Multidisciplinary Management of Acute Pulmonary Thromboembolism Following Lumbar Spinal Fusion Surgery: A Case Report

Abstract

Acute pulmonary thromboembolism (PTE) is a life-threatening complication. Although uncommon, acute PTE can develop silently during prolonged immobility associated with long-duration surgery, particularly in high-risk patients. Prompt diagnosis and effective management can help in salvaging such patients. Here, we present the case of a 40-year-old African female who developed acute PTE soon after turning the patient from prone to supine position with continuous monitoring following spinal fusion surgery. This case report highlights an unusual presentation of acute PTE, which was managed successfully by both the neuroanesthesia and cardiac sciences teams. An integrated, multidisciplinary team approach was the key to her revival.

Keywords

Pulmonary thromboembolism - lumbar spinal fusion - neuroanesthesia - cardiac anesthesia - pulmonary embolism response team

Introduction

Symptomatic PTE following spine surgery is rare.[1] The onset can be acute and often difficult to diagnose under general anesthesia (GA).[2] Given the precipitous pathophysiology, almost one-third of patients die of shock if not diagnosed or treated in time.[3] This report represents an unusual case of acute PTE, which was promptly diagnosed due to uninterrupted monitoring even during transfer of the patient from prone to supine, and treated by a multimodal team approach, which prevented mortality and morbidity.

Case Report

A 40-year-old, ASA II, African female presented to the neurosurgery department with a history of severe low back pain radiating to both her legs for the last 2 months. Magnetic resonance imaging of the lumbosacral spine revealed diffuse disc bulge and lumbar canal stenosis involving L2–L5. The patient was advised three-level transforaminal lumbar interbody fusion and pedicle screw and rod fixation.

On preoperative examination, the patient was obese (weight: 99 kg, height: 160 cm, body mass index: 38.67) and had a history of oral contraceptive use and occasional smoking. However, she had a good exercise tolerance. But, for the last 2 weeks, her mobility was restricted due to excruciating low back pain. Other systemic examinations were unremarkable. Her hematological and biochemical parameters were within an acceptable range, including D-dimer levels. Her chest X-ray, electrocardiogram (ECG), echocardiogram (ECHO), and lower limb Doppler for deep venous thrombosis (DVT) screening were also normal. However, she was hepatitis B positive.

In the operating room, the patient was monitored with ASA standard monitoring; i.e., ECG, heart rate (HR), blood pressure (BP), pulse oximetry (SpO₂), and end-tidal carbon dioxide (EtCO₂). The patient was induced with fentanyl 100 μg and propofol 140 mg, followed by rocuronium 80 mg to facilitate orotracheal intubation. Anesthesia was maintained using oxygen: air (50:50) and sevoflurane. Rocuronium (10 mg) and fentanyl (50 μg) boluses were used whenever deemed necessary. An intranasal temperature probe was placed in the oropharynx for monitoring of core temperature. The left radial artery was cannulated for continuous intra-arterial pressure monitoring. An intermittent pneumatic compression pump was applied to both legs. The patient was then turned to the prone position on bolsters. Normothermia was ensured using a forced-air warming device. The surgery was uneventful and lasted for 7 hours. Her hemodynamic parameters were stable throughout the intraoperative period. Estimated blood loss was 700 to 800 mL. She received 4,000 mL of crystalloids as a transfusion. Two arterial blood gas (ABG) analyses done post-induction and at the start of surgical closure were within an acceptable range ([Table 1]).

Table 1 Perioperative ABG trend

	pH	pCO2	pO2	Lactate	BE	HCO3 −	Hb	Na+	K+	Glucose
Post-induction	7.413	35.7	238.2	1.9	−2.3	24.3	13.4	138	3.98	154
Before closure	7.386	39.6	204.7	3.2	−3.5	22.1	9.1	142	3.59	117
After turning supine (30 min)	6.936	82.4	85.5	13.5	−13.9	14.6	6.5	148	2.9	229
Following resuscitation in the ICU (3 h)	7.284	26.6	389	4.5	−10.4	16.1	9.7	137	4.1	149

After the completion of surgical dressing, the patient was turned supine with monitors in situ. Immediately thereafter, there was a fall in BP (115/59 to 54/26 mm Hg), EtCO₂ (37–4 mm Hg), and SpO₂ (100–88%), with sustained cardiac activity (HR: 50–60/min). Cardiopulmonary resuscitation (CPR), vasopressor infusions (noradrenaline, adrenaline, vasopressin, and dobutamine), and other resuscitative measures were initiated immediately as per advanced cardiac life support protocol.[4] With the sudden and persistent fall in BP, EtCO₂, SpO₂, and absent ST-T changes, acute PTE was strongly suspected, and an urgent cardiac assistance was sought, who were nearby, to perform transesophageal echocardiography (TEE). TEE revealed dilated right atrium (RA) and right ventricle (RV), severe tricuspid regurgitation (TR), decreased flow across the pulmonary artery (PA), normal contracted left ventricle (LV) with no visible flow, and contracted inferior vena cava, substantiating PTE. Heparin 2,500 IU was administered, CPR continued, and vasopressor infusions were titrated to effect. Necessary corrections were initiated as per ABG ([Table 1]). To maintain preload and distal vascular bed oxygenation, packed red blood cells (PRBC) were transfused along with fluid boluses. Pulmonary angiography was deferred because of her cardiovascular instability, and the patient was shifted to the cardiology intensive care unit (ICU) for further management.

In the ICU, the patient experienced yet another episode of hypotension. Volume resuscitation with PRBC and 25% human albumin was conducted. Vasopressor infusions were escalated. Heparin 2,500 IU was administered and continued every 8 hours, as there was no operative site bleeding following the initial bolus. Transthoracic echocardiography (TTE) revealed decreasing RV dilatation and improved PA blood flow, while lower limb Doppler screening was negative for DVT. We maintained mild passive hypothermia (around 35°C) throughout the resuscitation period.

Following the sustained resuscitative measures of more than 3 hours, vitals gradually stabilized, with slow tapering of ionotropic support. The patient was kept ventilated overnight. ABG was repeated at regular intervals, and necessary corrections were conducted. With sustained improvement in hemodynamics, vasopressors were also gradually weaned off. On the first postoperative day (POD), the patient was conscious, and the hemodynamics were maintained within normal range with very little vasopressor support, and the patient was extubated. On the fourth POD, the patient was switched to a therapeutic dose of low-molecular-weight heparin. A repeat lower limb Doppler was also negative for DVT. However, on the sixth POD, the patient again developed tachypnea with desaturation. Transthoracic ECHO showed dilated RA, RV, inferior vena cava, severe TR, and embolus in PA bifurcation ([Fig. 1A, B]). Computed tomography pulmonary angiography (CTPA) was performed, which diagnosed a saddle thrombus extending from the level of bifurcation into bilateral right and left PA ([Fig. 2A]). The cardiothoracic and vascular surgery team performed surgical embolectomy with removal of the residual clots using Fogarty catheter ([Fig. 2B]). The patient was kept electively ventilated and extubated the following day. Her postoperative course was uneventful, and she was discharged from the hospital on the 25th POD.

Fig. 1 Transthoracic Echocardiography image showing dilated RA and RV (A) and an anechoic filling defect at the level of the pulmonary artery, suggesting probable embolus (B).

Fig. 2 Computed tomography pulmonary angiography image (A) showing a central hypodense filling defect at the level of the main pulmonary artery (PA) bifurcation, suggestive of a saddle embolus (red arrow), and extending into the left (pink arrow) and right PA (blue arrow). (B) The embolus, measuring around 25 cm, retrieved through surgical embolectomy.

Discussion

Acute PTE is a rapidly progressive, devastating complication. The risk of PTE is fivefold higher in the general surgical population.[5] However, the risk of acute PTE is much higher among patients undergoing invasive neurosurgical procedures.[6] The detection can be delayed or even missed as the clinical features are often masked under GA. However, in our case, there was non-ambiguity in the clinical diagnosis of PTE because of the severe hypotension, abrupt and sustained fall in EtCO₂, and SpO₂, which we could detect immediately due to continuous monitoring of the patient while shifting the patient from the prone to the supine position. Additionally, smoking, obesity, oral contraception use, hepatitis virus-positive status, long-distance travel in a sitting position, long-duration surgery, and invasive neurosurgical procedures were risk factors of PTE in our patient.[3] [6] We presume thrombus may have been formed in the pelvic veins following prolonged spine surgery, which ostensibly got dislodged while flipping the patient from the operating table to the bed.

Despite effective resuscitation, the patient remained hypotensive, for which the cardiac anesthesiologist's intervention was sought. They advised TEE to rule out acute myocardial infarction and PTE. The TEE evidence was strongly suggestive of PTE. Although CTPA remains the gold standard for diagnosis, it was deferred in our case as the patient was hemodynamically unstable. However, on the sixth POD, the patient developed tachypnoea with desaturation, for which TTE and later CTPA were done, which revealed a large thrombus on the pulmonary bifurcation.

The mortality rate following cardiac arrest secondary to PTE is as high as 95%.[7] So, the management of PTE centers around resuscitative measures till hemodynamic stability is restored. Norepinephrine was used to improve RV function and coronary perfusion, dobutamine to increase the cardiac output, and epinephrine to prevent the vasodilatory effect and increase the efficacy of dobutamine.[8] Vasopressin was used to increase the vascular response to catecholamine (norepinephrine) and decrease the risk of arrhythmia due to excessive catecholamine.[9] [10] If we had not resorted to external cardiac compression, the patient might have developed cardiac arrest.

Concurrent with resuscitation, systemic thrombolysis with heparin was started in the event of imminent threat to life despite increased risk of hemorrhagic complications. There was an initial gradual clinical recovery following thrombolysis. But the patient had a delayed onset of tachypnoea on the sixth POD, for which TTE followed by CTPA were done, which confirmed PTE. Subsequently, the patient underwent pulmonary thrombectomy, which was uneventful.

We strongly feel that in postoperative emergencies, cardiac anesthesiologists, if available, should be involved to perform the TEE or TTE for diagnostic evaluation. Second, they are much better trained in managing vasopressor therapy. Most importantly, in cases of refractory hypotension, they are better equipped to assess and initiate extracorporeal membrane oxygenation as a treatment modality.[11]

For the prevention and effective management of acute PTE, departments should have their own protocol, and we strongly recommend the creation of a multidisciplinary pulmonary embolism response team in hospitals for the timely and effective management of such acute life-threatening emergencies.

Conclusion

Acute PTE can develop silently in the perioperative period, and eternal vigilance with “no touch technique” to detach monitors “at any point” is the key to prompt diagnosis. Strong suspicion, early initiation of external cardiac massage if necessary, and sustained resuscitative measures in collaboration with cardiac anesthesiologists can prevent mortality, morbidity, and improve overall functional outcome.

Conflict of Interest

None declared.

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Publikationsverlauf

Artikel online veröffentlicht:
12. Dezember 2025