducing pulmonary vascular resistance and improving right ventricular function and cardiac index, nitric oxide was an appealing agent. Combining pharmacologic agents with different mechanisms of action may produce an additive effect or the same effect at lower doses of each drug (38).

In summary, we report a case of emergency caesarean section for decompensated pulmonary hypertension successfully treated with extracorporeal membrane oxygenation, localised catheter-directed pulmonary thrombolytic therapy using urokinase and catheter-directed suction embolectomy. Pregnant patients with confirmed or suspected thromboembolic pulmonary hypertension should be referred to a centre with expertise in the management of this disease, as tailored therapy will depend on the degree and location of the mechanical obstruction (central versus distal pulmonary arteries), the haemodynamic findings, the patient's comorbidities and the expertise of the treating centre. While the use of catheter-directed thrombolytic therapy, ECMO and combined advanced medical therapy proved successful in this case, specific therapy for this life-threatening problem should be on a case-by-case basis.

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(36.) Beck JR, Mongero LB, Kroslowitz RM, Choudhri AF, Chen JM, DeRose JJ et al. Inhaled nitric oxide improves hemodynamics in patients with acute pulmonary hypertension after high-risk cardiac surgery. Perfusion 1999; 14:37-42.

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(38.) Mathai SC, Girgis RE, Fisher MR, Champion HC, Housten Harris T, Zaiman A et al. Addition of sildenafil to bosentan monotherapy in pulmonary arterial hypertension. Eur Respir J 2007; 29:469-475.

L. WEINBERG *, C. KAY ([dagger]), F. LISKASER ([double dagger]), D. JONES ([section]), S. TAY ([dagger])([dagger]), S. JAFFE ([double dagger])([double dagger]), S. SEEVANAYAGAM ([double dagger])([double dagger]), L. DOOLAN ([section])([section])

Department of Anaesthesia, Austin Hospital, Heidelberg, Victoria, Australia

* B.Sc., M.B., B.Ch., M.R.C.P., F.A.N.Z.C.A., Dip. Crit Care. Echo., Anaesthetist, Department of Anaesthesia and Senior Fellow, Department of Surgery, University of Melbourne, Austin Hospital.

([dagger]) B.Sc., M.B., B.S. (Hons), Registrar.

([double dagger]) M.B., B.S., F.A.N.Z.C.A., Anaesthetist.

([section]) M.B., B.S., F.R.A.C.P., F.C.I.C.M., M.D., Intensivist, Department of Intensive Care.

** M.B., B.S., B.Med.Sci., Registrar.

([dagger])([dagger]) B.M., F.R.C.R., F.R.C.S. (Ed.), Fellow, Interventional Radiology, Department of Radiology.

([double dagger])([double dagger]) M.B., B.S., F.R.A.C.S., Cardiac Surgeon, Department of Cardiac Surgery.

([section])([section]) M.B., B.S., F.R.C.A., F.A.N.Z.C.A., Anaesthetist, Department of Anaesthesia and Intensivist, Department of Intensive Care.

Address for correspondence: Dr L. Weinberg, Staff Anaesthetist, Department of Anaesthesia, Austin Hospital, Studley Road, Heidelberg, Vic. 3081. Email: Laurence.Weinberg@austin.org.au

Accepted for publication on December 9, 2010.
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Title Annotation:Case Reports
Author:Weinberg, L.; Kay, C.; Liskaser, F.; Jones, D.; Tay, S.; Jaffe, S.; Seevanayagam, S.; Doolan, L.
Publication:Anaesthesia and Intensive Care
Article Type:Clinical report
Geographic Code:8AUST
Date:May 1, 2011
Words:3988
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