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.
