Saudi Journal for Health Sciences

: 2022  |  Volume : 11  |  Issue : 1  |  Page : 74--76

Challenges in managing postoperative pulmonary embolism after cesarean section

Manish Kumar Tiwary, Abhijit Sukumaran Nair 
 Department of Anaesthesiology, Ibra Hospital, Ministry of Health-Oman, Ibra, Sultanate of Oman

Correspondence Address:
Manish Kumar Tiwary
Department of Anaesthesiology, Ibra Hospital, Ministry of Health-Oman, P.O. Box 275, Ibra-414
Sultanate of Oman


Postoperative acute pulmonary embolism (APE) can be a life-threatening emergency and is associated with very high mortality. Approximately two-thirds of patients, who died of pulmonary embolism, die within the first hour after the presentation. We report a case of APE following an emergency lower segment cesarean section (LSCS) because of severe fetal distress. This 37-year-old female with no previous medical or surgical history underwent LSCS under general anesthesia. The surgery was uneventful and she was extubated uneventfully at the end of surgery. Six hours after surgery, there was a sudden drop in oxygen saturation on pulse oximetry, tachypnea which raised the suspicion of APE. An urgent chest radiograph computed tomographic pulmonary angiography (CTPA) and transthoracic echocardiogram along a sample for D-dimer were ordered immediately. CTPA was consistent with APE involving the main pulmonary artery. Given immediate postoperative status, therapeutic anticoagulation was done using low-molecular-weight heparin. The patient was discharged 10 days later. APE is a potentially high-risk event that can be challenging in the postoperative period. A high index of suspicion and therapeutic anticoagulation with meticulous monitoring is required in such cases to reduce morbidity.

How to cite this article:
Tiwary MK, Nair AS. Challenges in managing postoperative pulmonary embolism after cesarean section.Saudi J Health Sci 2022;11:74-76

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Tiwary MK, Nair AS. Challenges in managing postoperative pulmonary embolism after cesarean section. Saudi J Health Sci [serial online] 2022 [cited 2023 Jun 4 ];11:74-76
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Postoperative acute pulmonary embolism (APE) remains a significant medical problem.[1] Any surgery increases the risk of APE by five times in susceptible patients. The insult is triggered by vascular endothelial lesions due to surgical dissections, hypercoagulability induced by surgery per se, and venous stasis due to perioperative immobilization (Virchow's triad) which is characteristic in the peripartum period. The incidence of APE after lower segment cesarean section (LSCS) is 2.6 per 1000 (95% confidence interval, 1.7–3.5).[2] The following report describes a case of APE after an emergency LSCS.

 Case Report

A 37-year-old female, with a body mass index (BMI) of 28 kg/m2, and American Society of Anesthesiologist physical status II, was scheduled for emergency LSCS. There was no past medical history and the antenatal period was unremarkable. All relevant laboratory assessments were within normal limits. Emergency surgery was planned due to severe fetal distress (deceleration of fetal heart rate to 60/min). On arrival, the heart rate was 110/min and blood pressure of 128/82 mmHg. Preoxygenation with 100% oxygen was started and monitors were attached (non-invasive blood pressure, pulse oximeter, electrocardiography with lead II/V6). General anesthesia (GA) was administered with propofol 120 mg and succinylcholine 100 mg intravenously (IV). With a cricoid pressure applied by a colleague, endotracheal intubation was achieved using a 7.0 sized cuffed endotracheal tube which was confirmed on capnograph. Later, neuromuscular blockade was achieved with cisatracurium 8 mg. Mechanical ventilation was initiated with volume control mode (respiratory rate – 12–15/min, tidal volume – 400 ml). GA was maintained with oxygen: air (1:1) and sevoflurane 2 volume %. After the baby was delivered uneventfully, 100 μg IV fentanyl was administered, IV paracetamol 1 gm at the end of the time of skin closure, and skin infiltration using 40 ml of 0.25% bupivacaine. At the end of the surgery, neuromuscular blockade was reversed with neostigmine 2.5 mg and glycopyrrolate 0.4 mg, and tracheal extubation was done. Later, the patient was shifted to the ward for postoperative care after an observation period of 2 h in the recovery room.

Approximately 4 h later, the patient suddenly developed desaturation (Spo2 of 84–88%) and tachypnea (30–36/min). D-dimer revealed high values 5.5 (<0.5 μg/ml), suggesting APE. Arterial blood gas revealed respiratory alkalosis which was consistent with hyperventilation. Transthoracic echocardiogram showed a left ventricular ejection fraction of 55% along with mild tricuspid regurgitation. A computed tomographic pulmonary angiogram (CTPA) revealed filling defects in the segmental branches of the right and left pulmonary arteries suggestive of bilateral pulmonary embolism [Figure 1]a, [Figure 1]b, [Figure 1]c. There was also right lower lobe collapse with consolidation associated with mild displacement of mediastinal structures to the right. A bilateral lower limb Doppler was negative for deep vein thrombosis.{Figure 1}

Oxygen at 5 L/min with a face mask was initiated. As she was hemodynamically stable and being in an immediate postoperative state, therapeutic anticoagulation using low-molecular-weight heparin (enoxaparin) 6000 IU subcutaneous was started 12th hourly and was continued for 5 days. Subsequently, she was started on tablet warfarin 3 mg/day and was asked to continue for 3 months. Her condition improved gradually and she was discharged from the hospital uneventfully 10 days later.


Pregnancy is a hypercoagulable state and patients undergoing LSCS could develop deep vein thrombosis and subsequent APE. Theoretically, the chances are higher after GA than a central neuraxial blockade.[3],[4] Preoperative factors that could predict a postoperative APE are the use of second-generation oral contraceptive pills, cancer, elderly patients, smokers, obese patients, presence of indwelling central venous catheters. Intraoperative APE is usually associated with shock, changes in end-tidal carbon dioxide (an initial increase followed by decrease), tachycardia, desaturation, metabolic and respiratory acidosis. A postoperative APE in a spontaneously breathing patient manifests as tachycardia, tachypnea, desaturation, altered mentation, elevated jugular venous pressure, a gallop rhythm at the left sternal edge, an accentuated second heart sound, and occasionally wheezing.

An electrocardiogram could reveal new-onset changes such as sinus tachycardia, low-voltage complexes, right-axis deviation, complete or incomplete right bundle branch block, S1Q3T3 pattern (P-pulmonale, and T-wave inversion in anterior leads). Arrhythmias like atrial fibrillation/flutter, ventricular arrhythmias are seen in 5%–10% of patients. An ABG could reveal hypoxemia, hypocapnia, metabolic acidosis proportionate to underlying shock. A chest radiograph might not give essential information in an APE except in situations when there is pulmonary infarction manifesting as a Hampton's hump (wedge-shaped consolidation at the lung periphery), Westermark's sign (radiographic oligemia or increased lucency), and Fleischer sign (prominent pulmonary artery). A chest radiograph could be done to rule out other causes such as pneumothorax, pleural effusion, pneumonia, atelectasis.[5] The initial hemodynamic insult with APE is an obstruction to blood flow caused by emboli in the pulmonary vasculature and pulmonary outflow tract, leading to an acute increase in right ventricular impedance. The cardiovascular changes in APE are hypotension, increase right atrial pressure, increase pulmonary artery pressure and pulmonary vascular resistance, decreased cardiac output, decreased left atrial pressure, and an increased systemic vascular resistance. D-Dimer is although a sensitive test (96% to 98%) but is extremely nonspecific in the postoperative period as it can be elevated in many situations such as infection, cancer, trauma, and surgery itself. CTPA is considered the gold standard for diagnosing APE with a sensitivity of 85%.

There are no guidelines for anticoagulation in an APE in the immediate postoperative period. Thrombolysis is risky in the postoperative period and is reserved for patients who are hemodynamically unstable and are at less risk for bleeding. In a systematic review by Martillotti et al., the authors mentioned that more than 50% of women treated with thrombolysis in the postpartum period had major bleeding, which is much greater than the 9.9% risk of major bleeding for nonpregnant PE patients who underwent thrombolysis.[6] Pharmacological anticoagulation is preferred with subcutaneous LWMH and unfractionated heparin is preferred for patients with renal failure.[7] After the symptoms resolve, anticoagulants are recommended for 3 months and then a follow-up screening. Our patient was discharged with tablet warfarin 3 mg/day. Breastfeeding with warfarin has no serious consequences even with a dose as high as 25 mg/day.[8]

Declaration of patient consent

The authors certify that they have obtained all appropriate consent from the patient. The patient has given consent for the images and other clinical information to be reported in the journal. The patient understands that the name and initials will not be published and due efforts will be made to conceal the identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

The abstract of this case report was presented at KOREANESTHESIA-2021, which is the 98th annual scientific meeting of the Korean Society of Anesthesiologists' to be held in Busan, Korea, from November 4 to 6, 2021.


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