A 70-years-old male had no major medical history before until 4 years ago when he diagnosed as non-ST elevation myocardial infarction (NSTEMI), Killip 1. PCI was emergently introduced to the patient and coronary angiogram revealed coronary artery disease (CAD) with 2-vessel-occlusion. Successful percutaneous coronary angioplasty (PCA) from both radial arteries with 6F catheters and then drug-eluting stent (DES) for right coronary artery and left anterior descending artery were done. The patient had uneventful recovery following the procedure and he was discharged under DAPT control (aspirin at a dose of 100mg once daily and ticagrelor at a dose of 90mg twice daily). After 1 year of DAPT treatment, the medication was shifted to monotherapy with aspirin at a dose of 100mg once daily for 3 years.
Percutaneous coronary intervention
This time, he presented to a medical clinic with sudden onset retrosternal pain with radiation to back. After the transfer into our emergent room under the suspicion of ACS attack, the electrocardiogram disclosed equivocal ST-elevation with T-wave inversion. Ejection fraction of left ventricular was 61% in 2D-echocardiogram and Troponin-T was as high as 329.4 mg/dl. NSTEMI was impressed, 40mg methylprednisolone and local anesthesia with 2% lidocaine were prescribed as premedication. Cardiac catheterization revealed total occlusion of left circumflex artery majorly. PCI with 6F sheath was introduced from right radial artery and DES of Medtronic Resolute 2.5*38mm was placed to left circumflex artery. Activated clotting times of 290 to 300 seonds were maintained by using a weight-based dosing of 60 to 70 U/kg of heparin. DAPT (a aspirin at a dose of 100mg once daily and ticagrelor at a dose of 90mg twice daily) continued after the procedure.
Cauda equina syndrome
On admission to intensive care unit, vital signs were within normal ranges. Three hours after the PCI, he complained of severe backache from mid-thoracic to lower cervical level and it failed to relieve after acetaminophen 500mg oral intake. The patient stated no traumatic history since the last stent implantation 4 years ago. Then right leg weakness developed: Medical Research Council (MRC) scale down from 5/5 to 2/5, and it progressed to left lower extremity gradually. The strength of upper extremities remained intact. Bilateral pupil size was 3.0+/3.0+ and there was no sensation while urinating and defecating. Brain computed tomography for possible ischemic complication found no corresponding lesions. Neurological examination executed by the consulted neurologist disclosed acute paraplegia within 1 hour (MRC scale of bilateral lower extremities: 1/5) with hypoesthesia below T7 level, nearly anesthesia on lower limbs, and positive Babinski signs. Saddle anesthesia complicated with urine retention and incontinence led to indwelling catheter dependent. Rectal examination showed flaccid anal sphincter and reflex of bilateral Achilles’ tendon decreased.
The patient had no chest pain, dyspnea exacerbation, loss of consciousness, dizziness, upper limbs weakness, facial palsy, disorientation, and blurred speech. The neurologist suggested CES rather than ischemic stroke. The auxiliary data of the blood and coagulation parameters showed mildly decreased platelet count (145 /L) and high Troponin-T (2336 mg/dl) but other coagulation factors were within the normal range (Table 1). Magnetic resonance imaging (MRI) of the spine revealed multiple intraspinal hematomas, include: C5 to T3 segmental subdural hematoma ventral to the spinal cord (Fig. 1AB), T4 to T8 epidural hematoma compressed the spinal cord dorsally (Fig. 1CD), and intrathecal hematoma at L5 to S1 deviated the nerve roots from normal distribution (Fig. 1EF). Interrupted intraspinal hematomas distorted the cord and cauda equina.
Dexamethasone phosphate 5mg was given via intravenous route to reduce secondary neurological insults and acetaminophen was held due to critical bleeding with increasing Troponin-T. The neurosurgery team discussed the urgent situation about CES and possible treatment options with his daughter. After the hesitation of other family members, surgical decompression carried out immediately within 8 hours after neurological symptoms attacks. L5 to upper S2 wide laminectomy was performed initially for the incontinence (Fig. 2A). A 4.5 cm cyst content with blood compressed underlying eliminated (Fig. 2AB) and further neurolysis to roots of the cauda equina executed cautiously under the microscope (Fig. 2C). No anatomical variations were detected during surgery. Dural closure was accomplished after good hemostasis (Fig. 2D).
Due to incomplete spinal cord impairment below T7 level, we decided to perform limited T7 to T9 laminectomy to evacuate the epidural hematoma. Liquefied hematoma gashed out with pressure and was aspirated to achieve full cord decompression. Two epidural drains guaranteed the relief of epidural pressure then. Total operation time was 6 hours and blood loss was 400cc. 12U platelet transfusion was done following the operation. We took conservative observation to cervical subdural hematoma because no obvious neurological signs over upper limbs and no severe cord compromised by hematoma.
After the surgery, we withdrew ticagrelor and adjusted the DAPT as aspirin at a dose of 100mg once daily and clopidogrel at a dose of 90mg once daily. Intravenous dexamethasone phosphate 10mg continued four times daily. Immediately, muscle strength of left lower leg near totally recovered on postoperative day 1 (MRC scale of left lower extremity: 4/5). The neurological deficits kept improving include saddle sensation and he was transferred to neurosurgery ward under lumbar brace protection on postoperative day 2 as gradually declined Troponin-T level. On postoperative day 5, epidural drains were pulled out. Muscle strength of lower extremities continued improving after the hemovac drains removal on postoperative days 5 through 9. The movement became symmetry (MRC scale of bilateral lower extremities: 4+/5) on postoperative day 10 under comprehensive rehabilitation. And he started to aware urination and stool passage but still was unable to control it. He tried the catheter removal but failed due to hematuria and the difficulty in voiding after that. On postoperative day 15, he could sit at a wheelchair stably without numbness over the saddle area. On postoperative day 17, the patient was able to ambulation without assistance. He was discharged home without fecal incontinence on day 30. The outpatient urology follow-up was arranged since Foley catheter dependence.
DAPT therapy backed to aspirin and ticagrelor after the hematuria improved. Benign prostatic hyperplasia was diagnosed at the urology clinics. After medication, self urination achieved one month later (Fig. 3). Two months after the surgery, spinal MRI revealed the resolution of hematomas and the regression of the mass effect over the whole spinal cord but residual seroma over the lumbosacral junction left (Fig. 1G). The patient returned to his normal life independently without obvious neurological sequelae.
Half-year later, he received scheduled PCI for the restenosis of previous DES noted by the last coronary angiogram. DES for left main to the proximal anterior descending artery and distal right coronary artery were installed smoothly under proper sedation and analgesics control. There were no bleeding complications of the PCI. The same DAPT continued to prevent stent thrombosis and the benefits of neurosurgical intervention maintained without recurrence till now (Fig. 4). The seroma was replaced by contrast-enhancing granulation at L5 level in MRI follow-up 18 months after the operation leading to mild numbness over right calf laterally which didn’t influence the quality of daily life (Fig. 1H).