Journal of Datta Meghe Institute of Medical Sciences University

: 2017  |  Volume : 12  |  Issue : 4  |  Page : 289--291

Anesthetic management of chronic thromboembolic pulmonary hypertension for pulmonary endarterectomy

Nameirakpam Charan, Mangesh Choudhari, Manish Sonkusale, Rashmi Deshpande 
 Department of Cardiac Anaesthesia, JNMC, Wardha, Maharashtra, India

Correspondence Address:
Dr. Nameirakpam Charan
Room No. 6, New building Meghe heights, JNMC Campus, Sawangi Meghe, Wardha, Maharastra


Pulmonary endarterectomy (PEA) is considered treatment of choice for chronic thromboembolic pulmonary hypertension. The procedure dramatically improves functional status and provides an excellent immediate improvement and long-term survival, better than lung transplantation. PEA, until recently performed in only a few highly specialized centers, is now spreading worldwide with good results. We report successful anesthetic management of PEA under deep hypothermic circulatory arrest in our institute.

How to cite this article:
Charan N, Choudhari M, Sonkusale M, Deshpande R. Anesthetic management of chronic thromboembolic pulmonary hypertension for pulmonary endarterectomy.J Datta Meghe Inst Med Sci Univ 2017;12:289-291

How to cite this URL:
Charan N, Choudhari M, Sonkusale M, Deshpande R. Anesthetic management of chronic thromboembolic pulmonary hypertension for pulmonary endarterectomy. J Datta Meghe Inst Med Sci Univ [serial online] 2017 [cited 2020 Aug 3 ];12:289-291
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Full Text


Chronic thromboembolic pulmonary hypertension (CTEPH) is thromboembolic obstruction of the major pulmonary arteries resulting in pulmonary hypertension (mean PAP >25 mmHg).[1] CTEPH is a term proposed by Kenneth Moser from the University of California, San Diego.[2] The incidence of CTEPH is 0.1%–0.5% of nonfatal embolism cases, but in recent studies, the cumulative incidence of symptomatic CTEPH after an acute episode of pulmonary embolism without previous venous thromboembolism was found to be 1% at 6 months, 3.1% at 1 year, and 3.8% at 2 years of follow-up. Women are affected more frequently than men. Most patients have bilateral involvement.[3] In such patient's embolus do not resolve and thrombus becomes organized and form endothelialized, fibrotic obstruction of pulmonary vascular bed including the major branches of PA leading to pulmonary hypertension. They have no clinical symptoms for months (Honeymoon period) and develop dyspnea at exertion, and the clinical deterioration parallels to loss of right ventricle (RV) functional capacity.[3] Pulmonary endarterectomy (PEA) is considered permanently curative and the treatment of choice for CTEPH. It can only be done in multi-specialized centers. We report successful anesthetic management under deep hypothermic circulatory arrest (DHCA) of a case of CTEPH in our Institute.

 Case Report

A 41-year-old male patient was admitted with the complaints of difficulty in breathing and excessive sweating with mild exertion for 5 months and worsening of symptoms for 2 months. He was nonsmoker, nonalcoholic, nondiabetic, or hypertensive and not working in any factory. He was not responding to medical therapy and developed Grade III dyspnea. General physical examination revealed an anxious patient with RR 30/min, PR 100/min, BP 100/70 mmHg, and SPO2 on room air was 76%. His chest X-ray (CXR) showed increased bronchovascular markings. ECG showed a P Pulmonale, T-wave inversion in V1–V5, and right ventricular hypertrophy. Transthoracic echocardiography revealed hyperechoic filamentous oscillating mass (25 mm × 14 mm) in the right atrium, a dilated right atrium/RV and RV ejection fraction (RVEF) 20%, normal left ventricle ejection function (55%), and pulmonary artery systolic pressure of 50 mmHg. Venous Doppler ultrasound of the lower limbs showed no evidence of deep vein thrombosis. Pulmonary function tests showed a restrictive pattern. Arterial blood gas -Ph: 7.48, PaO2: 46.0, PCO2: 32.0, ABE: 3.8. Computed tomography pulmonary angiography revealed large nonenhancing heterogeneous lesion within the right atrium suggestive of thrombus or mass and also a thrombus in the distal right pulmonary artery and its segmental and nonsegmental branches [Figure 1] and [Figure 2]. Hb of 18 g% and negative D-dimer test.{Figure 1}{Figure 2}

The patient was given tablet nicoumalone (acitrom) 2 mg, tablet bosentan 125 mg OD, tablet sildinafil 20 mg OD, and tablet torsemide 10 mg OD 15 days before surgery.[4] Intraoperative monitoring was done with central venous pressure, intra-aortic balloon pump, SpO2, temperature, and entropy. General anesthesia was given with routine protocols in the presence of surgeon and perfusionist. After the full heparinization, patient was treated with cardiopulmonary bypass (CPB). Injection methylprednisolone 1 g was given before DHCA. The patient was gradually cooled to 20°C by standard protocols. Injection thiopental 500 mg and mannitol were given for cerebral protection. Pulmonary arteriotomy and embolectomy were done from the pulmonary arteries [Figure 3] and macro-emboli was removed with the help of Fogarty catheter. A total DHCA time of 5 min each was taken to perform the PEA. CPB was restarted after closing the pulmonary artery, the patient was rewarmed slowly up to 36.5°C and weaned off from the bypass with supports of injection milrinone and adrenaline.{Figure 3}

Postoperatively, the patient was kept on synchronized intermittent mandatory ventilation mode with 50%–70% FiO2 and a peep of 5–7 cm H2O to keep the PaO2 above 90 mmhg. Extubated after 48 h of ventilation with PaO2 80 mmhg with stable hemodynamics. CXR showed marked hyperperfusion of the lung which cleared over the next 3 days. The patient was treated with diuretics, methylprednisolone, and acitrom (international normalized ratio of 2.5–3).

BiPAP was given after extubation for 4 days as the saturation was falling (reperfusion injury) and O2 saturation maintained above 90%. Postoperative delirium was managed with haloperidol. The patient was shifted from Intensive Care Unit (ICU) on the 9th postoperative day (POD) with O2 supplementation. He was completely weaned off from oxygen therapy on the 20th POD and discharged from the hospital on 28 h day with O2 saturation of 96% on room air. Echo showed an RVEF of 40% and PA pressure of 35 mmHg. On follow-up after 1 month, he was asymptomatic and able to perform normal activities.


The idea in reporting this case is that a unique case was managed in our institution in a rural setup. The results are rewarding and creating awareness about the surgery. The problems faced by the anesthesiologist were preoperative pulmonary hypertension with chronic hypoxia, impending circulatory collapse during induction, problems of DHCA, postoperative prolonged ventilation and reperfusion injury.

Preoperatively, sildinafin and bosentan were started to reduce PH.[4] Acitrom was shifted to heparin. Induction was done with etomidate to avoid hemodynamic collapse in the presence of surgeon and perfusionist.[5],[6] During DHCA, thiopental, methylprednisolone, and mannitol were given along with slow rewarming for cerebral and vital organ protection.[7]

The specific complication observed in this surgery postoperatively is Reperfusion injury.(9.6%). It is defined as the presence of hypoxemia (PaO2/FiO2< 300 mmHg)[8] and new lung infiltrates in an area that had been reperfused, occurring in the absence of any other possible cause of hypoxemia or chest radiograph abnormality on days 1–3.[9],[10],[11] The underlying mechanism is thought to be the sudden onset of blood flow to the lung tissues which has not been exposed to the raised pulmonary vascular resistance.[12],[13] The patient had hypoxic episode after 8 h of extubation which might be attributed to reperfusion injury as there was no other obvious cause. Hence, the patient was treated with BIPAP and methylprednisolone for 3 days to reduce complement activation and cytokine release even though the role of steroid is doubtful. FiO2 was maintained as low as possible keeping O2 saturation above 90% with hematocrit 30%–32%.

In such patients, there is a potential for more subtle cognitive impairment due to prolonged CPB and DHCA. The patient had delirium which can be explained due to prolong ICU stay, CPB and DHCA. As a preventive measure, we had given thiopental, mannitol, steroids, and haloperidol.

Entropy monitoring might help us in diagnosing the major neurological events. The evidence for the inferior vena cava filter is low, and hence, we had not kept IVC filter. Management of persistent pulmonary hypertension after PEA can be done with ECMO [14] and medically with oral Rioaguat.[15]


PEA is a definitive and effective surgical treatment for CTEPH. A successful outcome depends on the proper preoperative diagnosis, evaluation, treatment of PH and intraoperative care. Conscientious postoperative management is required. Complications such as reperfusion injury, neurological deficit, and persistent PH should be remembered and needs multidisciplinary approach for management.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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